rhinitis pt4 1998

Diagnosis and Management of Rhinitis:Complete Guidelines of the Joint Task Forceon Practice Parameters in Allergy, Asthmaand ImmunologyMark S Dykewicz, MD, Stanley Fineman, MD, MBA, EditorsDavid P Skoner, MD, Chair, Workgroup on RhinitisRichard Nicklas, MD\; Rufus Lee, MD; Joann Blessing-Moore, MD; James T Li, MD, PhD**;I Leonard Bernstein, MD; William Berger, MD, MBA; Sheldon Spector, MD; andDiane Schuller, MD,\\ Associate Editors

This document contains complete guidelines for diagnosis and management ofrhinitis developed by the Joint Task Force on Practice Parameters in Allergy,Asthma and Immunology, representing the American Academy of Allergy, Asthmaand Immunology, the American College of Allergy, Asthma and Immunology andthe Joint Council on Allergy, Asthma and Immunology. The guidelines are com-prehensive and begin with statements on clinical characteristics and diagnosis ofdifferent forms of rhinitis (allergic, non-allergic, occupational rhinitis, hormonalrhinitis [pregnancy and hypothyroidism], drug-induced rhinitis, rhinitis from foodingestion), and other conditions that may be confused with rhinitis. Recommenda-tions on patient evaluation discuss appropriate use of history, physical examination,and diagnostic testing, as well as unproven or inappropriate techniques that shouldnot be used. Parameters on management include use of environmental controlmeasures, pharmacologic therapy including recently introduced therapies and aller-gen immunotherapy. Because of the risks to patients and society from sedation andperformance impairment caused by first generation antihistamines, second genera-tion antihistamines that reduce or eliminate these side effects should usually beconsidered before first generation antihistamines for the treatment of allergic rhi-nitis. The document emphasizes the importance of rhinitis management for co-morbid conditions (asthma, sinusitis, otitis media). Guidelines are also presented onspecial considerations in patients subsets (children, the elderly, pregnancy, athletesand patients with rhinitis medicamentosa); and when consultation with an allergist-immunologist should be considered.

Ann Allergy Asthma Immunol 1998;81:478518.

CONTRIBUTORS: Donald W Aaronson, MD;Allen D Adinoff, MD; James N Baraniuk, MD;Robert J Dockhorn, MD; William Dolen,MD; Howard M Druce, MD; Marianne Frieri,MD, PhD; Morton P Galina, MD; Leon Greos, MD;Alfredo A Jalowayski, PhD; Craig F La Force,MD; Eli O Meltzer, MD; Robert M Naclerio,MD; Keith M Phillips, MD; Gordon Raphael, MD;Michael Schatz, MD; Michael J Schumacher,MBBS; Howard J Schwartz, MD; Tommy CSim, MD; Chester T Stafford, MD; William WStorms, MD; Michael J Tronolone, MD; Mi-chael J Welch, MD; Chester C Wood, MD; andRobert S Zeiger, MD, PhD

PRINCIPAL REVIEWERS: Jean A Chap-man, MD; Robert A Nathan, MD; John Santilli,Jr, MD; Michael Schatz, MD; and Betty B Wray,MD

This document was developed by the JointTask Force on Practice Parameters in Allergy,Asthma and Immunology, representing theAmerican Academy of Allergy, Asthma and Im-munology (AAAAI), the American College ofAllergy, Asthma and Immunology (ACAAI) andthe Joint Council on Allergy, Asthma and Im-munology. The AAAAI and the AACAAI havejointly accepted responsibility for establishingthese practice parameters. Because this docu-

ment incorporated the efforts of many partici-pants, no single individual, including those whoserved on the Joint Task Force, is authorized toprovide an official interpretation of this docu-ment by the AAAAI or ACAAI. Any request forinformation about or an interpretation of thisdocument by the AAAAI or ACAAI should bedirected to the Executive Offices of the AAAAI,ACAAI and the Joint Council on Allergy,Asthma and Immunology.

* This parameter was developed with Dr.Nicklas in his private capacity and not in hiscapacity as a medical officer with the Food andDrug Administration. No official support or en-dorsement by the Food and Drug Administrationis intended or should be inferred.

Division of Allergy and Immunology, De-partment of Internal Medicine, Saint LouisUniversity School of Medicine, St. Louis, Mis-souri; Department of Pediatrics, Emory Uni-versity School of Medicine, Atlanta, Georgia; Departments of Pediatrics & Otolaryngology,Childrens Hospital of Pittsburgh, Universityof Pittsburgh School of Medicine, Pittsburgh,Pennsylvania; \ Department of Medicine,George Washington Medical Center, Washing-ton, DC; Departments of Medicine & Pediat-rics, Stanford University Medical Center, PaloAlto, California; ** Department of Medicine,Mayo Clinic & Medical School, Rochester, Min-nesota; Departments of Medicine & Environ-mental Health, University of Cincinnati Collegeof Medicine, Cincinnati, Ohio; Department ofPediatrics, Division of Allergy and Immunology,University of California College of Medicine,Irvine, California; Department of Medicine,University of California-Los Angeles, Los An-geles, California; \\ Department of Pediatrics,Pennsylvania State University, Milton S. Her-shey Medical College, Hershey, Pennsylvania.

The Joint Task Force has made an intenseeffort to appropriately acknowledge all contrib-utors to this parameter. If any contributors areinadvertently excluded, the Task Force will in-sure that appropriate recognition of such contri-butions is subsequently made.

478 ANNALS OF ALLERGY, ASTHMA, & IMMUNOLOGY

Contents and Organization of this DocumentSummaryStatement

Page

INTRODUCTION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 480

DEFINITION OF RHINITIS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 480

DIFFERENTIAL DIAGNOSIS OF RHINITIS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 480

Allergic Rhinitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 312 480

Non-Allergic rhinitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13 484

Infectious rhinitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14 485

Non-Allergic rhinitis without eosinophilia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15 485

Non-Allergic rhinitis with eosinophilia syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 486

Occupational rhinitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17 486

Hormonal rhinitis (pregnancy and hypothyroidism) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18 487

Drug-induced rhinitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19 487

Rhinitis from food ingestion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20 487

Other conditions that may be confused with rhinitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21 488

Nasal polyps . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22 489

EVALUATION OF RHINITIS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 489

History . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2324 489

Physical examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25 491

Testing for specific IgE . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26 492

Special diagnostic techniques . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27 493

Nasal cytology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 28 494

Total serum IgE, blood eosinophil counts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29 495

Unproven or inappropriate testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30 495

MANAGEMENT OF RHINITIS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 497

Environmental control measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31 497

Pharmacologic therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32 500

Antihistamines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3335 501

Issues with sedation/performance impairment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34 501

Cardiac effects of some antihistamines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35 501

Intranasal antihistamines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 36 505

Oral and nasal decongestants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37 505

Nasal corticosteroids . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38 506

Oral and parenteral corticosteroids . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39 506

Intranasal cromolyn . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40 507

Intranasal anti-cholinergics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41 508

Oral anti-leukotriene agents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 42 510

Allergen immunotherapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43 510

Surgical approaches for co-morbid conditions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 44 511

Important considerations in management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45 511

Education of patient and caregivers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 46 511

Importance of rhinitis management for concomitant asthma, sinusitis, and otitis media . . . . . . . . . . . . . . . . 47 512

Special considerations in children, the elderly, pregnancy, athletes, and rhinitis medicamentosa . . . . . . . . . 48 513

Consultation with an allergist-immunologist . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 49 518

VOLUME 81, NOVEMBER (PART II), 1998 479

INTRODUCTIONRhinitis may be caused by allergic,non-allergic, infectious, hormonal, oc-cupational and other factors. All toooften, important causes of rhinitis gounrecognized by both physicians andpatients. This leads to suboptimal con-trol of the disease.

Rhinitis is a significant cause ofwidespread morbidity. Althoughsometimes mistakenly viewed as atrivial disease, symptoms of rhinitismay significantly impact the patientsquality of life, by causing fatigue,headache, cognitive impairment andother systemic symptoms. Appropriatemanagement of rhinitis may be an im-portant component in effective man-agement of co-existing or complicatingrespiratory conditions, such as asthma,sinusitis, or chronic otitis media. Thecost of treating rhinitis and indirectcosts related to loss of workplace pro-ductivity resulting from the disease aresubstantial. The estimated cost of al-lergic rhinitis based on direct and in-direct costs is 2.7 billion dollars for theyear 1995, exclusive of costs for asso-ciated medical problems such as sinus-itis and asthma. Allergic rhinitis, themost common form of rhinitis, affects20 to 40 million people in the UnitedStates annually, including 10% to 30%of adults and up to 40% of children.

This document reviews clinicallyrelevant information about pathogene-sis and provides guidelines about diag-nosis and management of rhinitis syn-dromes. Throughout the document,summary statements that articulate keypoints precede supporting text and rel-evant citations of evidence-based pub-lications.

DEFINITION OF RHINITIS1. Rhinitis is defined as inflamma-

tion of the membranes lining thenose, and is characterized by na-sal congestion, rhinorrhea, sneez-ing, itching of the nose and/orpostnasal drainage.

Rhinitis can be defined as a heteroge-neous disorder characterized by one ormore of the following nasal symptoms:sneezing, itching, rhinorrhea, and/ornasal congestion. Rhinitis frequently is

accompanied by symptoms involvingthe eyes, ears, and throat. Post-nasaldrainage may also be present fre-quently.

Reference1. Druce HM. Allergic and nonallergic

rhinitis. In: Middleton EJ, Reed CE,Ellis EF, et al, eds. Allergy principlesand practice, 5th edition. St. Louis:Mosby-Year Book Inc, 1998:10051016.

DIFFERENTIAL DIAGNOSIS OFRHINITIS2. Rhinitis should be classified by

etiology as allergic or nonaller-gic.

Allergic rhinitis is a very commoncause of rhinitis. However, since ap-proximately 50% of patients with rhi-nitis do not have allergic rhinitis, otherpotential causes must also be ruledout.13 The following outline lists dif-ferent forms of allergic and non-aller-gic rhinitis, and conditions that maymimic rhinitis.I. Allergic rhinitis

A. SeasonalB. PerennialC. EpisodicD. Occupational (may also be non-

allergic)II. Non-allergic rhinitis

A. Infectious1. Acute2. Chronic

B. NARES syndrome(Nonallergic rhinitis with eo-sinophilia syndrome)

C. Perennial nonallergic rhinitis(Vasomotor rhinitis)

D. Other rhinitis syndromes1. Ciliary dyskinesia syndrome2. Atrophic rhinitis3. Hormonally-induced

A. HypothyroidismB. PregnancyC. Oral contraceptivesD. Menstrual cycle

4. Exercise5. Drug-Induced

A. Rhinitis medicamentosaB. Oral contraceptivesC. Anti-hypertensive ther-

apy

D. AspirinE. Nonsteroidal anti-in-

flammatory drugs6. Reflex-Induced

A. Gustatory rhinitisB. Chemical or irritant-in-

ducedC. Posture reflexesD. Nasal cycleE. Emotional factors

7. Occupational (may be aller-gic)

III. Conditions that may mimic symp-toms of rhinitisA. Structural/mechanical factors

1. Deviated septum/septal wallanomalies

2. Hypertrophic turbinates3. Adenoidal hypertrophy4. Foreign bodies5. Nasal tumors

A. BenignB. Malignant

6. Choanal atresiaB. Inflammatory/immunologic

1. Wegeners granulomatosis2. Sarcoidosis3. Midline granuloma4. Systemic lupus erythemato-

sus5. Sjogrens syndrome6. Nasal polyposis

C. Cerebrospinal fluid rhinorrhea

References1. Lieberman P. Rhinitis. In: Bone RC,

ed. Current practice of medicine. vol 2.Philadelphia: Churchill Livingstone1996; VII:5.1VII:5.10.

2. Mygind N, Anggard A, Druce HM.Definition, classification, and termi-nology [of rhinitis]. In: Mygind N,Weeke B, eds. Allergic and vasomotorrhinitis. Copenhagen, Munksgaard,1985;15.

3. Sibbald B, Rink E. Epidemiology ofseasonal and perennial rhinitis: clinicalpresentation and medical history. Tho-rax 1991;46:895901.

Allergic Rhinitis3. Allergic rhinitis affects 20 to

40 million people in the UnitedStates annually, including 10%to 30% of adults and up to 40%of children.


4. The severity of allergic rhinitisranges from mild to seriouslydebilitating.

5. The cost of treating allergic rhi-nitis and indirect costs related toloss of workplace productivityresulting from the disease aresubstantial. The estimated costof allergic rhinitis based on di-rect and indirect costs is 2.7 bil-lion dollars for the year 1995,exclusive of costs for associatedmedical problems such as sinus-itis and asthma. Rhinitis is also asignificant cause of lost schooldays.

6. Risk factors for allergic rhinitisinclude: (1) family history ofatopy; (2) serum IgE > 100IU/mL before age 6; (3) highersocioeconomic class; (4) expo-sure to indoor allergens such asanimals and dust mites; (5) pres-ence of a positive allergy skinprick test.

Rhinitis is reported to be a very fre-quent disease, although data regardingthe true prevalence of rhinitis are dif-ficult to interpret. Most population sur-veys rely upon physician-diagnosedrhinitis for their data, and this maygive rise to a much lower reporting ofrhinitis. Some population studies havebeen done with questionnaires admin-istered to the subjects followed inmany cases by telephone interviews totry to make a specific diagnosis ofrhinitis. These studies may reflect amore accurate prevalence of rhinitisbut probably still underreport this dis-ease.17

Most epidemiologic studies havebeen directed towards seasonal allergicrhinitis, or hay fever, since this symp-tom complex with its reproducible sea-sonality is somewhat easier to identifyin population surveys. Perennial aller-gic rhinitis is more difficult to identifybecause its symptom complex mayoverlap with chronic sinusitis, recur-rent upper respiratory infections, andvasomotor rhinitis.

The prevalence of rhinitis in variousepidemiologic studies ranges from 3%to 19%. Studies suggest that seasonalallergic rhinitis (hay fever) is found in

approximately 10% to 20% of the pop-ulation.2,810 One study showed a prev-alence of physician-diagnosed allergicrhinitis in 42% of 6-year-old children.3Overall, allergic rhinitis affects 20 to40 million individuals in the UnitedStates annually.11,12

In childhood, males with allergicrhinitis outnumber females, but thegender ratio becomes approximatelyequal in adults and may even favorfemales. Surveys of medical studentshave resulted in a higher prevalence ofrhinitis, but this may be related to thesurvey technique.1,6,8

Allergic rhinitis develops before age20 in 80% of cases. Studies haveshown that the frequency of allergicrhinitis increases with age until adult-hood and that positive immediate hy-persensitivity skin tests are significantrisk factors for the development of newsymptoms of seasonal allergic rhini-tis.1,8,13 There is a greater chance of achild developing allergic rhinitis ifboth parents have a history of atopy,than if only one parent is atopic. Chil-dren in families with a bilateral familyhistory of allergy generally developsymptoms before puberty; those with aunilateral family history tend to de-velop their symptoms later in life ornot at all.5,10

There tends to be an increased prev-alence of allergic rhinitis in higher so-cioeconomic classes, in non-whites, insome polluted urban areas, and in in-dividuals with a family history of al-lergy. Allergic rhinitis is more likely infirst-born children. Studies in childrenin the first years of life have shownthat the risk of rhinitis was higher inthose youngsters with early introduc-tion of foods or formula, heavy mater-nal cigarette smoking in the first yearof life, exposure to indoor allergenssuch as animals and dust mite, higherserum IgE levels (.100 IU/mL beforeage 6), and parental allergic disorders.3

Seasonal allergic rhinitis is appar-ently becoming more common. Onestudy showed that the prevalence ofhay fever increased from 4% to 8% inthe 10 years from 1971 to 1981.14 Inanother study, atopic skin test reactiv-

ity increased from 39% to 50% in dur-ing an 8-year period of evaluation.15

The impact on society is tremen-dous.16 The severity of allergic rhinitisranges from mild to seriously debilitat-ing. The cost of treating allergic rhini-tis and indirect costs related to loss ofworkplace productivity resulting fromthe disease are substantial. The esti-mated cost of allergic rhinitis based ondirect and indirect costs is 2.7 billiondollars for the year 1995, exclusive ofcosts for associated medical problemssuch as sinusitis and asthma. The totaldirect and indirect cost estimates forallergic rhinitis have been reported tobe $5.3 billion for 1996. This figureincluded the higher indirect costs asso-ciated with increased loss of produc-tivity, which, in turn, was related toextensive over-the-counter antihista-mine use. Such treatment can causedrowsiness and impair cognitive andmotor function (see summary state-ment #34).

Rhinitis is also a significant cause oflost school attendance, resulting inmore than 2 million absent school daysin the US annually. In children, there isevidence that symptoms of allergic rhi-nitis can impair cognitive functioning,which can be further impaired by theuse of first generation antihistamines.17

References1. Hagy GW, Settipane GA. Prognosis of

positive allergy skin tests in an asymp-tomatic population. J Allergy 1971;48:200.

2. Druce HM. Allergic and nonallergicrhinitis. In: Middleton EJ, Reed CE,Ellis EF, et al. Allergy principles andpractice, 5th edition. St. Louis: Mosby-Year Book Inc, 1998:10051016.

3. Wright AL, Holberg CJ, Martinez FD,et al. Epidemiology of physician-diagnosed allergic rhinitis in child-hood. Pediatrics 1994;94(6):895901.

4. Aberg N, Engstrom I. Natural historyof allergic diseases in children. ActaPediatr Scan 1990;79:206211.

5. Aberg N, Engstrom I, Lindberg U. Al-lergic diseases in Swedish school chil-dren. Acta Paediatr Scan 1989;78:246252.

6. Fougard T. Allergy and allergy-likesymptoms in 1,050 medical students.Allergy 1991;46:2026.


7. Aberg B, Hesselmar B, Eriksson B.Increase of asthma, allergic rhinitisand eczema in Swedish school chil-dren between 1979 and 1991. Clin ExpAllergy 1995;25:815819.

8. Settipane RJ, Hagy GW, SettipaneGA. Long-term risk factors for devel-oping asthma and allergic rhinitis: a23-year follow-up study of college stu-dents. Allergy Proc 1994;51:2125.

9. Varyonen E, Kalimo K, LammintaustaK. Prevalence of atopic disordersamong adolescents in Turku, Finland.Allergy 1992;47:243248.

10. Smith JM. A five-year prospective sur-vey of rural children with asthma andhay fever. J Allergy 1971;47:2331.

11. Fireman P. Allergic rhinitis. In: Fire-man P, Slavin RG, eds. Atlas of aller-gies. Philadelphia, PA: JB Lippincott,1991:9.29.18.

12. McMenamin P. Costs of hay fever inthe United States in 1990. Ann Allergy1994;73:3539.

13. Tang RB, Tsai LC, Hwang B, et al.The prevalence of allergic disease andIgE antibodies to house dust mite inschool children in Taiwan. Clin ExpAllergy 1990;20:3338.

14. Linna O, Kokkonen J, Lukin M. A10-year prognosis for childhood aller-gic rhinitis. Acta Pediatr 1992;81:100102.

15. Sibbald B, Rink E, OSouza M. Is theprevalence of atopy increasing? Br JGen Pract 1990;40:338340.

16. Ross RN. The costs of allergic rhinitis.Am J Managed Care 1996;2:285290.

17. Vuurman EF, van Veggel LM, Uiter-wijk MM, et al. Seasonal allergic rhi-nitis and antihistamine effects on chil-drens learning. Ann Allergy 1993;71:121126.

7. The symptoms of allergic rhinitis re-sult from a complex allergen-drivenmucosal inflammation resultingfrom an interplay between residentand infiltrating inflammatory cells,and a number of inflammatory me-diators and cytokines. Sensory nerveactivation, plasma leakage and con-gestion of venous sinusoids also con-tribute.

The nasal mucosa is designed to hu-midify and clean inspired air. The ac-tions of epithelium, vessels, glands,and nerves are carefully orchestrated toperform these functions.1 Dysfunctionof any of these structures may contrib-

ute to the symptoms of allergic andnonallergic rhinitis.2

References1. Raphael GR, Baraniuk JN, Kaliner

MA. How and why the nose runs. JAllergy Clin Immunol 1991;87:457467.

2. Baraniuk JN. Neural control of the up-per respiratory tract. In: Kaliner MA,Barnes PJ, Kunkel GK, Baraniuk JN,eds. Neuropeptides in respiratory med-icine. New York: Marcel Dekker, Inc1995;79123.

8. Allergic rhinitis may be character-ized by early and late phase re-sponses. Each type of response ischaracterized by sneezing, conges-tion and rhinorrhea, but congestionpredominates in the latter.

Atopic subjects inherit the tendency todevelop IgE-mast cell-TH2 lympho-cyte immune responses. Exposure tolow concentrations of dust mite fecalproteins, cockroach, cat, dog and otherdanders, pollen grains, or other aller-gens for prolonged periods of timeleads to the presentation of the allergenby antigen presenting cells (APC) toCD41 lymphocytes that release IL3,IL4, IL5, GM-CSF and other cyto-kines. These promote IgE productionagainst these allergens by plasma cells,mast cell proliferation and infiltrationof airway mucosa, and eosinophilia.

Early or immediate allergic re-sponse. With continued allergen expo-sure, increasing numbers of IgE-coatedmast cells move into the epithelium,recognize the mucosally-deposited al-lergen, and degranulate.1 Mast cellproducts include preformed mediatorssuch as histamine, tryptase (a mast cellspecific marker), chymase (in con-nective tissue mast cells only), kini-nogenase (generates bradykinin), hep-arin, and other enzymes. Newlyformed mediators include prostaglan-din D2 and the cysteinyl-leukotrienesLTC4, LTD4, and LTE4. These media-tors stimulate vessels to leak and pro-duce edema plus watery rhinorrhea;stimulate glands to exocytose their mu-coglycoconjugates and antimicrobialsubstances; and dilate arteriole-venuleanastomoses to cause sinusoidal filling

and occlusion of nasal air passages.Sensory nerves are stimulated that con-vey the sensations of nasal itch andcongestion, and initiate systemic re-flexes such as sneezing paroxysms.Release of these mast cell mediatorsand induction of these reactions occurwithin minutes of allergen exposure,and are termed the early or immediateallergic response.2 While most subjectsexperience sneezing and copious rhi-norrhea after allergen exposure, somesubjects have sensations of nasal con-gestion as their predominant symptom.

Late phase response. The mast cellsmediators, including the cytokines, arethought to act upon post-capillary en-dothelial cells to promote VCAM andE-selectin expression that permits cir-culating leukocytes to stick to the en-dothelial cells. Chemoattractants, suchas IL-5 for eosinophils, promote theinfiltration of the superficial laminapropria of the mucosa with some neu-trophils and basophils, many eosino-phils, and, at later time points, T lym-phocytes and macrophages.3,4 Over thecourse of 4 to 8 hours, these cells be-come activated and release their medi-ators, which in turn activate many ofthe proinflammatory reactions of theimmediate response. This late occur-ring inflammatory reaction is termedthe late phase response. While thisreaction may be clinically similar tothe immediate reaction, congestiontends to predominate.5 Eosinophilproducts such as major basic protein,eosinophil cationic protein, hypochlor-ate, leukotrienes and others are thoughtto damage the epithelium and othercells, an inflammatory response thatpromotes the tissue damage of chronicallergic reactions.

TH2 lymphocytes are thought toplay a critical role in promoting theallergic response by releasing theircombination of IL3, IL4, IL5, andother cytokines that promote IgE pro-duction, eosinophil chemoattractionand survival in tissues, and mast cellrecruitment.6 Cytokines released fromTH2 lymphocytes, mast cells, eosino-phils, basophils and epithelial cellsmay circulate to the hypothalamus andpromote the fatigue, malaise, irritabil-


ity, and neurocognitive deficits thatcommonly afflict those suffering fromallergic rhinitis. Glucocorticoids areeffective at reducing the release ofthese cytokines during late phase re-sponses.7

Priming response. When allergenchallenges are given repeatedly, theamount of allergen required to inducean immediate response decreases.8This priming effect is thought to bedue to the influx of inflammatory cellsduring ongoing, prolonged allergen ex-posure and repeated late phase re-sponses. This response is clinically im-portant, since exposure to one allergen(eg, early spring tree pollen) may pro-mote the more exaggerated later re-sponses to another allergen (eg, latespring grass pollen). This priming ef-fect demonstrates the importance ofknowing the full spectrum of allergensto which a patient responds, the sea-sons of their allergic responses, andhighlights the need to initiate effectiveanti-inflammatory therapies beforepollen seasons and allergen exposuresso that the inflammatory allergic phasewill not occur.

References1. Naclerio RM. Allergic rhinitis. N Engl

J Med 1991;325:860869.2. Mygind N, ed. Allergic and nonaller-

gic rhinitis clinical aspects. Phila-delphia: Saunders, PA, 1993.

3. Naclerio RM, Proud D, Togias AG, etal. Inflammatory mediators in late an-tigen-induced rhinitis. N Engl J Med1985;313:6570.

4. Bascom R, Pipkorn U, LichtensteinLM, Naclerio RM. The influx of in-flammatory cells into nasal washingsduring late response to antigenchallenge: effect of corticosteroid pre-treatment. Am Rev Respir Dis 1988;138:406412.

5. Skoner DP, Doyle WJ, Boehm S, Fire-man P. Late phase eustachian tube andnasal allergic responses associatedwith inflammatory mediator elabora-tion. Am J Rhinol 1988;2:155161.

6. Durham SR, Sun Ying M, Varney VA,et al. Cytokine messenger RNA ex-pression for IL-3, IL-4, IL-5 and gran-ulocyte/macrophage-cloning-stimulat-ing factor in the nasal mucosal afterlocal allergen provocation: relation-

ship to tissue eosinophilia. J Immunol1992;148:23902394.

7. Sim TC, Reece LM, Hilsmeier KA, etal. Secretion of chemokines and othercytokines in allergen-induced nasalresponses: inhibition by topical steroidtreatment. Am J Respir Crit Care Med1995;152:927933.

8. Connell JT. Quantitative intranasalpollen changes. III. The priming effectin allergic rhinitis. J Allergy 1969;50:4344.

Seasonal and Perennial AllergicRhinitis9. Symptoms of allergic rhinitis

may occur only during specificseasons, may be perennial with-out seasonal exacerbation, pe-rennial with seasonal exacerba-tion, or may occur sporadicallyafter specific exposures.

10. Seasonal allergic rhinitis iscaused by an IgE-mediated re-action to seasonal aeroallergens.Typical seasonal aeroallergensare pollens and molds. Thelength of seasonal exposure tothese allergens is dependent ongeographic location.

11. Perennial allergic rhinitis iscaused by an IgE-mediated re-action to perennial environmen-tal aeroallergens. These may in-clude dust mites, molds, animalallergens, or certain occupa-tional allergens, as well as pollenin areas where pollen is preva-lent perennially.

12. Allergic rhinitis often coexistswith allergic conjunctivitis.

Symptoms of allergic rhinitis may in-clude paroxysms of sneezing, nasalpruritus (itching) and congestion, clearrhinorrhea and palatal itching. In se-vere cases, mucous membranes of theeyes, eustachian tube, middle ear andparanasal sinuses may be involved.This produces conjunctival irritation(itchy, watery eyes), redness and tear-ing, ear fullness and popping, itchythroat, and pressure over the cheeksand forehead. Malaise, weakness andfatigue may be present. The coinci-dence of other allergic syndromes suchas atopic eczema or asthma, and a pos-itive family history of atopy, point to-

ward an allergic etiology. Around 20%of cases are accompanied by symp-toms of asthma.1

When all the typical rhinitis symp-toms are not expressed, the diagnosisis more difficult to make. Chronic na-sal obstruction alone may be the majorsymptom of perennial rhinitis due toongoing inflammation and late-phaseallergic reactions.2 Distinct temporalpatterns of symptom production mayaid diagnosis. Symptoms of rhinitiswhich occur whenever the patient isexposed to a furry pet suggest IgE-mediated sensitivity to that pet. Pa-tients who are exquisitely sensitive toanimal proteins may develop symp-toms of rhinitis and asthma when en-tering a house or laboratory eventhough the animal is no longer present.Exposure to airborne allergens in theworkplace may produce symptomsonly at work with symptom-free peri-ods away from work. Seasonal and pe-rennial forms of allergic rhinitis oftencoexist in the same individual. Symp-toms may be chronic and persistentand patients may present with second-ary complaints of mouth-breathing,snoring, or symptoms of sinusitis.3

Seasonal allergic rhinitis symptomstypically appear during a defined sea-son in which aeroallergens are abun-dant in the outdoor air. Familiaritywith the pollinating season of the ma-jor trees, grasses and weeds of the lo-cale makes the syndrome easier to di-agnose.4,5 Certain outdoor mold sporesalso display seasonal variation, withhighest levels in the summer and fallmonths.6 Tree (eg, birch, oak, maple,mountain cedar), grass, and weed (eg,ragweed) pollens, and fungi (molds:Alternaria, Aspergillus, Cladospo-rium) are common seasonal allergens.Priming effects, increases in sensorynerve irritability, and mucosal infiltra-tion by activated eosinophils, mastcells, and TH2 lymphocytes have beenidentified. Hyperresponsiveness to ir-ritant triggers such as tobacco smoke,noxious odors, changes in temperature,and exercise may persist beyond theactual pollen season.

In studies of allergic seasonal rhini-tis, a correlation between the daily pol-


len count and overall daily symptomscore and medication score has beenfound. The symptoms on any particu-lar day will be influenced by exposureon that day but also on previous daysdue to the priming phenomenon. As aconsequence, at the end of the pollenseason, it is usual to observe a declinein symptoms which is slower than thatof the pollen counts themselves.7 Indi-vidual sensitivity will also influencethe intensity of symptoms. In highlysensitive individuals, many symptomsoccur with pollen counts of 15 to 75pollen grains/m3 per 24 hours, whereasin the less sensitive, 4 to 10 times thisexposure may be necessary to provokeequivalent symptoms.8 The levels ofpollen counts that cause symptomsmay vary with an individuals degreeof sensitivity and with different pol-lens.9

In perennial allergic rhinitis the re-sponsible allergens are present in theenvironment throughout the year, andare usually indoor. Chronic exposureto dust mites (Dermatophagoidespteronyussinus, D. farinae), cock-roach, perennial molds, cat, dog andother danders leads to persistent tissueedema and infiltration with eosino-phils, mast cells, TH2 lymphocytes,and macrophages.10 Chronic allergenexposure with unremitting recruitmentof inflammatory cells often requirescorticosteroids for control. In somesubjects, nasal congestion and mucusproduction (post-nasal drip) symptomspredominate, and sneezing and wateryrhinorrhea may be minimal.

References1. Evans III R. Epidemiology and natural

history of asthma, allergic rhinitis, andatopic dermatitis. In: Middleton E, Jr,Reed CE, Ellis EF, et al, eds. Allergy:principles and practice. 4th edition. St.Louis: Mosby, 1993:11091136.

2. Skoner DP, Doyle WJ, Boehm S, Fire-man P. Late phase eustachian tube andnasal allergic responses associatedwith inflammatory mediator elabora-tion. Am J Rhinol 1988;2:155161.

3. Lucente FE. Rhinitis and nasal ob-struction. Otolaryngol Clin North Am1989;22:307318.

4. Jelks M. Allergy plants that cause

sneezing and wheezing, Tampa:Worldwide Publications, 1986.

5. Lewis WH, Vinay P, Zenger VE. Air-borne and allergic pollen of NorthAmerica, Baltimore: Johns HopkinsUniversity Press, 1983.

6. Platts-Mills TAE, Hayden ML, Chap-man MD, Wilkins SR. Seasonal varia-tion in dust mite and grass pollen al-lergens in dust from the houses ofpatients with asthma. J Allergy ClinImmunol 1987;79:781791.

7. Brostrom G, Moller CA. A newmethod to relate symptom scores withpollen counts. A dynamic model forcomparison of treatments of allergy.Grana 1990;28:123128.

8. Taudorf E, Moseholm L. Pollen count,symptom and medicine score in birthpollinoses. A mathematical approach.Int Arch Allergy Appl Immunol 1988;86:225233.

9. Solomon WR, Platts-Mills TAE. Aer-obiology and inhalant allergens. In:Middleton EJ, Reed CE, Ellis EF, et al,eds. Allergy principles and practice,5th edition. St. Louis: Mosby-YearBook Inc, 1998;367403.

10. Bradding P, Feather IH, Wilson S, etal. Immunolocalization of cytokines inthe nasal mucosa of normal and peren-nial rhinitis subjects. J Immunol 1993;151:38533865.

Non-Allergic Rhinitis13. Nonallergic rhinitis is character-

ized by sporadic or persistent pe-rennial symptoms of rhinitis thatdo not result from IgE-mediatedimmunopathologic events. Exam-ples of nonallergic rhinitis areinfectious rhinitis, hormonal rhi-nitis, vasomotor rhinitis, nonaller-gic rhinitis with eosinophilia syn-drome (NARES), certain types ofoccupational rhinitis, and gusta-tory and drug-induced rhinitis.

The differential diagnosis of nonaller-gic rhinitis is extensive.1 The mecha-nisms in each are poorly understood.Nonallergic rhinitis with inflammatorycells present in the mucosa can be clas-sified by inflammatory cell type.

Nonallergic rhinitis with eosino-philia syndrome (NARES) is charac-terized by nasal congestion and prom-inent nasal eosinophilia. (see summarystatement #15) The mechanism of theeosinophil infiltration is not known.

Eosinophilia is also prominent whennasal polyps are present, but again themechanism of eosinophil recruitmentis not known. Subjects with aspirinsensitivity have nasal eosinophilia. As-pirin and other nonsteroidal antiin-flammatory drugs (NSAIDs) block cy-clooxygenase activity, and shuntarachidonic acid to the 5-lipoxygenasepathway that increases production ofthe potent proinflammatory cysteinylleukotrienes (LTC4, LTD4, and LTE4).2

Neutrophilic infiltrates usually indi-cate the presence of bacterial rhinosi-nusitis, especially when humoral im-munodeficiency or ciliary dysmotilityare present. LTB4, IL8, bacterial prod-ucts, and complement fragments maycontribute to their recruitment and ac-tivation. Neutrophilic infiltrates mayalso be present in rhinoviral and otherviral rhinitis syndromes. Early in rhi-novirus infections there is an increasein vascular permeability that is likelydue to bradykinin. Later, there may bean increase in glandular secretion, par-ticularly of locally synthesized secre-tory IgA.

There are several causes of nonaller-gic rhinitis without inflammation/in-flammatory cells. Endocrine changesof hypothyroid and hyperthyroid dis-ease, and pregnancy can lead to unre-mitting nasal congestion. Damage tosympathetic nerves, as in Hornerssyndrome, can ablate sympathetic va-soconstrictor tone and lead to unop-posed vasodilatory parasympathetic re-flexes and chronic nasal congestion.Overuse of topical-adrenergic ago-nists/nasal decongestants also leads tochronic nasal congestion (rhinitismedicamentosa).

Vasomotor rhinitis is unrelated toallergy, infection, structural lesions,systemic disease, or drug abuse. (seesummary statement #16) Although theterm vasomotor implies increased neu-ral efferent traffic to the blood vesselssupplying the nasal mucosa, this hasnever been proven. Subjects with va-somotor rhinitis fall into two generalgroups: runners who have wet rhi-norrhea, and dry subjects with pre-dominant symptoms of nasal conges-tion and blockage to airflow, and


minimal rhinorrhea. These reactionscan be provoked by nonspecific irritantstimuli such as cold dry air, perfumes,paint fumes, and cigarette smoke. Sub-jects with predominantly rhinorrhea(sometimes referred to as cholinergicrhinitis) appear to have enhanced cho-linergic glandular secretory activity,since atropine effectively reduces theirsecretions.3 Subjects with predomi-nantly nasal congestion and blockagemay have nociceptive neurons thathave heightened sensitivity to innocu-ous stimuli.

Emotional factors such as stress andsexual arousal are known to have aneffect on the nose, probably due toautonomic stimulation.4

References1. Mygind N, Naclerio RM, eds. Allergic

and nonallergic rhinitis. Philadelphia,PA: 1993.

2. Christie PE, Tagari P, Ford-Hutchin-son AW, et al. Urinary leukotriene E4concentrations increase after aspirinchallenge in aspirin sensitive subjects.Am Rev Respir Dis 1991;143:10251102.

3. Stjarne P, Lundblad L, Lundberg JM,Anggard A. Capsaicin and nicotinesensitive afferent neurons and nasal se-cretion in healthy human volunteersand in patients with vasomotor rhinitis.Br J Pharmacol 1989;96:693701.

4. Eiser N. The hitch-hikers guide to na-sal airway patency. Respir Med 1990;84:179183.

Infectious Rhinitis14. Infectious rhinitis may be acute

or chronic. Acute infectious rhi-nitis is usually due to one of alarge number of viruses, but sec-ondary bacterial infection withsinus involvement is a commoncomplication. Symptoms ofchronic infectious rhinosinusitisinclude mucopurulent nasal dis-charge, facial pain and pressure,olfactory disturbance, and post-nasal drainage with cough.

Acute rhinitis is usually associatedwith a viral upper respiratory infection,but may follow trauma.1 Symptoms ofacute viral rhinitis include rhinorrhea,nasal obstruction, and fever. Initially,

viral rhinitis is characterized by clear,watery rhinorrhea that is accompaniedby sneezing and nasal obstruction.Edema of the nasal mucosa producesocclusion of the sinus ostia with result-ing facial pain or of the eustachian tubewith resulting ear fullness. The nasaldrainage may become cellular andcloudy due to the presence of organ-isms, white blood cells and desqua-mated epithelium. Responsible virusesinclude rhinoviruses, respiratory syn-cytial virus, parainfluenza, influenzaand adenoviruses. Unless there is bac-terial superinfection, the condition isself-limiting and usually resolveswithin 7 to 10 days. Acute bacterialrhinitis may occur de novo or mayfollow viral rhinitis. Nasal obstruction,cloudy drainage, vestibular crustingand facial pain occur. Not all patientsreport fever. Bacteria frequently recov-ered from nasal or sinus cultures in-clude Streptococcus pneumoniae,group-A beta-hemolytic Streptococciand Hemophilus influenzae.2 In pa-tients with immunodeficiency, HIVpositivity, or acquired immunodefi-ciency syndrome (AIDS), mycobacte-rial, fungal, and other opportunistic or-ganisms may be involved.

The symptoms of allergic rhinitisare frequently confused with infectiousrhinitis when patients complain of aconstant cold. Purulent nasal drainagemay be present in either infectious ornon-infectious rhinitis. Symptoms per-sisting longer than two weeks shouldprompt a search for causes other thaninfection. Foreign body rhinitis shouldbe considered in the differential diag-nosis, especially in children. Symp-toms may be acute or chronic, unilat-eral or bilateral, and the nasaldischarge may be blood-stained orfoul-smelling.

Exacerbations of rhinitis symptomswith predominant clear rhinorrhea inpatients with a known history of aller-gic rhinitis may prove to be a diagnos-tic difficulty. The distinction betweenactive infection and allergy should bemade. When the history or physicalexamination is not diagnostic, a nasalsmear may be obtained to aid in dif-ferentiation.

There is controversy about whetherchronic infectious rhinitis (diagnosedafter 8 to 12 weeks of symptoms) canexist in the absence of chronic sinus-itis. Symptoms of chronic infectiousrhinosinusitis can include nasal con-gestion, predominantly purulent nasaldischarge, facial pain, and pressure, ol-factory disturbances and post-nasaldrainage with cough.3

Allergy, mucociliary disturbance andimmune deficiency may predispose cer-tain individuals to the development ofchronic infection.4,5 Mucociliary abnor-malities may be congenital, as in primaryciliary dyskinesia,6 Youngs syndrome,7or cystic fibrosis, or secondary to infec-tion. Similarly, immune deficiency maybe congenital or acquired.

References1. Noble SL, Forbes RC, Woodbridge

HB. Allergic rhinitis. Am Fam Physi-cian 1995;51:837846.

2. Gwaltney JM, Scheld M, Sande MA,Sydnor A. The microbial etiology andantimicrobial therapy of adults withacute community-acquired sinusitis: afifteen-year experience at the Univer-sity of Virginia and review of otherselected studies. J Allergy Clin Immu-nol 1992;90:457462.

3. Kaliner MA, Osguthorpe JD, FiremanP, et al. Sinusitis: bench to bedside. JAllergy Clin Immunol 1997;99:S289S847.

4. MacKay IS, Cole P. Rhinitis, sinusitisand associated chest disease. In:MacKay IS, Null TR, eds. Scott-Browns otolaryngology. vol. 4. Rhi-nology. London: Butterworths. 1987;6192.

5. Lund VJ, Scadding GK. Immunologicaspects of chronic sinusitis. Can J Oto-laryngol 1991;105:181185.

6. Afzelius BA. A human syndromecaused by immotile cilia. Science1976;193:317319.

7. Young D. Surgical treatment of maleinfertility. J Reprod Fertil 1970;23:541542.

Non-Allergic Rhinitis WithoutEosinophilia15. Nonallergic, noninfectious rhini-

tis, generally termed vasomotorrhinitis, comprises a heteroge-neous group of patients with


chronic nasal symptoms that arenot immunologic or infectious inorigin and usually not associatedwith nasal eosinophilia. Most ofthese patients develop rhinitis inresponse to environmental con-ditions, such as cold air, highhumidity, strong odors and in-haled irritants.

The term vasomotor rhinitis has beenused loosely to describe patients withperennial rhinitis whose symptoms areintensified by changes in temperatureor relative humidity, alcohol, odorssuch as bleach, perfume or solvents,bright lights or hot spicy foods, andirritants such as tobacco smoke, dustsand automotive emission fumes. Thisdisorder is not due to allergy or infec-tion, nor is it associated with nasaleosinophilia. The symptoms are vari-able, consisting mainly of nasal ob-struction and increased secretion.Sneezing and pruritus are less com-mon. Although the term vasomotor im-plies increased neural efferent traffic tothe blood vessels supplying the nasalmucosa, this has never been proven.Some investigators prefer to use thedescriptive term nonallergic or id-iopathic rhinitis that does not implyknown pathophysiology.

Reference1. Druce HM. Allergic and nonallergic

rhinitis. In: Middleton EJ, Reed CE,Ellis EF, et al, eds. Allergy principlesand practice, 5th edition. St. Louis:Mosby-Year Book Inc, 1998:10051016.

Non-allergic Rhinitis withEosinophilia Syndrome16. The nonallergic rhinitis with eo-

sinophilia syndrome (NARES) ischaracterized by nasal eosino-phils in patients who have pe-rennial symptoms and occasion-ally loss of sense of smell. Thesepatients lack evidence of allergicdisease as demonstrated by lackof clinically significant positiveskin tests and/or specific IgE an-tibodies in the serum.

In the NARES syndrome, individualsexperience perennial symptoms of

sneezing paroxysms, profuse wateryrhinorrhea and nasal pruritus and oc-casional loss of smell.1,2 Patients aretypically middle-aged and have a char-acteristic perennial course but withparoxysmal episodes. Nasal smears re-veal eosinophils during symptomaticperiods. Patients lack evidence of al-lergic disease as determined by skintesting or by serum levels of IgE anti-body to specific allergens. It is difficultto assess the prevalence of this syn-drome in the general population. Theetiology of the syndrome is obscure,but may be an early stage of aspirinsensitivity.3

References1. Jacobs RL, Freedman PM, Boswell

RN. Non-allergic rhinitis with eosino-philia (NARES syndrome): clinicaland immunologic presentation. J Al-lergy Clin Immunol 1981;67:253.

2. Mullarkey MF. Eosinophilic nonaller-gic rhinitis. J Allergy Clin Immunol1988;82:941949.

3. Moneret-Vautrin DA, Shieh V, Way-off M. Non-allergic rhinitis with eosin-ophilia syndrome (NARES)a pre-cursor of the triad. Ann Allergy 1990;64:513518.

Occupational Rhinitis17. Occupational rhinitis refers to

rhinitis arising in response toairborne substances in theworkplace, which may be medi-ated by allergic or nonallergicfactors, eg, laboratory animalantigen, grain, wood dusts, andchemicals. It often coexists withoccupational asthma.

Occupational rhinitis may be definedas sneezing, nasal discharge and/orcongestion caused by exposure to anairborne agent present in the work-place. Triggering substances may beirritants, such as tobacco smoke, coldair, formaldehyde, hair sprays, orchemicals acting apparently throughnon-immunologic mechanisms. Alter-natively, occupational exposure mayinvolve IgE-mediated reactions trig-gered by allergens such as laboratoryanimals (rats, mice, guinea pigs, etc.),animal products, grain (bakers and ag-ricultural workers), coffee beans, wood

dusts (particularly hard woods such asmahogany, western red cedar, iroko),latex, chemicals (eg, acid anhydrides,platinum salts, glues), mites, moldspores, pollen, psyllium, enzymes, anda litany of other substances. This dis-order frequently coexists with occupa-tional asthma. Occupational rhinitismay precede development of occupa-tional asthma.

Symptoms may occur acutely atwork after intermittent exposure ormore chronically at work after contin-uous exposure. Occupational rhinitisshould be suspected in patients withnasal symptoms which are temporallyrelated to exposure at work and whichimprove away from the workplace. Foroccupational allergens, skin testingmay confirm sensitivity, if appropriatereagents are available. The most spe-cific diagnostic test for occupationalrhinitis is a challenge with the sus-pected agent, either naturally in theworkplace setting or in a medical set-ting. Optimally, in addition to symp-tom scores, such a challenge could in-clude pre-challenge and post-challengemeasures of nasal airway resistance us-ing anterior rhinomanometry.

The optimal management of occupa-tional rhinitis is avoidance of the oc-cupational trigger, either by modifyingthe workplace, use of filtering masks,or removing the patient from the ad-verse exposure. If this is impossible,pharmacologic therapy as discussed inearlier sections should be instituted,recognizing that chronic use of medi-cation will probably be required foradequate relief and prevention ofsymptoms. Strategies to prevent or re-duce symptoms may include the dailyuse of anti-inflammatory intranasalcorticosteroids or the administration ofantihistamines and/or intranasal cro-molyn immediately prior to allergenexposure. It is also important to insti-tute avoidance measure for non-occu-pational allergens that may contributeto rhinitis symptoms.

References1. Murphy EE, Slavin RS. Occupational

rhinitis: when to suspect, what to do. JRespir Dis 1995;16:135142.


2. Lund VJ, Aaronson D, Bousquet J andThe International Rhinitis Manage-ment Working Group. InternationalConsensus Report on the Diagnosisand Management of Rhinitis. Allergy1994;49(Suppl 19):134.

3. Druce HM. Allergic and nonallergicrhinitis. In: Middleton EJ, Reed CE,Ellis EF, et al, eds. Allergy principlesand practice, 5th edition. St. Louis:Mosby-Year Book Inc, 1998:10051016.

Hormonal Rhinitis18. Causes of hormonal rhinitis in-

clude pregnancy and hypothy-roidism. Although symptoms ofrhinitis, in particular nasal con-gestion, may occur during preg-nancy, most notably from thesecond month to term, thesesymptoms usually disappearrapidly after delivery. Othercauses of rhinitis such as allergicrhinitis, infectious rhinitis andrhinitis medicamentosa are alsocommon during pregnancy.

Pregnancy,1 puberty, the use of oralcontraceptives, hypothyroidism,2 orconjugated estrogens can be associatedwith nasal obstruction and/or hyperse-cretion. Evidence linking thyroid dis-ease directly with nasal pathology islimited.2 Increased nasal secretion inhypothyroidism has been reported onan anecdotal basis. The frequency ofrhinitis symptoms was unclear. Symp-toms of hypothyroidism such as leth-argy, constipation, and cold intoler-ance, should be sought. No clear dataexist which indicate that thyroid re-placement treatment alone leads to res-olution of an associated rhinitis.

During pregnancy, rhinitis symp-toms, especially congestion, often de-velop during the second month andpersist to term, but usually disappearshortly after delivery.2 These symp-toms are likely related to hormone-induced intranasal vascular engorge-ment and mucosal hypersecretion.3However, non-hormonal causes of rhi-nitis such as allergic rhinitis, vasomo-tor rhinitis, rhinitis medicamentosa andsinusitis are more common causes ofrhinitis in pregnancy.

References1. Mabry RL. Rhinitis in pregnancy.

South Med J 1986;79:965971.2. Incaudo GA, and Schatz M. Rhinosi-

nusitis associated with endocrineconditions: hypothyroidism and preg-nancy, In: Schatz M, Zeigler RS, Set-tipane GA, eds. Nasal manifestationsof systemic diseases, Providence:Oceanside, 1991.

3. Georgitis JW. Allergic and non-allergic rhinitis. Current concepts andtreatment. Immunol Allergy ClinNorth Am 1987;7:211234.

Drug-Induced Rhinitis19. Drug-induced rhinitis may be

caused by a number of medica-tions, including ACE (angioten-sin-converting enzyme) inhibi-tors, reserpine, guanethidine,phentolamine, methyldopa andprazosin, as well as beta block-ers, chlorpromazine, aspirin,other NSAIDs (non-steroidal an-ti-inflammatory drugs) and oralcontraceptives. Rhinitis medica-mentosa commonly refers tothe over-use of nasally inhaledvasoconstrictor (decongestant)agents such as the OTC (over-the-counter) products, oxymeta-zoline or phenylephrine. Re-peated use of cocaine may alsoproduce rhinitis.

Medications may induce symptoms ofnasal congestion and/or rhinorrhea.1Antihypertensive medications are mostfrequently incriminated. Reserpinewas thought to be the major cause ofnasal obstruction, but guanethidine,phentolamine, methyldopa, ACE in-hibitors (angiotensin-converting en-zyme) and prazosin (alpha receptor an-tagonist) have been implicated. Otherantihypertensive drugs from variedpharmacologic classes have been doc-umented to have similar side effects.Oral contraceptives, chlorpromazineand beta blockers have also been im-plicated.2 Aspirin and non-steroidal an-ti-inflammatory agents (NSAIDs) mayproduce rhinorrhea. The rhinorrheamay be isolated, or part of a complexinvolving hyperplastic rhinosinusitis,nasal polyposis and asthma. Drugs ofabuse, such as cocaine, should also be

considered potential causes of rhinitis.Nasal irritation and inflammation mayproduce a rhinitis picture before theend-stage effects, such as nasal septalperforation, occur.3

The repetitive use of topical alpha-adrenergic nasal decongestant spraysfor more than 5 to 7 days may inducerebound nasal congestion upon with-drawal. These agents include over thecounter products containing oxymeta-zoline or phenylephrine. Also, patientsmay develop tachyphylaxis, due to theneed for more frequent doses to pro-vide adequate decongestion. Prolongedusage may lead to a hypertrophy of thenasal mucosa termed rhinitis medica-mentosa. The nasal mucosa is oftenbeefy-red, appears inflamed, andshows areas of punctate bleeding andscant mucus. This condition may becaused by down regulation of the nasalmucosal alpha-adrenergic receptors.Similar consequences may occur withprolonged use of other vasoconstrictoragents such as cocaine.

Management of rhinitis medicamen-tosa is discussed in text for summarystatement #48.

References1. Druce HM. Allergic and nonallergic

rhinitis. In: Middleton EJ, Reed CE,Ellis EF, et al. Allergy principles andpractice, 5th edition. St. Louis: Mosby-Year Book Inc, 1998:10051016.

2. Ammar-Kohdja A. Influence des con-traceptifs oraux sur la muqueuse na-sale. Revue de Laryngologie OtologieRhinologie 1971;92:4042.

3. Dax EM. Drug dependence in the dif-ferential diagnosis of allergic respira-tory disease. Ann Allergy 1990;64:261.

Rhinitis from Food Ingestion20. Rhinitis may occur after inges-

tion of foods or alcoholic prod-ucts. This may be due to vagallymediated mechanisms, nasal va-sodilation, food allergy and/orother undefined mechanisms.Food allergy is a rare cause ofrhinitis without associated gas-trointestinal, dermatologic orsystemic manifestations.


Foods can provoke rhinitis symptomsby a variety of different mechanisms.1,2Ingested food allergens rarely produceisolated IgE mediated rhinitis withoutinvolvement of other organ systems.Urticarial rash, facial or lip swelling,or bronchospasm, strongly suggest anIgE mediated reaction.3 Symptomswhich promptly follow eating foods orfood additives may suggest a causaletiology, but this may or may not beIgE-mediated. In adults, food skin testsmay be appropriate in occasional casesif a careful history suggests food-re-lated rhinitis symptoms, particularly ifrhinitis symptoms are associated withother systemic symptoms. Although avariety of opinions have been ex-pressed in the literature,110 there is lit-tle or no credible data available to jus-tify routine performance of food skintests in the evaluation of rhinitis inadults. In the evaluation of rhinitis inchildren where the history may bemore difficult to interpret and food al-lergy is more common, there is greaterjustification to consider performanceof limited food skin testing. Beer, wineand other alcoholic drinks may pro-duce symptoms by nasal vasodilation.The syndrome of copious watery rhi-norrhea occurring immediately afteringestion of foods, particularly hot andspicy foods, has been termed gustato-ry rhinitis and is vagally mediated.10

References1. Metcalfe DD. The diagnosis of food

allergy: theory and practice. In: Spec-tor S, ed. Provocative challengeprocedures: bronchial, oral, nasal andexercise. vol. 2. Boca Raton: CRCPress. 1983:119125.

2. Bock SA, Lee WY, Remigio LK, MayCD. Studies of hypersensitivity reac-tions to food in infants and children. JAllergy Clin Immunol 1978;62:327334.

3. Atkins FM, Steinberg SS, and Met-calfe DD. Evaluation of immediate ad-verse reactions to foods in adult pa-tients. I. Correlation of demographic,laboratory, and prick skin test datawith response to controlled oral foodchallenge. J Allergy Clin Immunol1985;75:348.

4. Hendrick DJ, Davies RJ, DSouza MF,

Pepys J. An analysis of skin prick re-actions in 656 asthmatic patients. Tho-rax 1975;30:28.

5. Foucard T. Allergy and allergy-likesymptoms in 1050 medical students.Allergy 1991;46:2026.

6. Novembre E, de Martino M, VierucciA. Foods and respiratory allergy. J Al-lergy Clin Immunol 1988;81:10591065.

7. Pastorello E, Ortolani C, Luraghi MT,et al. Evaluation of allergic etiology inperennial rhinitis. Ann Allergy 1985;55:854856.

8. Pelikan Z, Pelikan-Filipek M. Bron-chial response to the food ingestionchallenge. Ann Allergy 1987;58:164172.

9. Heiner DC. Respiratory diseases andfood allergy. Ann Allergy 1984;53:657664.

10. James JM, Bernhisel-Broadbent J,Sampson HA. Respiratory reactionsprovoked by double-blind food chal-lenges in children. Am J Respir CritCare Med 1994;149:5964.

11. Raphael GD, Hauptschein-Raphael M,Kaliner M. Gustatory rhinitis: a syn-drome of food-induced rhinorrhea. JAllergy Clin Immunol 1989;83:110115.

Other Conditions that May BeConfused with Rhinitis21. Signs and symptoms suggestive

of rhinitis can be produced byother conditions including: na-sal septal deviation, tumors, ad-enoidal hypertrophy, hypertro-phy of the nasal turbinates.

Nasal obstruction may be caused bycongenital or acquired anatomic abnor-malities, which may mimic symptomsof rhinitis. Reduced air flow throughthe nasal passages in infants may bedue to congenital choanal atresia. Themost common acquired anatomiccause of nasal obstruction in infantsand children is adenoidal hypertrophy.

Nasal septal deviation, and nasalturbinate or adenoidal hypertrophymany block flow of nasal secretions,leading to rhinorrhea or postnasal drip,as well as causing nasal blockage.

Although comparatively rare, bothbenign and malignant tumors maycause rhinitis symptoms.1 Lesions mayocclude the nasal airway, often unilat-erally and invariably. Rapidly growing

nasal malignancies may cause nasalobstruction early in the disease. Le-sions arising in the maxillary sinuspresent intranasally in the late stages ofthe disease, after the tumor has pene-trated the medial wall of the antrum.Bleeding may occur, as well as hypos-mia or anosmia, pain and otalgia. Pro-longed occupational exposure to chem-icals such as nickel, wood or leatherdusts, chromate, formaldehyde andchlorophenol, have been associatedwith hypertrophic rhinosinusitis, meta-plasia and carcinoma. Refractory clearrhinorrhea may be due to CSF leakeven in the absence of trauma or recentsurgery.

Nasal mastocytosis presents withsymptoms of rhinorrhea and nasal con-gestion without pruritus.2 Patients withnasal mastocytosis display an espe-cially pale mucosa, which contains in-creased numbers of mast cells, and feweosinophils. Skin tests and other testsfor IgE-mediated disease are negative.

Primary atrophic rhinitis occurs inelderly patients who report nasal con-gestion and a constant bad smell (oze-na) in the nose.3 This persistent condi-tion is characterized by progressiveatrophy of the nasal mucosa and un-derlying bone of the conchae.4 Thickcrusts form that produce the character-istic foul odor. The nasal cavities areenlarged and squamous metaplasia ofthe surface epithelium is detectable.Patients report associated headachesand chronic sinusitis. The syndromeshould be separated from secondaryatrophic rhinitis, developing as a directresult of chronic granulomatous nasalinfections, chronic sinusitis, radical na-sal surgery, trauma and irradiation.The incidence of atrophic rhinitis indeveloped countries has declined, butthe disease is still prevalent in EasternEurope, Greece, Egypt, India, andChina. The etiology of primary atro-phic rhinitis has not yet been estab-lished. Theories include infection withKlebsiella ozaenae5 and other bacteria.Despite the sensation of congestion,rhinomanometric studies have shownno evidence of increased resistance toairflow.


Systemic immunologic and non-im-munologic diseases may affect thenose. In uremia and diabetes, ischemiamay cause an anterior rhinitis. Othersinclude Wegeners granulomatosis,sarcoidosis, relapsing polychondritisand midline granuloma.6 In certainsyndromes, the systemic symptomsmay be absent or undetected when pa-tients present with nasal complaints.Infections such as tuberculosis, syphi-lis, leprosy, sporotricosis, blastomyco-sis, histoplasmosis, and coccidiomyco-sis also may cause granulomatousnasal lesions. These are usually ulcer-ative, and crust formation may lead tonasal obstruction or bleeding. Rhino-scleroma is a rare chronic granuloma-tous disease associated with the bacte-rium Klebsiella rhinoscleromatis.Rhinoscleroma is endermic to EasternEurope and Central America, but isnow increasing in incidence in the US.Symptoms include purulent nasal dis-charge, crusting and nodule formationproducing nasal obstruction.

References1. Komisar A. Nasal obstruction due to

benign and malignant neoplasms. Oto-laryngol Clin North Am 1989;22:351365.

2. Connell JT. Nasal mastocytosis [Ab-stract]. J Allergy 1969;43:182.

3. Zohar Y, Talmi YP, Strauss M, et al.Ozena revisited. J Otolaryngol 1990;19:345349.

4. Goodman WS, deSouza FM. Atrophicrhinitis. In: English GM, ed. Otolaryn-gology. Philadelphia: JB Lippincott,1987;2:111.

5. Ferguson JL, McCaffrey TV, Kern EB,et al. Effects of Klebsilla ozaenae onciliary activity in vitro: implications inthe pathogenesis of atrophic rhinitis.Otolarygol Head Neck Surg 1990;102:207.

6. Falkoff RJ. Nasal manifestations ofsystemic disease, Providence: Ocean-side, 1991.

Nasal Polyps22. Nasal polyps may occur in con-

junction with chronic rhinitis orsinusitis and may contribute sig-nificantly to the patients symp-toms. Nasal polyps should al-

ways be considered in thedifferential diagnosis of patientswho present with invariant na-sal congestion and its sequelae.Allergy as a cause of nasal pol-yps has not been established butnasal polyps may occur in con-junction with allergic rhinitis.

Nasal polyps present as invariable na-sal obstruction and may occur in asso-ciation with chronic allergic rhinitis orsinusitis. They may occur in associa-tion with cystic fibrosis in children1and adults,2 asthma and as part of as-pirin idiosyncracy3 (acetylsalicylicacid sensitivity, sinusitis and asthma),but they most commonly occur alone.Allergy does not appear to predisposeto polyp formation, but mast cell reac-tions and eosinophil activation withsubsequent inflammation seem to beimportant and may explain why corti-costeroids are therapeutically effec-tive. Between 10% and 15% of pa-tients with allergic rhinitis also havenasal polyps.4

References1. Stern RC, Boat TF, Wood RE. Treat-

ment and prognosis of nasal polyps incystic fibrosis. Am J Dis Child 1982;136:10671070.

2. DiSantAgnese PA, David PB. Cysticfibrosis in adults: 75 cases and a re-view of 232 cases in the literature.Am J Med 1979;66:121132.

3. Stevenson DD, Simon RA. Sensitivityto aspirin and nonsteroidal anti inflam-matory drugs. In: Middleton E, Jr,Reed CE, Ellis EF, et al, eds. Allergy:principles and practice. 4th edition. St.Louis: Mosby, 1993:17471766.

4. Fireman P. Allergic rhinitis. In: Fire-man P, Slavin RG, eds. Atlas of aller-gies, ed 2. London: Mosby-Wolfe,Times Mirror International PublishersLimited, 1996:141159.

EVALUATION OF RHINITIS

History23. Full evaluation of the patient

with rhinitis should include adetermination of the pattern,chronicity, and seasonality ofsymptoms (or lack thereof), re-sponse to medications, presence

of coexisting conditions, occupa-tional exposure, a detailed envi-ronmental history and identifi-cation of precipitating factors.

A careful history will usually suggestthe diagnosis of rhinitis (Table 1). Athorough general medical historyshould be followed by questions spe-cific to rhinological symptoms, includ-ing information on environmental andoccupational factors and family his-tory. Allergic rhinitis can occur at anyage, including infancy, and the physi-cian should note the onset of symp-toms. Most patients with allergic rhi-nitis develop their symptoms prior tothe age of 20 years.1,2 The frequency ofsymptoms should be noted andwhether they are daily, episodic, sea-sonal or perennial. The duration andseverity of the symptoms should alsobe mentioned, and whether the severityhas increased, decreased, or remainedthe same over a period of time.

Presentation of allergic rhinitis mayvary considerably. Some patientspresent primarily with symptoms ofsneezing and rhinorrhea whereas oth-ers present with nasal blockage withlittle or no itching or sneezing.

Symptoms may be perennial, withor without seasonal exacerbations. Inevaluating the patient, it is important toobtain a detailed account of when andwhere the symptoms arise. Commonseasonal allergens include tree, grassand weed pollens, and airborne molds.In seasonal allergic rhinitis, there is adistinct relation between timing of pol-len release at various geographic loca-tions and the appearance of symptoms.

It is important to ask about the as-sociation of acute symptoms with ex-posure to specific allergens such asmites during house cleaning, episodicexposures to animals or mold spores,which are present in increased amountsduring harvesting, mowing, or leaf rak-ing. Perennial allergens, such as dustmites, cockroaches, pet danders andmold spores can cause chronic symp-toms.

Frequently, unsuspected occupa-tional allergens can stimulate an IgE-mediated response, and inquiriesshould be made about this and poten-


tial exposures to irritants in the work-place. (see Summary Statement #17)

Consistent obstruction on the sameside suggests a polyp, foreign body,structural problem, or rarely, a tumor.Hyposmia and anosmia are most oftenassociated with nasal polyps or severedisease. Symptoms related to blockageof the airways include: frequent sorethroats, dryness of the mouth and oro-pharynx, a nasal quality to the voiceand snoring. An allergic salute may becharacterized by an upward or side-ways thrust of the palm of the handagainst the tip of the nose when wateryrhinorrhea and itching are significant,resulting in a transverse crease in theskin of the lower third of the externalnose. If sneezing is present, it oftenoccurs in paroxysms.

The allergens, irritants and weatherconditions that precipitate or aggravatesymptoms should be detailed. Peren-nial symptoms more commonly occurwhen there are indoor pets, dust mitesor mold spores present throughout theyear. Moisture favors the growth ofmites and molds. Mattresses, pillows,upholstered furniture, curtains and car-pets are frequent sources of dust mites.House plants and stored paper goodsfavor mold growth. There is a directrelationship between the amount ofpollen exposure and severity of symp-toms.3 As the season progresses, thereis a gradual increase in severity ofsymptoms in relation to the pollencount due to immunologic enhance-ment of sensitivity or priming.4 Cer-tain foods can induce rhinitis symp-toms as has been confirmed by doubleblind challenges.5 Irritants can potenti-

ate the symptoms of allergic rhinitis.Emotional upsets can also exacerbaterhinitis symptoms. In an allergic indi-vidual, an upper respiratory infectioncan either mimic allergies or worsen orprolong the effects of allergies or othernon-specific irritants.6,7 Hormonal fac-tors or medications/drugs, such as anti-hypertensives or cocaine, can be re-sponsible for a persistent rhinitis. Apositive family history makes it morelikely that an allergy will develop,8 butthe pattern of inheritance seems to bepolygenic and a negative family his-tory by no means rules out the diagno-sis of allergic rhinitis. The level ofresponse to previous medication trialsis also important to assess. For exam-ple, a favorable response to antihista-mines would support a diagnosis ofallergy, while such a response to intra-nasal corticosteroids could support anyof a number of diagnoses, includingrhinitis due to allergy, or the NARESsyndrome.

References1. Haahtela R, Heiskala M, Slonemi I.

Allergic disorders and immediate skintest reactivity in Finnish adolescents.Allergy 1980;35:433441.

2. Hagy GW, Settipane GA. Bronchialasthma, allergic rhinitis and allergyskin tests among college students. JAllergy 1969;44:323.

3. Norman PS. Allergic rhinitis. J AllergyClin Immunol 1985;75:531548.

4. Connell JT. Quantitative intranasalpollen changes. III. The priming effectin allergic rhinitis. J Allergy 1969;50:4344.

5. Bock SA. Prospective appraisal ofcomplaints of adverse reactions to

foods in children during the first 3years of life. Pediatrics 1987;79:683688.

6. Lemanske RF, Dick EC, Swenson C,et al. Rhinovirus upper respiratory in-fection increases airway hyperreactiv-ity and late asthmatic reactions. J ClinInvest 1989;83:110.

7. Doyle WJ, Skoner DP, Seroky JT, etal. Effect of experimental rhinovirus39 infection on the nasal response tohistamine and cold air challenges inallergic and non-allergic subjects. J Al-lergy Clin Immunol 1994;93:534542.

8. Van Arsdel PP Jr, Motulsky AG. Fre-quency and hereditability of asthmaand allergic rhinitis in college students.Acta Genet 1959;9:101114.

Taking History of Impact onQuality of Life24. Symptoms of rhinitis may signif-

icantly impact the patientsquality of life, by causing fa-tigue, headache, cognitive im-pairment and other systemicsymptoms. An assessment of thedegree to which these symptomsinterfere with the patients abil-ity to function should be made.

The individuals subjective assessmentof his/her physical, physiologic and so-cial well being1 is the cornerstone ofevaluating the effect of the varioustherapies provided by physicians. Inrhinitis, it is not only the clinical out-comerelief of sneezing, itching, rhi-norrhea or congestionor the effecton measures of nasal patency studieswhich define success of treatment, butalso it is the functional impact of thetreatment on the patients daily lifewhich defines successful treatment.Diseases have a variety of impacts onpatients in addition to making themfeel ill. They also interfere in a varietyof ways with carrying out ones day today responsibilities. In patients withrhinitis, loss of sleep and concomitantfatigue, headache, poor concentration,repeated nose blowing, itchy wateryeyes and general irritability all impactnegatively on their ability to carry outphysical, social and work/school re-sponsibilities effectively.

There are several surveys whichhave been used to measure the out-

Table 1. Important Historical Points in the Evaluation of Rhinitis

Symptoms: magnitude, duration, timing in relation to exposure (ie, early and/or late-phaseallergic reactions), effects on daily living

Triggers/seasonality Environment, including home, job and school or day care for children History of other allergic symptoms (eg, asthma, conjunctivitis, eczema) Past medical history, including trauma Feeding history in young children Past treatment experience Current treatment Family history, including allergic diseases Review of systems


comes of treatment on a variety ofdiseases. The Medical OutcomesStudy Short Form Healthy Survey (SF-36) has been used to measure the out-comes on specific functions such asphysical and role functioning and onemotional well being. On the otherhand specific rhinitis questionnaires,such as the Rhinoconjunctivitis Qual-ity of Life Questionnaire (RQLQ),have been validated in the measure-ment of the effects of treatment of na-sal disease on important parameters ofevery day living.2,3

Another look at the Rhinoconjuncti-vitis Quality of Life Questionnaire re-veals that a questionnaire specificallydesigned for 12 to 17-year old patientsis necessary to determine significantquality of life impacts of different ther-apies for this age group.4

Another quality of life study evalu-ated the impact of the relief of rhinor-rhea on moods and daily activities inpatients with non-allergic rhinitis. Thisstudy revealed that patients treatedwith topical ipratropium had substan-tially greater improvement in moodthan those on placebo.5

Finally, one must note that numer-ous studies have demonstrated thatbetter health outcomes occurred in pa-tients who adhere to treatment recom-mendations as compared to those whoare not compliant with recommendeddrug regimens.6 This fact is worrisomein evaluating the results of clinicaldrug trials which require patients to becompliant with drug administrationand do not make allowances for thenon-compliant patient.

Allergic rhinitis, particularly whenperennial, can cause restrictions on thephysical, psychological, and socialwell-being of patients. In one studythat used the SF-36 questionnaire toevaluate the quality of life in patientswith perennial allergic rhinitis, valuesfor patients with moderate to severeperennial allergic rhinitis were signifi-cantly different from those for healthysubjects for 8 of 9 variables.7 Indeed,patients with allergic rhinitis had de-creased physical and social function-ing, energy, mental health, and generalhealth perception. They had increased

physical and emotional limitations andexperience of pain.

References1. Coons SJ, Kaplan RM. Assessing

health related quality of life; applica-tion to drug therapy. Clin Therap 1992;14:850858.

2. Juniper EF, Guyatt GH. Developmentand testing of a new measure of healthstatus for clinical trials in rhinocon-junctivitis. Clin Exp Allergy 1991;21:7783.

3. Juniper EF, Guyatt GH, Archer B, etal. Aqueous beclomethasone dipropi-onate in the treatment of ragweed pol-len-induced rhinitis; further explora-tion of as needed use. J Allergy ClinImmunol 1993;92:6672.

4. Juniper EF, Guyatt GH, Dolovich J. As-sessment of quality of life in adolescentswith allergic rhinoconjunctivitis: devel-opment and testing of a questionnaire forclinical trials. J Allergy Clin Immunol1993;93:413423.

5. Georgitis JW, Banov C, Boggs PB, etal. Ipratropium bromide nasal spray innon-allergic rhinitis, efficacy, nasalcytological response and patient eval-uation on quality of life. Clin Exp Al-lergy 1994;24:10491055.

6. Horwitz R, Horwitz SM. Adherence totreatment and health outcomes. ArchIntern Med 1993;153:18631868.

7. Bousquet J, Bullinger M, Fayol C, etal. Assessment of quality of life inpatients with perennial allergic rhinitiswith the French version of the SF-36health status questionnaire. J AllergyClin Immunol 1994;94:182188.

Physical Examination25. An examination of the nose

should be performed in patientswith a history of rhinitis. Thisshould include examination ofthe nasal passageways, secre-tions, turbinates, septum, anddetermination of whether nasalpolyps are present.

Examination of the nose is indicated inall cases of rhinitis (Table 2). This isaccomplished with a nasal speculumwith appropriate lighting, otoscopewith nasal adapter, rigid Hopkins rodor flexible nasopharyngoscope.1 Use ofthe latter procedure may be limited inthe pediatric population. If it is used,the middle meatus should also be ex-

amined, if possible, to evaluate bony ormucosal crowding with obstruction ofthe sinus ostia. The presence of muco-purulent material in this region is sug-gestive of sinusitis. Cobblestoningof the pharynx with lymphoid tissuemay be seen. A nasal speculum shouldbe inserted gently, since the septummay be tender. Elevating the end of thenose with the other hand provides abetter view of the nasal passage.

On physical examination, the patientwith rhinitis may appear quite uncom-fortable and distressed with mouthbreathing. On nasal examination, thetypical mucosa of the allergic patientappears pale and swollen, with a blu-ish-gray appearance when the mucosaledema is severe. Occasionally, the mu-cosa can be hyperemic. The mucosa isusually reddened in acute infectionsand with overuse of topical medica-tions. Mucosal appearance may notdistinguish between allergic and non-allergic rhinitis, because non-allergicrhinitis may also present with mucosalpallor, edema or hyperemia.

The quantity and quality of nasalsecretions should be noted. With aller-gic rhinitis, there may be watery mu-cus on the epithelial surface or on thefloor of the nasal passage. With abnor-mal mucociliary clearance or total na-sal obstruction, thick secretions can beseen pooling in the floor of the nose.

An examination of the nasal cavitymay identify polyps, tumors, foreignbodies, or septal deflections. Unlikethe nasal turbinates with which theyare often confused, polyps appear glis-tening, mobile, and opaque and areinsensitive to touch.3 Nasal polyps maybe differentiated from severely edem-atous mucosa by applying a smallamount of a topical vasoconstrictorsuch as phenylephrine to the mucosa,and reexamining the mucosa 5 to 10minutes later. Nasal polyps will notshrink in size after topical vasocon-strictor has been applied, unlike edem-atous mucosa. Crusting on an inflamedmucosa may suggest atrophic rhinitisor a systemic disease such as sarcoid-osis. The presence of a septal perfora-tion should raise the possibility of co-caine abuse, previous surgery or,


again, systemic granulomatous dis-eases.

In allergic rhinitis associated withconjunctivitis, the palpebral conjuncti-vae may be injected with watery dis-charge and puffiness of the eyelids.Subconjunctival edema may bepresent. With chronic or severe acuteallergic rhinitis, a transverse crease isoften seen across the bridge of thenose, particularly in children, as a re-sult of rubbing of the nose to relievenasal obstruction and itching. Thecharacteristic gesture in which the pa-tient elevates the tip of the nose withthe palm of the hand to relieve itchingand obstruction has acquired the namethe allergic salute. Allergic shiners(infraorbital dark skin discoloration),3and facial pallor may be present. Theeyes and periorbital region also shouldbe examined for evidence of Dennie-Morgan lines (accentuated lines orfolds below the margin of the inferioreyelid) and cataracts, particularly ifatopic dermatitis is present.

With prolonged nasal obstructionand constant mouth breathing in child-hood, an individual may have eleva-tion of the upper lip, an overbite (den-tal malocclusion) and a high archedpalate.4 The tympanic membranes

should be examined for evidence ofassociated middle-ear disease, includ-ing middle-ear effusion and tympanicmembrane retraction or immobility.5This may provide evidence of allergen-induced Eustachian tube dysfunction.6The examination should also focus onthe possible involvement of the si-nuses. Evidence of associated allergicdiseases, such as asthma and atopicdermatitis, should be sought. Examina-tion of the lungs may reveal wheezingor a persistent cough, since there areoften accompanying symptoms andsigns of asthma when allergic rhinitisis present.7 In the evaluation of patientswith rhinitis it may be necessary to ruleout involvement of any other relevantorgan system.

References1. Rohr A, Hassner A, Saxon A. Rhino-

pharyngoscopy for the evaluation ofallergic-immunologic disorders. AnnAllergy 1983;50:380384.

2. Slavin RG. Nasal polyps and sinusitis.In: Middleton E Jr, Reed CE, Ellis EF,et al, eds. Allergy principles and prac-tice, 5th ed. St. Louis: Mosby-YearBook, 1998:10241035.

3. Marks MB. Significance of discolora-tion in the lower orbitopalpebralgrooves in allergic children (allergic

shiners). Ann Allergy 1963;21:2632.4. Bresolin D, Shapiro CG, Shapiro PA,

et al. Facial characteristics of childrenwho breathe through the mouth. Pedi-atrics 1984;73:622625.

5. Badhwar AK, Druce HM. Allergic rhi-nitis. Med Clin North Am 1992;76:789803.

6. Skoner DP, Doyle WJ, Chamovitz A,Fireman P. Eustachian tube obstruc-tion (ETO) after intranasal challengewith house dust mite. Arch Otolaryn-gol 1986;112:840842.

7. Noble SL, Forbes RC, WoodbridgeHB. Allergic rhinitis. Am Fam Physi-cian 1995;51:837846.

Testing for Specific IgE26. The demonstration of specific

IgE antibodies to known aller-gens by skin testing or in-vitrotests (as delineated in the Pa-rameters for Diagnostic Test-ing1) is of particular impor-tance in determining whetherthe patient has allergic rhinitisand for identifying specific aller-gens for which avoidance mea-sures and/or allergen immuno-therapy are warranted.

A careful history is the most importantstep toward the diagnosis of allergicdisease. Skin testing to allergens is in-dicated to provide evidence of an al-lergic basis for the patients symptoms,to confirm suspected causes of the pa-tients symptoms, or to assess the de-gree of sensitivity to a specific aller-gen. The simplicity, ease and rapidityof performance, low cost, and highsensitivity of these tests makes themfavorable for use in patients with rhi-nitis. Quality control measures andproper performance of skin testing arevital to produce accurate and reproduc-ible results. The number of skin teststhat are necessary may vary dependingon the age, potential allergen expo-sures, and area of the country. To prop-erly interpret skin tests or in vitro testsfor specific IgE, it is essential to knowwhich aeroallergens are present lo-cally, are clinically important and haveallergenic cross-reactivity with botani-cally related species (see Practice Pa-rameter for Allergy Diagnostic Test-ing).

Table 2. Elements of Physical Examination and Procedures to Consider in Patients WithRhinitis

General observations: facial pallor, allergic shiners, mouth breathing, and nasal crease,evidence of systemic disease (e.g. nail clubbing).

Growth percentiles for children. Eyes: evidence for conjunctivitis, Dennie-Morgan lines (accentuated lines or folds below

the margin of the inferior eyelid). Nose: presence or absence of external deformity, nasal mucosal swelling, nasal polyps,

deviated septum, septal perforation, discharge (noting color and consistency), blood.Consider examining the nasopharynx using indirect mirror visualization or fiberopticendoscope

Ears: Consider pneumatic otoscopy to look for abnormalities of tympanic membranes,including abnormal mobility patterns, retraction, air-fluid levels, bubbles behind tympanicmembrane; consider tympanometry to confirm the presence or absence of effusion andmiddle ear under- or over-pressures.

Mouth: Observe for malocclusion or high arched palate associated with chronic mouthbreathing, tonsilar hypertrophy, lymphoid streaking in the oropharynx, pharyngealpostnasal discharge, halitosis, and pain upon mouth occlusion suggestive of temporo-mandibular joint syndrome.

Neck: Lymphadenopathy, thyroid enlargement. Chest: Signs of asthma. Skin: Eczema, skin dryness, dermographism. Other relevant organ systems.


Reference1. Bernstein IL, Storms WW. Practice

parameters for allergy diagnostic test-ing. Joint Task Force on Practice Pa-rameters for the Diagnosis and Treat-ment of Asthma. The AmericanAcademy of Allergy, Asthma and Im-munology and the American Collegeof Allergy, Asthma and Immunology.Ann Allergy Asthma Immunol 1995;75:543.

Special Diagnostic Techniques27. In selected cases, special tech-

niques such as fiberoptic nasalendoscopy and/or rhinomanom-etry may be useful in evaluatingpatients presenting with rhinitissymptoms. These tests may re-quire special expertise for ap-propriate administration and in-terpretation. Patients with nasaldisease require appropriate ex-amination for associated dis-eases, such as sinusitis and otitismedia.

History and routine physical examina-tion are usually sufficient for a defini-tive diagnosis of rhinitis. Patients withupper airway complaints may initiallyreport symptoms suggestive of rhinitis.When symptoms or physical findingsare atypical, complications or otherconditions are suspected, or whensymptoms do not respond appropri-ately to therapy, endoscopy may beindicated. Traditional examination ofthe nasal cavity consists of inspectionwith a nasal speculum following mu-cosal decongestion; mirrors are usedfor examination of the nasopharynxand larynx. Unfortunately, it is notpossible to view many of the importantrecessed structures of the upper airwayby these methods. A more completeupper airway examination can easilybe performed endoscopically, using ei-ther the rigid Hopkins instruments orthe flexible fiberoptic endoscope. Ra-diologic imaging techniques, such asplain films, computed tomography(CT), and magnetic resonance imaging(MRI) have limited use in the evalua-tion of patients with uncomplicatedrhinitis which responds well to ther-apy.

Upper Airway Endoscopy. Upperairway endoscopy (rhinolaryngos-copy) is the most useful diagnosticprocedure in an evaluation for ana-tomic factors causing upper airwaysymptoms. Endoscopy provides a clearview of the nasal cavity and allows fordetailed examination of the middle me-atus, superior meatus, sphenoeth-moidal recess, and posterior nasophar-ynx, as well as structures of theoropharynx and larynx.1,2 The proce-dure is usually performed in the officefollowing decongestion and topical an-esthesia. Some children may requiresedation. Analysis of videotaped fiber-optic upper airway endoscopy has alsobeen used as a research technique tomeasure cross sectional area of the na-sal cavity.

rhinitis pt4 1998

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