The diagnosis and management of rhinitis: An updated practice parameter

Article Outline

• Abstract
• Contributors
• Chief editor—joint task force
• Chief editor—parameter workgroup chair
• Task force reviewers
• Assigned reviewers
• Parameter workgroup members
• Preface [summary statements 8, 9, 13]
  • Components and organization of this parameter
• Abbreviations
• Collation of summary statements
  • Definition and classification of rhinitis
  • Differential diagnosis of rhinitis and associated conditions
  • Burden and epidemiology of rhinitis
  • Allergic rhinitis
    • Pathogenesis
    • Seasonal and perennial allergic rhinitis
    • Associated allergic conjunctivitis
  • Nonallergic rhinitis syndromes
    • Vasomotor rhinitis
    • Rhinitis from foods and alcohol
    • Infectious rhinitis
    • NARES
    • Occupational rhinitis
    • Hormonal rhinitis
    • Drug-induced rhinitis
    • Atrophic rhinitis
  • Conditions that mimic rhinitis
    • Nasal polyps
    • Anatomic abnormalities
    • Cerebral spinal fluid rhinorrhea
    • Ciliary dysfunction
  • Evaluation and diagnostic studies
    • History
    • Physical examination
    • Testing for specific IgE antibody
      • Skin testing
    • In vitro assays for specific IgE
    • Special diagnostic techniques
    • Special testing considerations in children
    • Testing for comorbid conditions
    • Tests without diagnostic validity
  • Management of rhinitis
    • Environmental control measures
    • Pharmacologic therapy
      • Oral antihistamines
      • Intranasal antihistamines
      • Oral and topical decongestants
      • Over-the-counter cough and cold medications for young children
      • Intranasal corticosteroids
      • Oral corticosteroids
      • Intranasal cromolyn
      • Intranasal anticholinergics
      • Oral anti-LT agents
      • Omalizumab
      • Nasal saline
    • Allergen immunotherapy
    • Surgery
    • Management decisions
      • Education of patient and caretakers
      • Major comorbid conditions
    • Special considerations
      • Pregnancy
      • Elderly patients
      • Athletes
    • Consultation with an allergist/immunologist
• Executive summary
  • Definition of rhinitis [Summary Statement 1]
  • Classification and differential diagnosis of rhinitis and associated conditions [Summary Statements 2-7]
    • Allergic rhinitis: Risk factors and presentation [Summary Statements 8-17]
      • Risk factors for allergic rhinitis
      • Presentation of allergic rhinitis
      • Early-phase and late-phase responses in allergic rhinitis
    • Allergic conjunctivitis [Summary Statements 17-19]
    • Vasomotor rhinitis [Summary Statements 20-22]
    • Acute infectious rhinitis [Summary Statements 23, 24]
    • Acute and chronic sinusitis [Summary Statements 23, 24]
    • Nonallergic rhinitis with eosinophilia syndrome [Summary Statement 25]
    • Occupational rhinitis [Summary Statement 26]
    • Pregnancy and menstrual cycle rhinitis [Summary Statement 27]
    • Drug-induced rhinitis [Summary Statement 28]
    • Rhinitis medicamentosa [Summary Statement 28]
    • Atrophic rhinitis [Summary Statement 29]
  • Conditions that mimic rhinitis
    • Nasal polyps [Summary Statement 30]
    • Anatomic abnormalities and cerebral spinal fluid rhinorrhea [Summary Statements 31-33]
    • Ciliary dysfunction syndromes [Summary Statement 34]
  • Evaluation and diagnostic studies in patients with rhinitis
    • History [Summary Statements 35, 36]
    • Physical examination [Summary Statement 37]
    • Testing for specific IgE [Summary Statements 38-41]
    • Special diagnostic techniques [Summary Statement 42]
    • Rhinomanometry and acoustic rhinometry [Summary Statement 42]
    • Nasal provocation testing [Summary Statement 42]
    • Nasal cytology [Summary Statement 43]
    • Saccharin test and cilia biopsy [Summary Statements 44, 45]
    • Additional laboratory testing [Summary Statements 46-48]
    • Sleep apnea study [Summary Statement 49]
    • Studies based on the link between the upper and lower airway (pulmonary function test) [Summary Statement 50]
    • Diagnostic tests with no validity [Summary Statement 51]
  • Management of rhinitis
    • Environmental control measures for allergens [Summary Statement 52]
      • Pollens [Summary Statements 53, 54]
      • Fungi [Summary Statements 55, 56]
      • Dust mites and cockroaches [Summary Statements 57, 59]
      • Animals [Summary Statement 58]
      • Irritants [Summary Statement 60]
    • Pharmacologic therapy
      • Second-generation oral antihistamines [Summary Statements 61-64]
      • Intranasal antihistamines [Summary Statements 65-69]
      • Oral decongestants [Summary Statements 70, 71]
      • Topical decongestants [Summary Statements 71, 72]
      • OTC cough and cold medications in young children [Summary Statement 73]
      • Intranasal corticosteroids [Summary Statements 74-80]
      • Systemic corticosteroids [Summary Statement 81]
      • Intranasal cromolyn sodium [Summary Statement 82]
      • Intranasal anticholinergics [Summary Statements 83, 84]
      • LT receptor antagonists [Summary Statement 85]
      • Omalizumab [Summary Statement 86]
      • Saline [Summary Statement 87]
    • Allergen immunotherapy [Summary Statements 88-90]
    • Surgery [Summary Statement 91]
    • Management decisions [Summary Statements 92, 93]
    • Education of patients and family members or other patient advocates [Summary Statement 94]
    • Major comorbid conditions
      • Asthma [Summary Statements 95, 96]
      • Recurrent OME [Summary Statement 97]
    • Special considerations
      • Pregnancy [Summary Statements 98-105]
      • Elderly patients [Summary Statement 106]
      • Athletes [Summary Statement 107]
    • Consultation with an allergist/immunologist [Summary Statements 108, 109]
• Annotations
  • Box 1: Patient presents with symptoms of rhinitis (Fig 6)
  • Box 2: Is history and examination suggestive of allergic rhinitis?
  • Box 3: Therapeutic trial for allergic rhinitis symptoms
  • Box 4: Therapeutic trial for nonallergic rhinitis symptoms
  • Box 5: Does the patient respond?
  • Box 6: Further follow-up, meets consultation criteria?
  • Box 7: Consultation with an allergist/immunologist
  • Box 8: Does patient have an allergic basis for rhinitis?
  • Box 9: Management of allergic rhinitis
  • Box 10: Management of nonallergic rhinitis
  • Box 11: Cooperative follow-up
• Summary statements with discussion
  • Definition
  • Differential diagnosis of rhinitis
  • Classification of allergic rhinitis
  • Allergic rhinitis
    • Early or immediate allergic response
    • Late-phase response
    • Priming response
  • Seasonal and perennial allergic rhinitis
  • Allergic conjunctivitis
  • Nonallergic rhinitis
  • Vasomotor rhinitis
  • Rhinitis from food ingestion
  • Infectious rhinitis
  • Infectious rhinitis in children
  • NARES
  • Occupational rhinitis
  • Hormonal-induced rhinitis
  • Drug-induced rhinitis
  • Atrophic rhinitis
  • Nasal polyps
  • Other conditions that may be confused with rhinitis
    • Anatomic abnormalities
    • CSF rhinorrhea
    • Ciliary dysfunction syndromes
  • Evaluation of rhinitis
    • History
    • Physical examination
    • Testing for specific IgE antibody
      • Skin testing
      • In vitro assays for specific IgE
    • Special diagnostic techniques
      • Upper airway endoscopy
      • Imaging techniques
      • CT and MRI
      • Aerodynamic methods for estimation of nasal airway obstruction
      • Acoustic rhinometry
      • Nasal provocation testing
    • Nasal cytology, ciliary functional studies, and biopsy
    • Additional laboratory testing
      • Special testing considerations in children
    • Testing for comorbid conditions
    • Unproven tests
  • Management of rhinitis
    • Environmental control measures
    • Pharmacologic therapy
      • Oral antihistamines
      • Intranasal antihistamines
      • Oral and topical decongestants
      • OTC cough and cold medications for young children
      • Intranasal corticosteroids
      • Oral corticosteroids
      • Intranasal cromolyn
      • Intranasal anticholinergics
      • Oral anti-LT agents
      • Omalizumab
      • Saline
    • Allergen immunotherapy
    • Surgical approaches for comorbid conditions.
    • Important considerations in management
    • Education of patients and family members or other patient advocates
    • Major comorbid conditions
    • Special considerations
      • Treatment of rhinitis during pregnancy
      • Rhinitis in the elderly
      • Rhinitis in the athlete
    • Allergist/immunologist consultation and referral guidelines
      • Referral guidelines8,11,50,468
      • Referral rationale and evidence level
• References
• Copyright

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 will be 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:

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

Back to Article Outline

Contributors 

The Joint Task Force has made a concerted effort to acknowledge all contributors to this parameter. If any contributors have been excluded inadvertently, the Task Force will ensure that appropriate recognition of such contributions is made subsequently.

Back to Article Outline

Chief editor—joint task force 

Dana V. Wallace, MD

Assistant Clinical Professor

Nova Southeastern University

Davie, Fla

Back to Article Outline

Chief editor—parameter workgroup chair 

Mark S. Dykewicz, MD

Professor of Internal Medicine

Chief, Section of Allergy and Clinical Immunology, Division of Immunobiology

Director, Allergy and Immunology Fellowship Program

Saint Louis University School of Medicine

St Louis, Mo

Back to Article Outline

Task force reviewers 

David I. Bernstein, MD

Professor of Clinical Medicine and Environmental Health

Division of Allergy/Immunology

University of Cincinnati College of Medicine

Cincinnati, Ohio

I. Leonard Bernstein, MD

Clinical Professor of Medicine and Environmental Health

University of Cincinnati College of Medicine

Cincinnati, Ohio

Joann Blessing-Moore, MD

Clinical Associate Professor of Medicine and Pediatrics

Stanford University Medical Center

Department of Immunology

Palo Alto, Calif

Linda Cox, MD

Assistant Clinical Professor of Medicine

Nova Southeastern University College of Osteopathic Medicine

Davie, Fla

David A. Khan, MD

Associate Professor of Internal Medicine

University of Texas Southwestern Medical Center

Dallas, Tex

David M. Lang, MD

Head, Allergy/Immunology Section

Division of Medicine

Director, Allergy and Immunology Fellowship Training Program

Cleveland Clinic Foundation

Cleveland, Ohio

Richard A. Nicklas, MD

Clinical Professor of Medicine

George Washington Medical Center

Washington, DC

John Oppenheimer, MD

Department of Internal Medicine

New Jersey Medical School

Pulmonary and Allergy Associates

Morristown, NJ

Jay M. Portnoy, MD

Chief, Section of Allergy, Asthma and Immunology

Children's Mercy Hospital

Professor of Pediatrics

University of Missouri–Kansas City School of Medicine

Kansas City, Mo

Christopher C. Randolph, MD

Clinical Professor of Pediatrics

Yale Affiliated Hospitals

Center for Allergy, Asthma, and Immunology

Waterbury, Conn

Diane E. Schuller, MD

Professor of Pediatrics

Pennsylvania State University Milton S. Hershey Medical College

Hershey, Pa

Sheldon L. Spector, MD

Clinical Professor of Medicine

University of California–Los Angeles School of Medicine

Los Angeles, Calif

Stephen A. Tilles, MD

Clinical Assistant Professor of Medicine

University of Washington School of Medicine

Redmond, Wash

Back to Article Outline

Assigned reviewers 

Kathleen R. May, MD

Allegany Allergy and Asthma

Cumberland, Md

Travis A. Miller, MD

University of Michigan

Capital Allergy and Respiratory Disease Center

Sacramento, Calif

Howard M. Druce, MD, FAAAAI

Clinical Associate Professor of Medicine

University Hospital

Morris Plains, NJ

Back to Article Outline

Parameter workgroup members 

Faud M. Baroody, MD

Professor of Otolaryngology–Head and Neck Surgery and Pediatrics

Pritzker School of Medicine

University of Chicago

Chicago, Ill

Jonathan A. Bernstein, MD

Professor of Medicine

Division of Immunology/Allergy Section

Department of Internal Medicine

University of Cincinnati College of Medicine

Cincinnati, Ohio

Timothy J. Craig, DO

Professor of Medicine, Pediatrics and Graduate Studies

Pennsylvania State University

Hershey, Pa

John W. Georgitis, MD

LaFayette Clinic

Fayetteville, NC

Ruby Pawankar, MD, PhD

Professor of Medicine

Division of Rhinology and Allergy

Department of Otolaryngology

Nippon Medical School

Tokyo, Japan

Gary S. Rachelefsky, MD

Clinical Professor of Allergy and Immunology

Center for Asthma, Allergy and Respiratory Diseases

University of California–Los Angeles Medical Center

Los Angeles, Calif

Russell A. Settipane, MD

Clinical Associate Professor of Medicine

Brown University Medical School

Providence, RI

David P. Skoner, MD

Professor of Pediatrics

Drexel University College of Medicine

Director, Division of Allergy, Asthma and Immunology

Allegheny General Hospital

Pittsburgh, Pa

Stuart W. Stoloff, MD

Clinical Professor of Family and Community Medicine

University of Nevada School of Medicine

Reno, Nev

Classification of recommendations and evidence

Category of evidence

Strength of Recommendation

Diagnosis and management of rhinitis: An updated practice parameter

PrefaceS3

AbbreviationsS4

Collation of Summary StatementsS4

Executive SummaryS9

AnnotationsS27

Summary Statements with discussionS32

ReferencesS65

Back to Article Outline

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, and itching. Rhinitis is usually associated with inflammation, but some forms of rhinitis such as vasomotor rhinitis or atrophic rhinitis are not predominantly inflammatory.

Rhinitis is a significant cause of widespread morbidity, medical treatment costs, reduced work productivity, and lost school days. Although sometimes mistakenly viewed as a trivial disease, symptoms of allergic and nonallergic rhinitis may significantly affect a patient's quality of life and can be associated with conditions such as fatigue, headache, cognitive impairment, and sleep disturbance. Appropriate management of rhinitis may be an important component in effective management of coexisting or complicating respiratory conditions, such as asthma, sinusitis, and sleep apnea. The financial burden to society for allergic rhinitis is substantial. The total direct ($7.3 billion) and indirect costs ($4.28 billion, including loss of productivity) estimated in the United States for 2002 were $11.58 billion.¹

Allergic rhinitis affects between 10% and 30% of all adults and as many as 40% of children.², ³, ⁴, ⁵, ⁶ In most studies, the ratio of allergic to pure nonallergic rhinitis is 3:1.² Preliminary data suggest that 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: An Updated Practice Parameter” is to improve the care of patients by providing the practicing physician with an evidence-based approach by reviewing data in the medical literature and incorporating this evidence into development of this guideline. While giving an overview of all categories of rhinitis, the parameter will focus on the diagnosis and treatment of allergic rhinitis. Using the 1998 practice parameter on “Diagnosis and Management of Rhinitis”⁸ as the basis, the working draft of this updated rhinitis practice parameter was prepared by a work group chaired by Mark S. Dykewicz, MD, and was revised and edited by the Joint Task Force on Practice Parameters under the leadership of Dana V. Wallace, MD. Preparation of this draft included a review of the recent medical literature using a variety of search engines such as PubMed. Published clinical studies were rated by category of evidence and used to establish the strength of the recommendations, as defined in the preamble to this parameter. The parameter was then reviewed by experts on rhinitis selected by the sponsoring organizations of the American Academy of Allergy, Asthma & Immunology and the American College of Allergy, Asthma, and Immunology. Based on this process, this parameter represents an evidence-based document.

Components and organization of this parameter 

The “Diagnosis and Management of Rhinitis: An Updated Practice Parameter” contains an annotated algorithm that presents the major decision points for the appropriate evaluation and treatment of patients with suspected rhinitis. This is followed by a collation of Summary Statements, which represent key points in the evaluation and management of this condition. Tables that provide clinically useful information in a concise format precede the body of the practice parameter, which provides a referenced narrative discussion of each Summary Statement. The graded references and figures complete the document. The Executive Summary emphasizes the key updates since the 1998 rhinitis parameter (Box).

To obtain the maximum value from this practice parameter in the most time-efficient manner, the clinician should review the Executive Summary, annotated algorithm, Summary Statements, and tables because these are created to provide the key information. The text and graded references provide the foundation on which the Joint Task Force formulated and graded the Summary Statements.

Back to Article Outline

Abbreviations 

ACE:Angiotensin-converting enzyme

AERD:Aspirin-exacerbated respiratory disease

ARIA:Allergic Rhinitis and its Impact on Asthma

BHR:Bronchial hyperresponsiveness

CF:Cystic fibrosis

CNS:Central nervous system

CSF:Cerebral spinal fluid

CT:Computed tomography

cysLT:Cysteinyl leukotriene

ECP:Eosinophilic cationic protein

FDA:US Food and Drug Administration

HEPA:High-efficiency particulate air

IOC:International Olympic Committee

IOP:Intraocular pressure

LT:Leukotriene

LTRA:Leukotriene receptor antagonist

MRI:Magnetic resonance imaging

NARES:Nonallergic rhinitis with eosinophilia syndrome

NSAID:Nonsteroidal anti-inflammatory drug

OA:Occupational asthma

OME:Otitis media with effusion

OSAS:Obstructive sleep apnea syndrome

OTC:Over-the-counter

PCD:Primary ciliary dyskinesia

PRN:When necessary (from Latin pro re nata)

QOL:Quality of life

RFVTR:Radiofrequency volumetric tissue reduction

RQLQ:Rhinoconjunctivitis Quality of Life Questionnaire

RUDS:Reactive upper-airways dysfunction syndrome

SIT:Specific immunotherapy

SPT:Skin prick test

USOC:US Olympic Committee

Back to Article Outline

Collation of summary statements 

Definition and classification of rhinitis 

Differential diagnosis of rhinitis and associated conditions 

Burden and epidemiology of rhinitis 

Allergic rhinitis 

Nonallergic rhinitis syndromes 

Conditions that mimic rhinitis 

Evaluation and diagnostic studies 

Skin testing 

Management of rhinitis 

Oral antihistamines 

Intranasal antihistamines 

Oral and topical decongestants 

Over-the-counter cough and cold medications for young children 

Intranasal corticosteroids 

Oral corticosteroids 

Intranasal cromolyn 

Intranasal anticholinergics 

Oral anti-LT agents 

Omalizumab 

Nasal saline 

Education of patient and caretakers 

Major comorbid conditions 

Pregnancy 

Elderly patients 

Athletes 

Back to Article Outline

Executive summary 

Definition of rhinitis [Summary Statement 1] 

Rhinitis is characterized by 1 or more of the following symptoms: nasal congestion, rhinorrhea (anterior and posterior), sneezing, and itching. Rhinitis is usually associated with inflammation, but some forms of rhinitis such as vasomotor rhinitis or atrophic rhinitis are not predominantly inflammatory. Rhinitis frequently 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. For example, occupational rhinitis has been classified separately from allergic and nonallergic because it may have components of both allergic and nonallergic rhinitis. Conditions that mimic symptoms of rhinitis include nasal polyps, cerebrospinal fluid rhinorrhea, ciliary dyskinesia syndrome, and structural/mechanical factors, such as deviated septum and pharyngonasal reflux (Table I, Table II).

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 induced
1	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 bodies
5	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

There is no generally accepted method of grading rhinitis severity. In an attempt to do this, an international working group (Allergic Rhinitis and its Impact on Asthma [ARIA])⁹ has proposed a classification for allergic rhinitis that placed patients into 1 of 4 categories: (1) mild intermittent, (2) mild persistent, (3) moderate/severe intermittent, and (4) moderate/severe persistent.¹⁰ This classification system discarded the terms seasonal and perennial, emphasizing that an aeroallergen (eg, grass pollen) that occurs seasonally in one region may be detected throughout the year in another geographical area. The ARIA definition of mild rhinitis may be a useful comparative reference point for other severity grading schemes; this states that none of the following items is present: sleep disturbance; impairment of daily activities, leisure, and/or sport; impairment of school or work; and symptoms present but not troublesome.¹¹ This updated parameter supports the concept that more severe rhinitis is defined as more symptoms or interference with QOL, because data show that it may not be possible to separate patients into moderate and severe categories.¹² A modified 7-point visual analog (graphic rating) scale for grading severity of nasal and nonnasal symptoms of allergic rhinitis and the effects of this disorder on the QOL has been developed (but not validated) and published by the Joint Task Force on Practice Parameters and is included, with minor modification, in Fig 1, Fig 2, Fig 3, Fig 4.¹³

• 
  • View Large Image
  • Download to PowerPoint

• Fig 1. 

  Assessment of nasal symptom severity.

• 
  • View Large Image
  • Download to PowerPoint

• Fig 2. 

  Assessment of non-nasal symptom severity.

• 
  • View Large Image
  • Download to PowerPoint

• Fig 3. 

  Global assessment of nasal and non-nasal symptom severity.

• 
  • View Large Image
  • Download to PowerPoint

• Fig 4. 

  Assessment of quality of life.

In this document, the Joint Task Force retains and uses the terms seasonal and perennial in classifying patients with allergic rhinitis. These traditional descriptive terms are clinically useful and allow for accurate categorization of the vast majority of patients as having seasonal, perennial, or perennial allergic rhinitis with seasonal exacerbations. It has become well recognized that the traditional seasonal/perennial and ARIA schemes define different patient populations.¹² This parameter introduces the term episodic allergic rhinitis, denoting allergic nasal symptoms elicited by sporadic exposures to inhalant aeroallergens that are not usually encountered in the patient's indoor or outdoor environment, such as while visiting a farm where there is exposure to horses or while visiting a home with pets when a patient has no pet exposure in their own home or work environments.

Risk factors for allergic rhinitis 

Risk factors for allergic rhinitis include (1) family history of atopy, (2) serum IgE >100 IU/mL before age 6 years, (3) higher socioeconomic class, and (4) the presence of a positive allergy SPT.⁴, ¹⁴, ¹⁵, ¹⁶ The influence of early childhood exposure to infections (the hygiene hypothesis), animals, and secondary tobacco smoke on the development of atopy and allergic rhinitis is still unknown.¹⁷, ¹⁸, ¹⁹, ²⁰, ²¹, ²², ²³, ²⁴

Presentation of allergic rhinitis 

In childhood, allergic rhinitis is more frequent in boys, but in adults, it is more frequent in women. Children with a bilateral family history of atopy may develop symptoms more frequently and at 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 born to atopic families are sensitized to pollen aeroallergens more frequently than to indoor aeroallergens in the first year of life.²⁷ Seasonal allergic rhinitis symptoms generally do not develop until 2 to 7 years of age.²⁸, ²⁹, ³⁰ Food ingestion rarely causes allergic rhinitis in infants, children, or adults unless there are associated gastrointestinal, dermatologic, or systemic manifestations. The prevalence of seasonal allergic rhinitis is higher in children and adolescents, whereas perennial allergic rhinitis has a higher prevalence in adults.³¹

Early-phase and late-phase responses in allergic rhinitis 

As in patients with asthma, early-phase and late-phase responses may be seen in allergic rhinitis. Both the early-phase and late-phase responses in allergic rhinitis are characterized by symptoms of sneezing, rhinorrhea, and nasal congestion. However, nasal congestion is predominantly a late-phase response. Mediators released from eosinophils during the late phase contribute to tissue damage.³², ³³ Pretreatment with glucocorticoids effectively reduces eosinophils and the release of cytokines during the late-phase response.³⁴, ³⁵, ³⁶

When allergen challenges are given repeatedly, the amount of allergen required to induce an immediate response decreases. This priming effect is thought to be a result of the release of inflammatory mediators from effector cells during ongoing, prolonged allergen exposure and repeated late-phase responses. Consequently, at the end of a pollen season, symptoms may decline at a slower rate than the pollen count. Therefore, it is important to know the full spectrum of aeroallergens to which the patient responds as well as seasonal variations in symptoms. Initiating anti-inflammatory therapy before pollen season or before any repetitive aeroallergen exposure, as indicated, will modify the late-phase response that is associated with the priming effect.

Oral antihistamines, intranasal antihistamines, oral anti-LT agents, intranasal corticosteroids, and allergen immunotherapy are treatments for allergic rhinitis that have been reported to relieve associated ocular allergy symptoms in controlled trials.³⁷, ³⁸, ³⁹, ⁴⁰, ⁴¹, ⁴², ⁴³, ⁴⁴, ⁴⁵, ⁴⁶, ⁴⁷, ⁴⁸, ⁴⁹, ⁵⁰, ⁵¹, ⁵² In systematic reviews of randomized controlled studies, intranasal corticosteroids compared with oral antihistamines⁵³, ⁵⁴ and intranasal 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 of allergic conjunctivitis. Topical ophthalmic agents are indicated for specific treatment of itching or symptoms of allergic conjunctivitis. Vasoconstrictors are indicated for relief of ocular redness, although they do not reduce the allergic response. Prolonged use of ocular decongestants may lead to rebound hyperemia, which is often referred to as “conjunctivitis medicamentosa.”⁵⁵ Use limited to 10 days does not appear to induce this condition.⁵⁶ The combination of an ocular antihistamine and a vasoconstrictor works better than either agent alone.⁵⁷ Mast cell stabilizers, also approved for vernal and atopic keratoconjunctivitis, have a slow onset of action and may require several days of treatment before optimal symptom relief is achieved,⁵⁸ making them more suitable for prophylactic or longer-term treatment of chronic ocular allergies than for acute symptom relief. Topical NSAIDs reduce prostaglandin production involved in mediating ocular allergy.⁵⁹ Multiple-action agents possess both antihistamine and mast cell stabilizer activities, generally have onset of action within 30 minutes, and are suitable for acute and long-term treatment of allergic conjunctivitis symptoms. Ocular corticosteroids should be reserved for more severe symptoms of allergic conjunctivitis considering that the ocular side effects from their use can threaten vision because of the increased risk of cataract formation, elevated intraocular pressure (IOP), and secondary infections. The modified steroid loteprednol is indicated for the temporary relief of symptoms and signs of seasonal allergic conjunctivitis and has a greatly reduced risk of causing increased IOP compared with many other ocular corticosteroids.⁶⁰, ⁶¹, ⁶², ⁶³, ⁶⁴

Vasomotor rhinitis, a type of nonallergic rhinitis, may be episodic or perennial.⁷ The exact pathophysiology of vasomotor rhinitis has never been established, and for this reason, it is often classified as “idiopathic” rhinitis.⁹ When rhinorrhea is the predominant symptom, there appears to be enhanced cholinergic glandular secretory activity based on the fact that atropinelike agents effectively reduce secretions.⁶⁵ Gustatory rhinitis (rhinitis symptoms associated with eating) is a form of nonallergic rhinitis felt to be vagally mediated that may respond to intranasal anticholinergic agents.⁶⁶ Patients with predominant nasal congestion may have nociceptive neurons that have heightened sensitivity to stimuli such as temperature change, airborne irritants, foods (especially hot and spicy foods), alcoholic beverages, cold dry air, and exercise.⁶⁷, ⁶⁸, ⁶⁹, ⁷⁰ Temperature change has also been noted to increase symptoms and the inflammatory nasal response in patients with allergic rhinitis.⁷¹

Acute viral upper respiratory infections are the most common predisposing factor for bacterial sinusitis, accounting for 90% to 98% of all episodes of sinusitis in children and adults.⁷², ⁷³, ⁷⁴, ⁷⁵, ⁷⁶ In uncomplicated cases of viral rhinitis, a 7-day to 10-day observation period for spontaneous resolution of symptoms is recommended before prescribing antibiotics.⁷⁷ Acute bacterial rhinosinusitis is usually associated with a viral upper respiratory infection and is characterized by symptoms persisting beyond the usual 7-day to 10-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 bacterial drug resistance.⁷⁸, ⁷⁹, ⁸⁰, ⁸¹, ⁸² Furthermore, the administration of antimicrobials increases the carriage of antimicrobial-resistant strains of certain bacterial pathogens, such as Streptococcus pneumonia, especially in children. ⁷⁸, ⁷⁹, ⁸³, ⁸⁴ Although it is generally believed that atopic children experience more episodes of acute otitis media and acute sinusitis compared with nonallergic children, this has not been firmly established.⁷⁷, ⁸⁵, ⁸⁶ Differentiating allergic rhinitis from infectious rhinosinusitis or adenoiditis may be difficult, especially in children, because the symptoms overlap and even purulent nasal drainage may be present in noninfectious rhinitis.

Distinguishing noninfectious perennial rhinitis from acute and chronic sinusitis can be difficult because many symptoms, such as mucosal erythema, increased pharyngeal secretions, olfactory disturbance, cough, nasal congestion, and headache, are found in both types of rhinitis. Although nasal cytology may be useful in differentiating infectious from noninfectious nasal and/or sinus disease, the clinical value, particularly for the diagnosis of allergic rhinitis, is limited by low specificity and sensitivity.⁸⁷, ⁸⁸, ⁸⁹, ⁹⁰, ⁹¹ For example, neutrophils may be present not only in acute and chronic sinusitis but also in conjunction with eosinophils in patients with allergic rhinitis who also have an acute infection process.⁹² Cultures of the nasopharynx without visualization in children with rhinitis is of no value because pathogenic bacteria, as part of the normal flora, have been recovered in as many as 92% of asymptomatic healthy children.⁹³ In adults, endoscopically directed middle meatus cultures have given promising results in diagnosing acute bacterial sinusitis.⁹⁴, ⁹⁵, ⁹⁶, ⁹⁷

Patients with NARES have paroxysmal exacerbations of symptoms, including sneezing, profuse watery rhinorrhea, nasal pruritus, nasal congestion, and occasional anosmia. These patients are typically middle-age. The prevalence in the general population is unknown. NARES is characterized by large numbers (inconsistently defined as >5% to >20%) of eosinophils on nasal smear.⁹⁸, ⁹⁹, ¹⁰⁰, ¹⁰¹, ¹⁰² The etiology is unknown. In some patients, NARES may precede the development of nasal polyposis and aspirin sensitivity.¹⁰³ Patients with NARES are at increased risk for the development of obstructive sleep apnea.¹⁰⁴

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, ¹⁰⁸, ¹⁰⁹ Allergic occupational rhinitis frequently coexists with OA.¹¹⁰ Irritant exposures elicit neutrophilic inflammation in the nasal mucosa,¹⁰⁷, ¹⁰⁸, ¹⁰⁹ whereas allergic exposures are associated with eosinophils, basophils, eosinophilic cationic protein (ECP), and tryptase in the nasal lavage.¹¹¹, ¹¹², ¹¹³ However, immunologic mechanisms may also be important in the response to chemical sensitizers, such as acid anhydrides, where both neutrophils and eosinophils are increased in nasal lavage fluid of workers with serum specific IgE to the relevant anhydride-human serum albumin (HSA) antigen.¹¹⁴ The prevalence of occupational rhinitis is essentially 100% among workers with OA who are sensitized to high-molecular-weight proteins, whereas only 50% of those with OA caused by chemicals have been identified with work-related rhinitis.¹¹⁰ Atopy and intensity of exposure are risk factors for developing occupational rhinitis.¹¹⁵ An asymptomatic latency period of exposure lasting weeks to years often precedes work-related symptoms.¹⁰⁵, ¹¹⁶ Symptoms are temporally related to exposure at work and often improve away from the workplace. The diagnostic validity of nasal allergen challenge for occupational allergens has not been evaluated.¹¹², ¹¹⁴ Optimal management is avoidance of the occupational trigger, but avoidance of nonoccupational allergens that contribute to the nasal symptoms is also recommended. Chronic pharmacologic therapy as used for allergic and nonallergic rhinitis can be instituted. In general, there is insufficient evidence to support the efficacy of immunotherapy for IgE-dependent occupational rhinitis, and it is inappropriate to use immunotherapy to treat occupational rhinitis caused by low-molecular-weight chemical allergens.¹¹⁷

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 symptoms during pregnancy are allergic rhinitis, sinusitis, rhinitis medicamentosa, and vasomotor rhinitis. Symptoms of allergic rhinitis increase in 1/3 of pregnant patients,¹¹⁸ perhaps attributed to nasal vascular pooling caused by vascular dilatation and increased blood volume.¹¹⁹ A type of rhinitis unique to the pregnant patient is “vasomotor rhinitis of pregnancy” or “pregnancy rhinitis.” Pregnancy rhinitis had been defined as rhinitis without an infectious, allergic, or medication-related cause that starts before the last 6 weeks of pregnancy (corresponding to 34 weeks gestation), persists until delivery, and resolves completely within 2 weeks after delivery.¹²⁰ When pregnancy rhinitis causes snoring, it may even 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 be an association of nasal congestion with ovulation and the rise in serum estrogen during the normal menstrual cycle in some women.¹²²

Drug-induced rhinitis may be caused by ACE inhibitors,¹²³ α-receptor antagonists used in the treatment of benign prostatic hypertrophy,¹²⁴ and phosphodiesterase-5 selective inhibitors used for treatment of erectile dysfunction.¹²⁵ There is no direct evidence that the current combined oral contraceptive pills cause nasal symptoms.¹²⁶ Aspirin and other NSAIDs may produce rhinorrhea as an isolated symptom or as part of aspirin-exacerbated respiratory disease (AERD), formerly termed “Samter's triad.”¹²⁷, ¹²⁸

Rhinitis medicamentosa may develop after the repetitive and prolonged use of topical α-adrenergic nasal decongestant sprays such as oxymetazoline and phenylephrine. The recreational use of cocaine may result in a rhinitis medicamentosa–like state.¹²⁹, ¹³⁰ Benzalkonium chloride in vasoconstrictor spray products, when used for 30 days or more, may augment local pathologic effects.¹³¹, ¹³² Patients may develop rebound congestion, tachyphylaxis, reduced mucociliary clearance because of loss of ciliated epithelial cells,¹³³ and on rare occasions, nasal septal perforation.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 rebound effects of the nasal decongestant spray to resolve. At times, a short course of oral corticosteroids may be needed to control the patients' symptoms while the effects of the nasal decongestant spray dissipate.¹²⁹, ¹³⁵ Once the rhinitis medicamentosa is treated, the patient should be evaluated for an underlying condition, such as allergic rhinitis.

Primary (idiopathic) atrophic rhinitis is a chronic condition characterized by progressive atrophy of the nasal mucosa, nasal crusting, nasal dryness (caused by atrophy of glandular cells), and fetor.¹³⁶, ¹³⁷ The nasal cavities appear abnormally wide on examination, and there is absence of identifiable turbinates on sinus CT, referred to as the “empty nose syndrome.”¹³⁸ Secondary atrophic rhinitis is most commonly a result of chronic sinusitis or excessive surgery to the nasal turbinates.¹³⁸ Although saline irrigation is the mainstay of treatment, topical or systemic antibiotics are indicated with the appearance of purulent nasal secretions.¹³⁹, ¹⁴⁰

Conditions that mimic rhinitis 

Conditions that mimic rhinitis must be considered in the differential diagnosis of nasal symptoms.

Nasal polyps may coexist with allergic rhinitis; however, allergy as a cause of nasal polyps has not been established. Nasal polyps have a prevalence of 2% to 4%¹⁴¹, ¹⁴², ¹⁴³ and usually occur after age 40 years.¹⁴³ Although previous studies showed a 2:1 male to female prevalence of nasal polyps,¹⁴², ¹⁴⁴, ¹⁴⁵ a recent large population study showed no sex preference.¹⁴³ AERD, previously referred to as the aspirin triad, consists of nasal polyps, acetylsalicylic acid 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 nasal polyps are associated with asthma, there is hypersecretion of cysteinyl LTs (cysLTs).¹⁴⁸ Oral steroids may be required in severe nasal polyposis to reduce polyp size, improve airflow, and allow for effective topical medication delivery. A short course of oral steroids followed by maintenance use of intranasal corticosteroid administered twice daily should follow.¹⁴⁹, ¹⁵⁰, ¹⁵¹ Subjective improvement has been observed when LT modifiers are administered in addition to intranasal corticosteroids.¹⁵², ¹⁵³ One study demonstrated that after surgery, reoccurrence rates and rescue medication requirements were the same in patients treated postoperatively with montelukast or beclomethasone.¹⁵⁴ In some adult patients with nasal polyps and AERD, aspirin desensitization followed by long-term daily aspirin treatment has successively reduced the need for removal of nasal polyps and systemic corticosteroids.¹⁵⁵, ¹⁵⁶, ¹⁵⁷

Nasal septal deviation and turbinate hypertrophy may lead to postnasal drip or nasal obstruction. Unilateral obstruction, especially 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 of trauma or recent surgery, may rarely be a result of a CSF leak.¹⁶⁰ Nasal symptoms, particularly congestion, may be noted in infants and children with pharyngonasal reflux resulting from prematurity, neuromuscular disease, or cleft palate.¹⁶¹ In infants and children, the most common acquired anatomic cause of nasal obstruction is adenoidal hypertrophy.

Ciliary dysfunction syndromes cause ineffective mucociliary clearance and include (1) PCD¹⁶² (also known as immotile-cilia syndrome), a rare genetic disorder, and (2) secondary ciliary dysfunction,¹⁶³, ¹⁶⁴ a more common condition caused by acute or chronic 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 unresponsive to therapy, and bronchiectasis.¹⁶⁵ Approximately 50% of subjects with PCD are affected by situs inversus (Kartagener syndrome). Whereas screening diagnostic tests for mucociliary clearance use saccharine¹⁶⁶ or Teflon (DuPont) tagged particles, definitive diagnosis requires biopsy and examination by electron microscopy.¹⁶⁷, ¹⁶⁸, ¹⁶⁹ After an infection, resolution of secondary ciliary dysfunction and cytopathic epithelial damage may require weeks.¹⁶³, ¹⁶⁴, ¹⁷⁰, ¹⁷¹, ¹⁷² An adverse effect of tobacco smoke on mucociliary clearance in the upper airways in healthy smokers has not been established.¹⁷³, ¹⁷⁴

Evaluation and diagnostic studies in patients with rhinitis 

A thorough allergic history remains the best diagnostic tool available. The history will include the patient's chief concerns and symptoms and often includes the pattern, chronicity, seasonality, and triggers of nasal and related symptoms, family history, current medications, response to previous treatment modalities, presence of coexisting conditions, occupational exposure, and a detailed environmental history. Questions relating symptoms to pollen and animal exposure have been shown to have positive predictive value for diagnosing allergic rhinitis.¹⁷⁵ In addition to upper respiratory symptoms, it is important to determine the effect of rhinitis 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, ¹⁷⁷, ¹⁷⁸, ¹⁷⁹ The psychological ramifications of untreated allergic rhinitis can lead to low self-esteem, shyness, depression, and anxiety.¹⁸⁰ Recent findings that the sexual QOL is affected by seasonal allergic rhinitis and that appropriate treatment improves the patient's sexual functioning emphasizes that allergic rhinitis is an underappreciated disease with systemic effects.¹⁸¹ As evidence of the disparities 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 underrecognized and inadequately treated by the patient's physician.¹⁸²

The effect of rhinitis on QOL has been measured using both generic and disease-specific questionnaires (Table III, Table 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 specific for rhinitis, describe disease-associated problems more accurately and seem to be more responsive to measuring the change with therapeutic interventions. Although both the generic and disease-specific QOL questionnaires are often used in research trials, their sensitivity and precision for use with individual patients have not been determined.¹⁸⁵, ¹⁸⁶, ¹⁸⁷, ¹⁸⁸, ¹⁸⁹, ¹⁹⁰

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, 626, 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.htmhttp://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, 632, 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: george.parkerson@duke.edu	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, 640, 641, 642
Health Utilities Index Mark 2 and 3 (HUI2 & 3)	http://www.healthutilities.com/hui2.htmhttp://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.

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: adultrqlqpack@qoltech.co.uk	643, 644, 645
Standardized Rhinoconjunctivitis Quality of Life Questionnaire	http://www.qoltech.co.uk/Rhinocon.htm#rqlqs	Free request: adultrqlqpack@qoltech.co.uk	646
Mini Rhinoconjunctivitis Quality of Life Questionnaire	http://www.qoltech.co.uk/Rhinocon.htm#minirqlq	Free request: adultrqlqpack@qoltech.co.uk	647
Nocturnal Rhinoconjunctivitis Quality of Life Questionnaire	http://www.qoltech.co.uk/Rhinocon.htm#noct	Free request: adultrqlqpack@qoltech.co.uk	648
Rhinitis Quality of Life Questionnaire	http://www.qoltech.co.uk/Rhinocon.htm#rhinqlq	Free request: adultrqlqpack@qoltech.co.uk	649
Rhinitis Symptom Utility Index			650
Rhinitis QOL pediatric and adolescent
Paediatric Rhinoconjunctivitis Quality of Life Questionnaire	http://www.qoltech.co.uk/PaedRhinocon.htm#prqlq	Free, request: paedrqlqpack@qoltech.co.uk	651
Adolescent Rhinoconjunctivitis Quality of Life Questionnaire	http://www.qoltech.co.uk/PaedRhinocon.htm#arqlq	Free, request: paedrqlqpack@qoltech.co.uk	652

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

The physical examination (Table V) of all organ systems potentially 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 patient 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.

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

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.

The nasal and oropharyngeal examination may be accomplished with a nasal speculum with appropriate lighting, otoscope with nasal adapter, indirect mirror, and/or rigid or flexible nasopharyngoscope, based on the expertise of the examiner and/or the assessment needs.¹⁹⁴ If after applying a topical decongestant there is a reduction of turbinate mucosa edema, this may assist in delineating mucosal versus bony hypertrophy and in differentiating 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 tympanic membrane mobility and the presence or absence of fluid, especially in children.

Many typical allergic findings are supportive of but not specific for allergic rhinitis.¹⁹⁵ Mucosal appearance may not distinguish between allergic and nonallergic noninfectious rhinitis or even infectious rhinitis, because hyperemia, for example, may be present with all 3. Likewise, classic “allergic shiners” are reported in 38% of nonatopic individuals.¹⁹⁶

Determination of specific IgE, preferably by skin testing, is indicated to (1) provide evidence of an allergic basis for the patient's symptoms, (2) confirm suspected causes of the patient's symptoms, or (3) assess the sensitivity to a specific allergen for avoidance measures and/or allergen immunotherapy.¹⁹⁷, ¹⁹⁸ The number of skin tests and the allergens selected for skin testing should be determined on the basis of the patient's age, history, and environment and living situation, such as area of the country, occupation, and activities.⁹ The precise sensitivity of specific IgE immunoassays compared with skin prick/puncture tests can vary with the technique used, from less than 50% to greater than 90%, with the average 70% to 75%.¹⁹⁹, ²⁰⁰, ²⁰¹, ²⁰², ²⁰³, ²⁰⁴, ²⁰⁵, ²⁰⁶, ²⁰⁷, ²⁰⁸, ²⁰⁹ Similar sensitivity has been reported when these immunoassays are compared with symptoms induced after natural or controlled challenge—that is, nasal provocation challenge. The simplicity, ease, and rapidity of performance, low cost, and high sensitivity make skin testing preferable to in vitro testing for determining the presence of specific IgE antibodies in patients with rhinitis. However, specific IgE immunoassays may be preferable to skin testing in certain clinical situations, such as extensive 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 anaphylaxis from skin testing. Positive results of testing for specific IgE antibody to allergens must be correlated with history and physical findings to assess their clinical significance.²¹⁰, ²¹¹ A positive immediate hypersensitivity skin test in the absence of symptoms has been shown to be a significant risk factor for the later development of seasonal allergic rhinitis.⁴, ¹⁴, ¹⁵

Special diagnostic techniques may be useful in selected cases. Fiber optic nasal endoscopy²¹², ²¹³ may be especially useful when symptoms or physical findings are atypical, complications or other conditions are suspected, or symptoms do not respond adequately to therapy. Although CT and magnetic resonance imaging (MRI) are not indicated in the evaluation of patients with uncomplicated rhinitis, they may be useful with suspected complications or comorbidities such as nasal polyposis and/or concomitant sinusitis.²¹⁴, ²¹⁵ MRI provides better imaging of soft tissue than CT, but it is less suited to imaging the bony anatomy. Standard radiographs are generally not indicated because of the availability of preferred procedures, as noted. When available, dynamic video rhinoscopy is more accurate at assessing adenoidal hypertrophy than a lateral nasopharyngeal radiograph.²¹⁶

Rhinomanometry, a technique that measures functional obstruction to airflow in the upper airway, may be used (1) to obtain objective assessment of nasal congestion, and may be particularly helpful in occupational rhinitis, or in assessing response to therapeutic interventions; (2) to assess the severity of anatomical abnormalities; or (3) to assist in the evaluation of patients with obstructive sleep apnea.²¹⁷ Acoustic rhinometry reflects acoustic signals from structures in the nasal cavity, thereby producing an image that represents variations in the cross-sectional dimensions of the nasal cavity.²¹⁸, ²¹⁹, ²²⁰ This produces an approximate nasal cavity volume and identifies the distance to the minimal cross-sectional area from the nares. Measurement by acoustic rhinometry has been validated by comparison to CT and MRI.²²¹ Using this comparison, there is high correlation for the anterior 2/3 of the nasal cavity, but the posterior nasal cavity shows more variance.²²², ²²³, ²²⁴, ²²⁵ Clinically, acoustic rhinometry may be of value to monitor response and adherence to medical therapy as well as nasal pharyngeal surgical outcome.²²⁶, ²²⁷ Although nasal congestion does not interfere with acoustic rhinometry, profuse nasal secretions may lead to measurement inaccuracy.²²⁸ Acoustic rhinometry is rapid, safe, and noninvasive; requires minimal patient training and cooperation; and may obviate the need of CT and MRI in some situations, such as when septoplasty and turbinoplasty are considered, as well as for postoperative evaluation.²²⁹, ²³⁰ Acoustic rhinometry and rhinomanometry have similar reproducibility²³¹ and compare favorably in challenge studies,²³² but measure nasal obstruction differently and are therefore best viewed as complementary.²³³, ²³⁴, ²³⁵

Nasal allergen challenge may be used for confirmation of sensitivity to an allergen. A single allergen dose may be used to measure nasal reactivity, whereas incremental doses of allergen can be used to assess sensitivity.²³⁶ The clinical utility of measuring nasal sensitivity/hyperresponsiveness to histamine and methacholine is limited because of a considerable overlap in the response of patients with allergic and nonallergic rhinitis.²³⁷, ²³⁸, ²³⁹, ²⁴⁰

Nasal smears for eosinophils are not recommended for routine use in diagnosing allergic rhinitis, but a positive nasal smear (>10% eosinophils)⁹⁰ may prompt nasal or conjunctival challenge when there remains a high index of suspicion of allergy in a history-positive, skin test–negative patient.²⁴¹ A negative allergen challenge in a patient with >5% eosinophils on nasal smear would support a diagnosis of NARES.¹⁰² If nasal smears are obtained, nasal secretions from both nostrils should be studied.²⁴² A prominence of neutrophils on nasal smear suggests an infectious process,⁹² with nasal neutrophils usually higher in bacterial than viral infections.²⁴³ However, the presence of neutrophils on nasal smear is not diagnostic because as many as 79% of asymptomatic school children have neutrophils in their nasal secretions.⁸⁸

The saccharin test for nasal mucociliary clearance can be performed in the office but has limited utility as a screening test for ciliary dyskinesis. It cannot be relied on for a definitive diagnosis of primary nasal ciliary dyskinesis but may be useful in diagnosing and following the resolution of secondary nasal ciliary dysfunction.¹⁶³, ¹⁶⁴, ¹⁶⁵ For a definitive diagnosis of primary nasal ciliary dyskinesis, a brush biopsy is obtained from the inferior concha and examined by electron microscopy.²⁴⁴, ²⁴⁵ Combining electron microscopy with computer-based image processing algorithms can improve the visualization of ultrastructural defects.¹⁶⁵, ¹⁶⁹

Laboratory studies that may be indicated in some patients with rhinitis include immune function studies and sweat test and/or genetic typing for CF. Total IgE, including cord blood samples, and specific IgG₄ subclasses have limited clinical benefit and should not be routinely performed in patients with rhinitis.²⁴⁶, ²⁴⁷, ²⁴⁸, ²⁴⁹, ²⁵⁰, ²⁵¹, ²⁵², ²⁵³, ²⁵⁴ The presence of β-2-transferrin in the nasal secretions is a sensitive method of confirming CSF rhinorrhea.²⁵⁵, ²⁵⁶

Atopy has been associated with habitual snoring in infants.²⁵⁷ In children, the presence of rhinitis is a strong predictor of habitual snoring.²⁵⁸ Children who are African American, have upper respiratory disease, and have a family history of sleep apnea are at enhanced risk for sleep-disordered breathing.²⁵⁹ Thus, formal evaluation for obstructive sleep apnea syndrome (OSAS) may be considered in children as well as adults presenting with chronic rhinitis and other risk factors associated with sleep-disordered breathing.

In snoring adults with rhinitis and sleep apnea symptoms, increased nasal airway resistance has been associated with apnea and hypopnea.²⁶⁰, ²⁶¹ Intranasal corticosteroids reduce nasal airway resistance and apnea-hypopnea frequency in patients with OSAS and rhinitis and may be of benefit in the treatment of some patients with OSAS.²⁶¹

Rhinitis and asthma are linked by common epidemiologic, physiologic, and pathologic mechanisms, as well as common comorbidities and therapeutic approaches.²⁶², ²⁶³, ²⁶⁴, ²⁶⁵ Therefore, it has been suggested that patients with persistent allergic rhinitis be evaluated for asthma.⁹ Because allergic rhinitis frequently coexists with asthma and patients may not recognize symptoms of asthma, pulmonary function tests should be considered in patients with rhinitis. The presence of asthma may not be apparent because such patients (1) may have difficulty in recognizing their symptoms, (2) may not have consistent symptoms throughout the day, (3) may have a physical examination of the respiratory system that appears normal, and (4) may present with symptoms that are atypical (see Major Comorbid Conditions, Summary Statements 95-97).

There is no evidence that the following procedures have diagnostic validity for allergic rhinitis: cytotoxic tests, provocation-neutralization, electrodermal testing, applied kinesiology, iridology, and hair analysis (see “Allergy Diagnostic Testing: An Updated Practice Parameter”⁹).

Management of rhinitis 

The success of environmental control measures for rhinitis should be judged by clinical improvement, such as reduction in symptoms and medication scores, and not by a decrease in allergen concentration.²⁶⁶ Individual host sensitivity to an aeroallergen influences the intensity of symptoms; for example, the pollen counts that causes symptoms may vary on the basis of an individual's degree of sensitivity and may be different for different pollens. Studies have not been consistently able to demonstrate symptom and/or medication reduction with any of the commonly used environmental control measures in patients with rhinitis.

Pollens [Summary Statements 53, 54] 

Patients with allergic rhinitis caused by pollens may be exposed to allergen from (1) nonpollen plant fragments, (2) allergenic bioaerosols without intact pollen grains, and (3) even high pollen concentrations of insect-pollinated plants.²⁶⁷, ²⁶⁸, ²⁶⁹ Pollen counts are generally highest on sunny, windy days with low humidity. Because the interplay of different weather factors (eg, wind, temperature, rain, and humidity) is complex, it may not be possible reliably to predict levels of outdoor aeroallergens on the basis of the influence of a single weather factor.²⁷⁰, ²⁷¹, ²⁷²

Fungi [Summary Statements 55, 56] 

Hydrophilic fungi, such as Fusarium and Phoma, are most abundant during rainy weather,²⁷³ whereas Alternaria and Cladosporium have elevated levels during dry, windy weather.²⁷⁴, ²⁷⁵, ²⁷⁶ When involved in plant-disturbing activity, such as gardening and lawn mowing, facemasks can reduce exposure to fungi.²⁷⁷, ²⁷⁸ The first step in reduction of indoor fungal exposure consists of eliminating the source of moisture, such as water intrusion, cold surfaces, and elevated humidity. As a second step, dilute bleach solution with detergent denatures fungal allergens and may prevent regrowth with application to nonporous surfaces, whereas porous surfaces must be removed and/or replaced.

Dust mites and cockroaches [Summary Statements 57, 59] 

Dust mite exposure can be reduced through measures that kill the mites or degrade and/or prevent their fecal pellets from becoming airborne. This may include HEPA air filtration²⁷⁹ and vacuum cleaning with a HEPA filter,²⁸⁰ low humidity,²⁸¹ hard surface flooring,²⁸² hot water laundry,²⁸³ barrier protection on pillows and mattresses,²⁷⁹, ²⁸⁴, ²⁸⁵ and the use of acaricides.²⁷⁹, ²⁸⁶, ²⁸⁷, ²⁸⁸ The patient should be encouraged to use multiple interventions because an isolated intervention, such as use of dust mite–impermeable bedding, is unlikely to offer clinical benefit.²⁸⁸ On the other hand, regular dusting and duct cleaning have not been shown to offer significant benefit. Some of these measures are also helpful for animal and insect allergen reduction, but none are as effective as removing the animal and/or insects. Cockroach allergen, a significant cause of nasal allergy in urban populations, is most abundant in the kitchen area. Environmental control of cockroach allergen involves an integrated pest management with the combination of family education—for example, emphasis on food debris removal and sealing of all sources of food and repetitive home cleaning; the use of newer gel or bait pesticides, such as odorless and colorless hydramethylnon and abamectin; and structural elimination of harborages. As with animal dander, it may take more than 6 months of aggressive pest management control to remove residual cockroach allergen.²⁸⁹, ²⁹⁰

Animals [Summary Statement 58] 

Cat and dog allergens have been shown to produce symptoms in sensitized individuals when there is contamination of animal-free homes and schools with passive transport, such as on clothing.²⁹¹, ²⁹², ²⁹³, ²⁹⁴ After cat removal from the home, an average of 20 weeks is required before the allergen concentration reaches levels found in the animal-free home.²⁹⁵ Confining a cat to an uncarpeted room (other than bedroom) with HEPA filtration may reduce by 90% airborne allergen dissemination to the remainder of the house.²⁹², ²⁹⁶ Some²⁹⁷, ²⁹⁸, ²⁹⁹ but not all²⁹², ²⁹⁶, ³⁰⁰ studies have demonstrated reduced airborne cat allergen by washing the animal on a weekly to biweekly basis.

Irritants [Summary Statement 60] 

Irritants reported to cause nasal symptoms include tobacco smoke,³⁰¹ microbially derived volatile organic compounds from bacteria and fungi, formaldehyde,³⁰², ³⁰³ chlorine, and perfume.³⁰⁴ The symptoms of rhinitis are directly related to the duration of exposure and usually resolve when the irritant is removed. Hyperresponsiveness to irritant triggers such as chlorine is enhanced among patients with seasonal allergic rhinitis during the season when they have symptoms. Formaldehyde, a recognized nasal and ocular irritant, produces symptoms only at concentrations well above those that produce a detectable odor.³⁰⁵, ³⁰⁶

The selection of pharmacotherapy for a patient depends on multiple factors, including the type of rhinitis present (eg, allergic, nonallergic, mixed, episodic), most prominent symptoms, severity, and patient age (Summary Statements 92, 93). Principal medication options are summarized in Table VI. The following sections provide a more expansive discussion of medication options.

Table VI. Principal medication options for rhinitis (see indicated Summary Statement [SS] discussion for supporting data) (listed in alphabetical order)

Allergic rhinitis: Seasonal allergic rhinitis and perennial allergic rhinitis
Monotherapy	Therapeutic considerations
Oral agents
Antihistamines, oral (H1 receptor antagonists; SS 61-64)	Continuous use most effective for SAR and PAR, but appropriate for PRN use in episodic AR because of relatively rapid onset of action
	Less effective for nasal congestion than for other nasal symptoms
	Other options, in general, are better choices for more severe AR
	Less effective for AR than INS (SS 74), with similar effectiveness to INS for associated ocular symptoms (SS 19)
	Because generally ineffective for nonallergic rhinitis, other choices are typically better for mixed rhinitis
	To avoid sedation (often subjectively unperceived), performance impairment, anticholinergic effects of first-generation antihistamines, second-generation agents generally preferred (SS 61)
	Of second-generation agents, fexofenadine, loratadine, desloratadine without sedation at recommended doses (SS 63)
Corticosteroids, oral (SS 81)	A short course (5-7 days) of oral corticosteroids may be appropriate for very severe nasal symptoms
	Preferred to single or recurrent administration of intramuscular corticosteroids, which should be discouraged (SS 81)
Decongestants, oral (SS 70-72)	Pseudoephedrine reduces nasal congestion (SS 70)
	Side effects include insomnia, irritability, palpitations, hypertension
Leukotriene receptor antagonists (SS 85)	Montelukast approved for SAR and PAR
	No significant difference in efficacy between LTRA and oral antihistamines (with loratadine as usual comparator; SS 85)
	Approved for both rhinitis and asthma; may be considered in patients who have both conditions (SS 85)
	Side effects minimal
Intranasal agents
Intranasal antihistamines (SS 65-69)	Effective for SAR and PAR (SS 65)
	Have clinically significant rapid onset of action, making them appropriate for PRN use in episodic AR (SS 65-69)
	Effectiveness for AR equal or superior to oral second-generation antihistamines (SS 64), with clinically significant effect on nasal congestion (SS 68)
	Less effective than INS (SS 69) for nasal symptoms
	Appropriate choice for mixed rhinitis, because also approved for vasomotor rhinitis
	Side effects with intranasal azelastine: bitter taste, somnolence (SS 69)
Intranasal anticholinergic (ipratropium; SS 83)	Reduces rhinorrhea but not other symptoms of SAR and PAR
	Appropriate for episodic rhinitis because of rapid onset of action
	Side effects minimal, but dryness of nasal membranes may occur
Intranasal corticosteroids (SS 74-80)	Most effective monotherapy for SAR and PAR (SS 74)
	Effective for all symptoms of SAR and PAR, including nasal congestion
	PRN use (eg, >50% days use) effective for SAR (SS 76)
	May consider for episodic AR
	Usual onset of action is less rapid than oral or intranasal antihistamines, usually occurs within 12 hours, and may start as early as 3 to 4 hours in some patients
	More effective than combination of oral antihistamine and LTRA for SAR and PAR (SS 75)
	Similar effectiveness to oral antihistamines for associated ocular symptoms of AR
	Appropriate choice for mixed rhinitis, because agents in class also effective for some nonallergic rhinitis
	Without significant systemic side effects in adults
	Growth suppression in children with PAR has not been demonstrated when used at recommended doses
	Local side effects minimal, but nasal irritation and bleeding occur, and nasal septal perforation rarely reported (SS 80)
Intranasal cromolyn (SS 82)	For maintenance treatment of AR, onset of action within 4 to 7 days, full benefit may take weeks
	For episodic rhinitis, administration just before allergen exposure protects for 4 to 8 hours against allergic response (SS 82)
	Less effective than nasal corticosteroids, inadequate data for comparison to leukotriene antagonists and antihistamines (SS 82)
	Minimal side effects (SS 82)
Intranasal decongestants (SS 71,72)	For short-term and possibly for episodic therapy of nasal congestion, but inappropriate for daily use because of the risk for rhinitis medicamentosa
	May assist in intranasal delivery of other agents when significant nasal mucosal edema present

Nonallergic (idiopathic) rhinitis
Monotherapy	Therapeutic considerations (for side effects, see AR table)
Oral agents
Antihistamines, oral (H1 receptor antagonists; SS 61, 62)	Generally ineffective for nonallergic rhinitis
Decongestants, oral (SS 70, 71)	Pseudoephedrine reduces nasal congestion (SS 70, 71)
Intranasal agents
Intranasal antihistamines (SS 65-69)	Effective for vasomotor rhinitis
Intranasal anticholinergic (ipratropium; SS 83)	Effective only for rhinorrhea of nonallergic rhinitis syndromes
	Special role for preventing rhinorrhea of gustatory rhinitis
Intranasal corticosteroids (SS 78)	Effective for some forms of nonallergic rhinitis, including vasomotor rhinitis and NARES
Combination therapy	Inadequate data to provide firm recommendations in nonallergic rhinitis

AR, Allergic rhinitis; INS, intranasal corticosteroids; PAR, perennial allergic rhinitis; SAR, seasonal allergic rhinitis.

Second-generation oral antihistamines [Summary Statements 61-64] 

Second-generation antihistamines are generally preferred over first-generation antihistamines for treatment of allergic rhinitis because they have less tendency to cause sedation, performance impairment, and/or anticholinergic adverse effects.³⁰⁷, ³⁰⁸, ³⁰⁹, ³¹⁰, ³¹¹ First-generation antihistamines may produce performance impairment in school¹⁷⁶, ³¹², ³¹³ and driving³¹⁴, ³¹⁵, ³¹⁶, ³¹⁷, ³¹⁸ that can exist without subjective awareness of sedation;³¹⁰ and the use of first-generation antihistamines has been associated with increased automobile and occupational accidents.³¹⁴, ³¹⁵, ³¹⁶, ³¹⁷, ³¹⁸, ³¹⁹ Individual variation exists with respect to development of sedative effects with first-generation antihistamines.³⁰⁷, ³⁰⁹, ³¹³ Concomitant use of other central nervous system (CNS)–active substances, such as alcohol and sedatives, may further enhance performance impairment from these antihistamines.³⁰⁷, ³⁰⁹ In part because of prolonged plasma half-life and metabolites (Table VII), these undesirable and potentially dangerous side effects cannot be eliminated by administration of first-generation antihistamines only at bedtime.³²⁰, ³²¹, ³²², ³²³, ³²⁴, ³²⁵ Anticholinergic effects include dryness of mouth and eyes, constipation, inhibition of micturition, and an increased risk for provocation of narrow-angle glaucoma. Increased sensitivity and a greater incidence of pre-existing comorbid conditions, such as prostatic hypertrophy, elevated IOP, and cognitive impairment, place older adults in a high-risk category for the side effects of first-generation antihistamines. The anticholinergic effects of the first-generation antihistamines may explain the reported better control of rhinorrhea compared with the second-generation antihistamines. The overall efficacy of first-generation antihistamines compared with second generation for the management of allergic rhinitis symptoms has not been adequately studied. Second-generation antihistamines differ in their onset of action, sedation properties, skin test suppression, and dosing guidelines (Table VIII). No single agent has been conclusively shown to have superior efficacy.³²⁶, ³²⁷ Exceeding the recommended dosage may result in increased sedation with many of these products³⁰⁹, ³²³, ³²⁸, ³²⁹, ³³⁰ that do not produce sedation at recommended doses. Although antihistamines can be used on an intermittent basis, such as for episodic allergic rhinitis, it has been shown that continuous treatment for seasonal or perennial allergic rhinitis is more effective,³³¹ primarily because of unavoidable, ongoing allergen exposure.

Table VII. Oral and intranasal antihistamines

Generic drug	Trade name example	Metabolites if significant (T 1/2 in hours of product or metabolite)	Tmax hours (metabolite)	Skin test suppression mean (max) days	% Sedation/somnolence or CNS impairment (control)	Dosage forms	Age limit	Adult dose
Second generation
Acrivastined	Semprex-D	(1.4-3.1)653	1.15654 1.4653	∼3, T 1/2 =1.7 h	8655 12 (6)PI	8 mg	12 y	8 mg qid
Azelastine hydrogen chloride	Astelin nasal	Desmethylazelastine (22)PI	2.5656 .25∗341	2656, 657	11.5 (5.4)PI	137 mcg/spray	5 y	2 sp/nostril bid
Cetirizined	Zyrtec	None (7-11)653	1.0 ± 0.5656	3656	14 (10)PI	5, 10 mg 5 mg/5 mL	6 mo	5-10 mg q d
Desloratadined	Clarinex	3 Hydroxy desloratadine (7.8 ± 4.2)653	3.17 (4.76)658	∼7 (T 1/2 = 21-31 h)	2.1 (1.8)PI	5 mg 2.5 mg/5 mL	6 mo	5 mg q d
Fexofenadined	Allegra	None (14.4-14.6)653	2.6656	2656	1.3 (.9)PI	30, 60, 180 mg 30 mg/5 mL	2 y	180 mg q d or 60 mg bid
Levocetirizine	Xyzal	None (7 ± 1.5)653	.9659 1.25PI	Unknown	6 (2)PI	5 mg	6 y	5 mg q d
Loratadined	Claritin	Descarboethoxyloratadine (7.8 ± 4.2)653	1.2 ± 0.3656 (1.5 ± 0.7)656	7656	8 (6)PI	10 mg 5 mg/5 mL	2 y	10 mg q d
Olopatadine hydrochloride	Patanase nasal	No major metabolites (8-12)PI	.5-1.0PI	Unknown	0.9 (0.3)PI	665 mcg/spray	12 y	2 sp/nostril bid
First generation
Brompheniramine	Dimetapp	24.9 ± 9.3660	4661	>2660 4662	24 (5)322	12 mg
1 mg/5 mL	2 y	1-2 bid
Chlorpheniramined	Chlor-Trimeton	Mono and didesmethyl chlorpheniramine (27.9 ± 8.7)653	2-6663 2.8653	3664 (6665)	45%661	4, 8, 12 mg 2 mg/5 mL	2 y	4 mg qid
Clemastined	Tavist	(21.3 ± 11.6)666	4.77 ± 2.26666	5667 (10667)	14 (1.5)668	1.34, 2.68 mg .67 mg/5 mL	6 y	1.34 mg bid to tid
Cyproheptadine	Periactin	(16)669	4670	9671 (11671)	8-50672	4 mg 2 mg/5 mL	2 y	4 mg tid
Diphenhydramine	Benadryl	Nordiphenhydramine (9.2 ± 2.5)653	2.6673, 674 1.7 ± 1.0653	2664 (5664)	50%661	25, 50 12.5 mg/mL	2 y	25-50 mg qid
Hydroxyzine	Atarax	(20 ± 4.1)653	2.1 ± 0.4653	5664 (8664)	80%661	10, 25, 50, 100 mg 10 mg/5 mL	All ages	25 mg qid
Promethazine	Phenergan	Promethazine sulfoxide & N-desmethylpromethazine (9-16)PI	4.4675	3664 (5664)	60-73676	12.5, 25, 50 mg 6.25 mg/5 mL	2 y	25 mg qid
Triprolidine	Actifed	(3.2)PI	2.0677	3654, 660, 661, 664 (7[7])	10% to 25%

T 1/2, Half life; ^d, available with decongestant; ^PI, package insert; qid, 4 times a day; q d, every day; bid, 2 times a day; tid, 3 times a day.

Table VIII. Intranasal corticosteroid sprays

nos, Nostril; bid, 2 times a day; q d, every day; tid, 3 times a day; NA, not applicable; BKC, benzalkonium chloride.

Intranasal antihistamines [Summary Statements 65-69] 

Intranasal antihistamines have demonstrated efficacy that is equal to³³² or superior to³³³, ³³⁴, ³³⁵ oral second-generation antihistamines in the treatment of seasonal allergic rhinitis. They are also effective and have been associated with a clinically significant effect on nasal congestion for nonallergic rhinitis³³⁶, ³³⁷, ³³⁸ but are generally less effective than intranasal corticosteroid for treatment of allergic rhinitis.⁴⁶ Combination therapy with intranasal corticosteroids may provide added benefit.³³⁹ The only intranasal antihistamines currently available in the United States, azelastine,³³², ³³³, ³³⁴, ³³⁵, ³³⁶, ³³⁷, ³³⁸ and olopatadine,³⁴⁰ have a rapid onset of action.³⁴¹ Bitter taste has been reported with both preparations, and sedation may occur³⁴² (Table VII).

Oral decongestants [Summary Statements 70, 71] 

Oral decongestants, such as pseudoephedrine, are effective at relieving nasal congestion in patients with allergic and nonallergic rhinitis but can result in side effects such as insomnia, loss of appetite, irritability, and palpitations.³⁴³ The efficacy of an oral decongestant in combination with an antihistamine in the management of allergic rhinitis has not been adequately documented to increase the efficacy of either drug alone.³⁴⁴

Pseudoephedrine is a key ingredient used in making methamphetamine. In an effort to reduce illicit production of methamphetamine, restrictions have been placed on the sale of pseudoephedrine in the United States.³⁴⁵ This has promoted substitution of phenylephrine for pseudoephedrine in many OTC cold and cough remedies. However, phenylephrine, which appears to be less effective than pseudoephedrine, is extensively metabolized in the gut.³⁴⁶, ³⁴⁷ In fact, the efficacy of phenylephrine as an oral decongestant has not been well established.³⁴⁵, ³⁴⁸, ³⁴⁹

Elevation of blood pressure after taking an oral decongestant is very rarely noted in normotensive patients and only occasionally in patients with controlled hypertension. However, because of variation in patient response, patients receiving oral decongestants should be followed for changes in blood pressure. Concomitant use of caffeine and stimulants, such as medications used for management in attention-deficit/hyperactivity disorder, may be associated with an increase in adverse events.³⁵⁰ Oral decongestants should be used with caution in patients with rhinitis with certain conditions, such as cerebrovascular or cardiovascular disease, hyperthyroidism, closed-angle glaucoma, and bladder neck obstruction.

Oral decongestants, when used in appropriate doses, are usually very well tolerated in children over 6 years of age. However, use in infants and young children has been associated with agitated psychosis, ataxia, hallucinations, and even death³⁵¹, ³⁵², ³⁵³ (see Summary Statement 73). At times, even at recommended doses these agents may cause increased stimulatory effects resulting in tachyarrhythmias, insomnia, and hyperactivity, especially when combined with other stimulant medications, such as stimulants used in attention deficit hyperactivity disorder management.³⁵⁴ Therefore, the risks and benefits must be carefully considered before using oral decongestants in children below age 6 years.

Topical decongestants [Summary Statements 71, 72] 

Topical decongestants such as phenylephrine or imidazoline derivatives—for example, oxymetazoline and xylometazoline–cause nasal vasoconstriction and decreased nasal edema but have no effect on antigen-provoked nasal response.³⁵⁵ Xylometazoline was found to have superior efficacy for nasal decongestion compared with intranasal corticosteroids in a 28-day study.³⁵⁶ However, topical decongestants are not recommended for continuous use because of the potential development of rhinitis medicamentosa.³⁵⁷ Furthermore, they have no effect on itching, sneezing, or nasal secretion. The development of rhinitis medicamentosa is highly variable; it may develop within 3 days of use³⁵⁷ or fail to develop after 6 weeks of daily use.³⁵⁸, ³⁵⁹, ³⁶⁰ Topical decongestants can be associated with local stinging or burning, sneezing, and dryness of the nose and throat. Intermittent use of topical decongestants is frequently prescribed; however, the efficacy and safety of this approach have not been formally studied.

OTC cough and cold medications in young children [Summary Statement 73] 

Controlled trials have shown that antihistamine-decongestant combination products are not effective for symptoms of upper respiratory tract infections in young children.³⁶¹, ³⁶², ³⁶³, ³⁶⁴, ³⁶⁵ Furthermore, there has been increasing concern over the safety of OTC cough and cold medications in children. An Adverse Event Reporting System review³⁶⁶ showed that between 1969 and September 2006, there were 54 fatalities associated with 3 reviewed decongestants and 69 fatalities associated with 3 antihistamines found in OTC and prescription preparations. Drug overdose and toxicity were common events reported in these cases.

Currently cough and cold OTC preparations indicate the user should “consult a physician” for dosing recommendations below age 2 years for decongestants and below age 6 years for antihistamines. In mid-October 2007, the FDA's Nonprescription Drugs and Pediatric Advisory Committees recommended that the OTC medications used to treat cough and cold no longer be used for children below 6 years of age.³⁶⁶ The FDA has yet to respond to these recommendations. In contrast, second-generation antihistamines such as cetirizine, desloratadine, fexofenadine, levocetirizine, and loratadine, when used in young children, have been shown to be well tolerated and to have a very good safety profile.³⁶⁷, ³⁶⁸, ³⁶⁹, ³⁷⁰, ³⁷¹, ³⁷², ³⁷³, ³⁷⁴

Intranasal corticosteroids [Summary Statements 74-80] 

Intranasal corticosteroids are the most effective medications for treating allergic rhinitis. In most studies, intranasal corticosteroids are more effective than the combined use of an antihistamine and a LT antagonist.³⁷⁵, ³⁷⁶, ³⁷⁷, ³⁷⁸, ³⁷⁹ The clinical response does not appear to vary significantly between intranasal corticosteroids that are currently available (Table VIII).⁵³, ³⁸⁰, ³⁸¹, ³⁸² The onset of therapeutic effect of intranasal corticosteroid occurs between 3 and 12 hours.³⁸³, ³⁸⁴, ³⁸⁵ The as-needed dosing (which equated to 55% to 62% of days) of an intranasal corticosteroid (fluticasone propionate) has been shown to be effective in the treatment of seasonal allergic rhinitis³⁸⁰, ³⁸⁶, ³⁸⁷ but may not be as efficacious as continuous use. In 1 study, PRN use of an intranasal corticosteroid (fluticasone propionate) was superior to PRN use of an oral antihistamine (loratadine) for seasonal allergic rhinitis.³⁸⁰ Intranasal corticosteroids are also effective in the treatment of nonallergic rhinitis, especially NARES³⁸⁸, ³⁸⁹, ³⁹⁰ and vasomotor rhinitis.³⁸⁹, ³⁹¹, ³⁹² Intranasal corticosteroids may also benefit ocular allergy symptoms associated with allergic rhinitis (see Summary Statement 19).

Intranasal corticosteroids when given in recommended doses are not generally associated with clinically significant systemic side effects. Studies in both children and adults have failed to demonstrate any consistent, clinically relevant effect from intranasal corticosteroids on the hypothalamic-pituitary-adrenal (HPA) axis,³⁹³, ³⁹⁴, ³⁹⁵, ³⁹⁶, ³⁹⁷, ³⁹⁸, ³⁹⁹, ⁴⁰⁰, ⁴⁰¹ ocular pressure or cataract formation,³⁹³, ⁴⁰², ⁴⁰³, ⁴⁰⁴ or bone density.⁴⁰⁵, ⁴⁰⁶, ⁴⁰⁷ In children, growth effect may be a better indicator of systemic effect than HPA axis suppression. The transient effect on growth suppression that has been demonstrated in children after administration of intranasal corticosteroids is dependent on the specific intranasal corticosteroid, and the dose administered, technique used for measuring growth, time of administration, and concomitant use of oral or inhaled corticosteroid. Studies with intranasal fluticasone propionate, mometasone furoate, and budesonide have shown no effect on growth at recommended doses compared with placebo⁴⁰⁸, ⁴⁰⁹, ⁴¹⁰ and reference values (at as much as 2 times the recommended doses).⁴⁰⁰ Growth suppression from intranasal corticosteroids has been reported only with long-term use of beclomethasone dipropionate that exceeded recommended doses⁴⁰⁹ or administration to toddlers.⁴¹¹

Local side effects of intranasal corticosteroids such as nasal irritation, bleeding, and nasal septal perforation⁴¹², ⁴¹³ are rare and can be avoided with proper administration technique. The patient should be periodically examined to assure that these side effects are not present. Preparations containing propylene glycol and benzalkonium chloride may result in local irritation or ciliary dysfunction, respectively⁴¹⁴, ⁴¹⁵ (Table VIII).

Systemic corticosteroids [Summary Statement 81] 

Oral corticosteroids, prescribed for a few days, may be required for the treatment of very severe intractable rhinitis or nasal polyposis.⁴¹⁶, ⁴¹⁷ The use of parenteral and intraturbinate injections of corticosteroids is discouraged.⁴¹⁸, ⁴¹⁹, ⁴²⁰, ⁴²¹, ⁴²², ⁴²³

Intranasal cromolyn sodium [Summary Statement 82] 

Nasal cromolyn sodium, an inhibitor of mast cell degranulation, is effective in the prevention of symptoms and in the treatment of other types of rhinitis.⁴²⁴, ⁴²⁵, ⁴²⁶, ⁴²⁷, ⁴²⁸, ⁴²⁹, ⁴³⁰, ⁴³¹ It has a strong safety profile and has a reported onset of action of 4 to 7 days for seasonal or perennial rhinitis. Nasal cromolyn is effective in the treatment of episodic allergic rhinitis—for example, before anticipated allergen exposure, in which case there appears to be a more rapid onset of action.⁴³², ⁴³³, ⁴³⁴ Although cromolyn sodium is less effective than intranasal corticosteroids, it has never been adequately studied to determine its effectiveness in comparison with antihistamines or LT antagonists.⁴³⁵

Intranasal anticholinergics [Summary Statements 83, 84] 

The nasal anticholinergic ipratropium bromide is effective in reducing rhinorrhea caused by allergic rhinitis, nonallergic rhinitis (including cold-induced rhinitis⁴³⁶ and gustatory rhinitis⁶⁶), and the common cold.⁴³⁷, ⁴³⁸, ⁴³⁹, ⁴⁴⁰, ⁴⁴¹, ⁴⁴², ⁴⁴³, ⁴⁴⁴, ⁴⁴⁵, ⁴⁴⁶, ⁴⁴⁷ Ipratropium bromide is only approved (down to the age of 5 years) for the treatment of rhinorrhea, although 1 pediatric study showed modest benefit for controlling nasal congestion.⁴⁴⁸ Ipratropium bromide has no adverse effect on physiologic nasal functions (eg, sense of smell, ciliary beat frequency, or mucociliary clearance) and has a low incidence of adverse events, in particular epistasis and nasal dryness.⁴⁴⁹ Concomitant use of ipratropium bromide and intranasal corticosteroid or antihistamines has an additive effect in controlling rhinorrhea.³⁹⁰, ⁴⁴²

LT receptor antagonists [Summary Statement 85] 

LT receptor antagonists (LTRAs) are effective in the treatment of seasonal and perennial allergic rhinitis.⁴⁵⁰, ⁴⁵¹, ⁴⁵², ⁴⁵³ There is no significant difference in efficacy between LTRA and antihistamines (with loratadine as the usual comparator), and their concomitant use may be additive.⁴⁰, ⁴², ³⁷⁷ However, not all studies with the concomitant administration of an antihistamine and a LTRA have shown an additive effect. Although the concomitant administration of a LTRA and an antihistamine can have an additive effect, in general this approach is less efficacious than administering intranasal corticosteroids as monotherapy.⁴⁸, ³⁷⁵, ³⁷⁷, ³⁷⁹ However, such combination therapy may provide an alternative treatment for patients who are unresponsive to or not compliant with intranasal corticosteroids.

Montelukast has an excellent safety profile and has been approved down to 6 months of age. As many as 40% of patients with allergic rhinitis have coexisting asthma. Because montelukast has been improved for both rhinitis and asthma, it may be considered in such patients.⁴⁵⁴, ⁴⁵⁵, ⁴⁵⁶ The combination of montelukast and a second-generation antihistamine may protect against seasonal decrease in lung function in patients with allergic rhinitis.⁴⁵⁷

Omalizumab [Summary Statement 86] 

Omalizumab has been shown to have the potential for improvement in nasal and ocular symptoms as well as QOL in 1 study of patients with both seasonal and perennial allergic rhinitis.⁴⁵⁸ However, superiority to currently approved rhinitis treatments has not been shown. In addition to the limited data of omalizumab on symptoms of rhinitis, the high cost of omalizumab treatment precludes its use for rhinitis without concomitant asthma to perennial allergens.

Saline [Summary Statement 87] 

Although less effective than intranasal corticosteroids and no more effective than other active agents for rhinitis, isotonic and hypertonic saline solutions, used as either single or adjunctive agents, are of modest benefit for reducing symptoms and improving the QOL in patients with allergic rhinitis and rhinosinusitis.⁴⁵⁹ Various mechanisms, such as improvement in mucus clearance; enhanced ciliary beat activity; removal of antigen, biofilm, or inflammatory mediators; and a protective effect on sinonasal mucosa, have been proposed but not confirmed to explain the reported symptom improvement. The use of topical saline is associated with minimal side effects, such as burning, irritation, and nausea; has low cost; and has overall good patient acceptance.⁴⁶⁰, ⁴⁶¹ The preferred method of delivery, the volume, the concentration—that is, the ratio of isotonic to hypertonic saline⁴⁶², ⁴⁶³ (Table IX)—and the dose frequency have not been established.

Table IX. Saline irrigation solutions

Allergen immunotherapy is effective for therapy for allergic rhinitis and can potentially modify the disease.⁵¹, ⁴⁶⁴, ⁴⁶⁵ Unlike pharmacotherapy, the clinical benefits may be sustained years after discontinuation of treatment⁴⁶⁶, ⁴⁶⁷ (see allergen immunotherapy practice parameter⁵⁰ for more details). Allergen immunotherapy for allergic rhinitis may prevent the development of new allergen sensitization⁴⁶⁹, ⁴⁷⁰, ⁴⁷¹ and reduce the risk for the future development of asthma in some patients.⁴⁷², ⁴⁷³, ⁴⁷⁴, ⁴⁷⁵, ⁴⁷⁶, ⁴⁷⁷, ⁴⁷⁸, ⁴⁷⁹, ⁴⁸⁰, ⁴⁸¹ Immunotherapy has been associated with significant improvement in rhinitis symptom and medication scores and QOL measures as well as objective parameters such as nasal provocation challenge.⁴⁶⁶, ⁴⁷¹, ⁴⁷⁹, ⁴⁸², ⁴⁸³, ⁴⁸⁴, ⁴⁸⁵, ⁴⁸⁶, ⁴⁸⁷, ⁴⁸⁸, ⁴⁸⁹, ⁴⁹⁰, ⁴⁹¹, ⁴⁹², ⁴⁹³, ⁴⁹⁴, ⁴⁹⁵, ⁴⁹⁶, ⁴⁹⁷, ⁴⁹⁸, ⁴⁹⁹, ⁵⁰⁰, ⁵⁰¹, ⁵⁰², ⁵⁰³, ⁵⁰⁴, ⁵⁰⁵, ⁵⁰⁶, ⁵⁰⁷, ⁵⁰⁸, ⁵⁰⁹, ⁵¹⁰, ⁵¹¹, ⁵¹², ⁵¹³, ⁵¹⁴, ⁵¹⁵, ⁵¹⁶, ⁵¹⁷, ⁵¹⁸ Immunotherapy is usually no more costly than pharmacotherapy over the projected course of treatment.⁵¹⁹, ⁵²⁰

Allergen immunotherapy should be considered for patients who have symptoms of allergic rhinitis after natural exposure to allergens and who demonstrate specific IgE antibodies to relevant allergens. There is no specific upper or lower age limitation for allergen immunotherapy. Other factors that justify consideration of immunotherapy include (1) severity and duration of symptoms, (2) responsiveness to other forms of therapy, (3) unacceptable adverse effects of medications, (4) the patient's desire to avoid long-term pharmacotherapy, (5) reduction of the risk of future asthma, and (6) the presence of comorbid conditions, such as sinusitis or asthma. Contraindications include, for example, severe, uncontrolled asthma and significant or unstable cardiovascular disease.⁵⁰ There should be a cautious attitude in regard to the concomitant use of β-adrenergic blocking agents and allergen immunotherapy⁵⁰, ⁴⁶⁸ because β-adrenergic blocking agents might make allergen immunotherapy–related systemic reactions more difficult to treat (see allergen immunotherapy practice parameter⁴⁶⁸).

Clinical improvement can usually be noted after reaching the patient's maintenance dose. Lack of improvement after 1 year of maintenance treatment should prompt a review of the patient's immunotherapy program and possible discontinuation of immunotherapy. If allergen immunotherapy is effective, treatment may be continued for 3 years or longer. If discontinuation of effective inhalant allergen immunotherapy is considered, there are no specific tests or clinical markers currently available that will distinguish between patients who will or will not remain in long-term clinical remission. Thus, the decision to continue or stop immunotherapy must be individualized. Patients may experience local swelling at the injection site of subcutaneous immunotherapy and, on rare occasions, an anaphylactic reaction to allergen immunotherapy (refer to “Allergen Immunotherapy: A Practice Parameter Second Update”⁵⁰, ⁴⁶⁸ for further information regarding allergen immunotherapy).

Surgery may be indicated for the management of structural/mechanical problems or comorbid conditions of allergic rhinitis, such as nasal polyps and adenoidal hypertrophy.⁷⁷, ⁵²¹, ⁵²², ⁵²³ The most common surgical procedures include (1) septoplasty,⁷⁷ (2) reduction of inferior turbinate hypertrophy,³ (3) adenoidectomy, (4) functional endoscopic sinus surgery, and (5) nasal polypectomy.⁵²⁴ The reduction of nasal obstruction after surgery not only improves nasal airflow but also allows for better delivery of topical medications.

At times, the nasal congestion of rhinitis may be confused with obstruction created by structural or mechanical problems. A disturbance of normal airflow resistance and turbulent flow pattern creates the perception of nasal obstruction, regardless of the actual size of the air passage.⁵²⁵ Anterior septal deviation, with or without nasal valve collapse, and anterior inferior turbinate hypertrophy are the major structural components resulting in the symptom of nasal obstruction.⁵²⁴, ⁵²⁶ Whenever there is septal deviation, typically there is compensatory turbinate hypertrophy on the opposite side. Septoplasty is infrequently performed in children because it may have a negative effect on nasal growth, particularly of the nasal dorsum.⁵²⁷

Septoplasty,⁵²⁸ which involves reshaping, repositioning, or recontouring the cartilage, has a high reported success rate⁵²⁹ and is preferred over submucosal resection, a procedure that involves more extensive resection of cartilage and bone.⁵²⁹, ⁵³⁰ Turbinate hypertrophy reduction surgery may be performed in conjunction with or separate from septoplasty, depending on the surgical assessment.⁵³¹, ⁵³² The various surgical procedures available (eg, bipolar cautery or radiofrequency ablation)⁵²⁴, ⁵³³, ⁵³⁴, ⁵³⁵ alleviate the mucosal hypertrophy, the bony hypertrophy (eg, submucosal resection), or a combination of bony and mucosal hypertrophy (eg, powdered turbinoplasty or laser turbinectomy).⁵³⁶, ⁵³⁷, ⁵³⁸, ⁵³⁹ If the patient with rhinitis and coexisting turbinate hypertrophy has been unresponsive to medical therapy, a surgical evaluation can be considered.⁵⁴⁰, ⁵⁴¹, ⁵⁴²

In children, the indications for adenoidectomy are sleep apnea caused by adenotonsillar hypertrophy, chronic adenoiditis, and chronic sinusitis.⁵⁴³ For OME, an adenoidectomy is usually recommended after the first set of tympanostomy tubes extrudes, effusion returns, and a second set of tympanostomy tubes are being considered. An adenoidectomy may also be considered for adenoiditis, postnasal obstruction, or chronic sinusitis.⁵⁴³ Recent clinical studies recommend a trial of intranasal corticosteroids for adenoidal hypertrophy before surgical intervention.⁵⁴⁴, ⁵⁴⁵, ⁵⁴⁶, ⁵⁴⁷

Management decisions must be individualized and guided by (1) age; (2) frequency, severity, and spectrum of symptoms (eg, predominant congestion versus rhinorrhea); (3) allergen exposure pattern; and (4) comorbidities.¹¹, ⁵⁴⁸, ⁵⁴⁹ Response to previous treatment, patient and family preferences, compliance with therapy, and cost are additional factors that enter management decisions for the patient with rhinitis.¹¹, ⁵⁵⁰ Rhinitis medication management frequently will require consideration of a step-up approach, if therapy is inadequate, or a step-down approach, if symptom relief is achieved or maximized with other approaches, such as avoidance measures.⁵⁵⁰ Medications may be required only on an intermittent or short-term basis for the treatment of episodic rhinitis. The patient and physician should agree on what therapeutic approach can realistically be instituted. These therapy decisions can be committed to a Rhinitis Action Plan developed jointly with the patient and family (see Fig 5 for sample).

• 
  • View Large Image
  • Download to PowerPoint

• Fig 5. 

  Sample rhinitis action plan.

When a patient is compliant with the prescribed medication and yet is not responding to treatment, substitution of another class of medication can be considered. Adding another medication to the patient's treatment regimen will not always improve the patient's symptoms to a degree that outweighs the cost of this approach.³⁷⁵, ⁴⁵⁰, ⁵⁵¹

Appropriate follow-up for patients with rhinitis increases therapeutic success, improves compliance, and identifies complications from rhinitis or its treatment. During each follow-up patient visit, the treatment plan should be reviewed and possibly modified on the basis of physician and patient assessment of how effectively the treatment regimen is, judging from symptom control and improvement in QOL. In large part this will relate to the patient's compliance with the agreed-on therapeutic interventions.

Education is a key element in promoting adherence and optimizing treatment outcomes in allergic rhinitis. Education for the patient and family members or other patient advocates begins at the initial encounter and continues at following visits. The education program should emphasize the chronicity of rhinitis as a disease, the realistic outcome of therapy, an understanding of how to implement appropriate environmental changes, appropriate methods of medication administration, medication benefits and possible side effects, the comorbidity of other allergic diseases, and the effect that disease control can make in overall improvement in QOL.¹¹

Although it is recognized that education is important for rhinitis, the best delivery method, frequency, and educational setting have yet to be determined. One-on-one allergy treatment educational sessions about rhinitis treatment may not be any more effective than a handout.⁵⁵² Reduced use of medication, reduced office visits, or improvement in QOL has not been consistently shown when educational programs are implemented for rhinitis.⁵⁵³, ⁵⁵⁴, ⁵⁵⁵, ⁵⁵⁶, ⁵⁵⁷, ⁵⁵⁸, ⁵⁵⁹, ⁵⁶⁰, ⁵⁶¹, ⁵⁶², ⁵⁶³ Whatever rhinitis educational delivery method is selected, it is important to review the content of the educational material.⁵⁶⁴

Asthma [Summary Statements 95, 96] 

Patients with allergic rhinitis are at increased risk of developing asthma.²⁶², ⁵⁶⁵, ⁵⁶⁶, ⁵⁶⁷ Patients with allergic rhinitis without asthma, especially those sensitized to dust mites, often have nonspecific bronchial hyperresponsiveness (BHR),⁵⁶⁸, ⁵⁶⁹, ⁵⁷⁰, ⁵⁷¹ and many patients with seasonal allergic rhinitis experience a seasonal increase in BHR.⁵⁷² Conversely, subsegmental bronchial allergen challenge in patients with allergic rhinitis has been shown to result in both bronchial and nasal inflammatory responses.⁵⁷³ It has been suggested that in patients with moderate to severe allergic rhinitis, especially those with longstanding rhinitis and sensitization to dust mites, a reduced forced expiratory flow at 25% to 75% of forced vital capacity may be a marker of early bronchial pathology.⁵⁷⁴, ⁵⁷⁵, ⁵⁷⁶ Treatment with intranasal corticosteroids has been shown to prevent the seasonal increase in BHR experienced by patients with allergic rhinitis, to reduce existing BHR, and to improve pulmonary function tests.⁵⁷⁰, ⁵⁷⁶, ⁵⁷⁷, ⁵⁷⁸ Allergen immunotherapy for allergic rhinitis may reduce the development of asthma in children and possibly in adults.⁴⁷³, ⁴⁷⁵, ⁴⁷⁶, ⁴⁷⁷, ⁵⁷⁹, ⁵⁸⁰ Treatment of allergic rhinitis with intranasal corticosteroids and certain second-generation antihistamines may improve asthma control when both diseases coexist.⁵⁸¹, ⁵⁸², ⁵⁸³, ⁵⁸⁴, ⁵⁸⁵, ⁵⁸⁶, ⁵⁸⁷, ⁵⁸⁸

Recurrent OME [Summary Statement 97] 

Recurrent otitis media and OME are frequently associated with allergic rhinitis. Eustachian tube dysfunction remains the most common etiology for otitis media. Mediators released after allergen exposure result in nasal allergic inflammation and contribute to the dysfunction of the eustachian tube by producing eustachian tube edema and inflammation.⁵⁴³, ⁵⁸⁹, ⁵⁹⁰ Under natural circumstances, the middle ear is not exposed to allergens. However, measurements of elevated ECP,⁵⁹¹ IL-5,⁵⁹² and IgA⁵⁹² within the middle ear during chronic OME support a localized inflammatory process. Similar cytokine and cellular profiles have been noted concurrently in the middle ear and nasopharynx of atopics.⁵⁹⁰ These findings suggest that the ear may be part of the united airway in atopic patients.⁵⁹⁰

Pregnancy [Summary Statements 98-105] 

When selecting medications for the pregnant patient, the FDA pregnancy risk categories (Table X) should be considered. However, these are based largely on animal studies with limited human data. Therefore, human cohort and case-control studies as well as birth registry data should be reviewed before making a medication selection. Concern about the potential for congenital malformation because of medication use occurs primarily during the first trimester, when organogenesis is occurring.

Table X. FDA pregnancy risk categories

First-generation antihistamines have previously been recommended as first-choice agents because of their observed safety and longevity of use.⁵⁹³ However, in general, their sedative and impaired performance characteristics make them less desirable choices than second-generation antihistamines. The accumulated safety data during pregnancy on the second-generation antihistamines are comparable to those of the first-generation antihistamines (Table XI, Table XII). Although there are no reports of increased congenital malformations with the use of fexofenadine during pregnancy and animal studies are negative for teratogenicity, no epidemiologic studies in human pregnancy have been published.⁵⁹⁴ Currently, there are also limited data on desloratadine, azelastine, and levocetirizine. Although diphenhydramine is frequently used during pregnancy and has good overall safety data, administration of diphenhydramine has been associated with the development of cleft palate.⁵⁹⁵, ⁵⁹⁶, ⁵⁹⁷, ⁵⁹⁸, ⁵⁹⁹ Hydroxyzine should be used cautiously during the first trimester based on animal data.⁵⁹⁴

Table XI. Antihistamines in pregnancy first trimester H1 first-generation antihistamines

NS, Not significant; RR, relative risk.

Table XII. Antihistamines in pregnancy first trimester H1 second-generation antihistamines live birth data

NS, Not significant; RR, relative risk.

Oral decongestants should be avoided, if possible, during the first trimester because of conflicting reports of an association of phenylephrine and pseudoephedrine with congenital malformations such as gastroschisis and small intestinal atresia.⁵⁹⁴, ⁶⁰⁰ The risks of such malformations have been reported to be increased by combining a decongestant with acetaminophen or salicylates.⁶⁰⁰, ⁶⁰¹ The safety of intranasal decongestants during pregnancy has not been studied.

Sodium cromolyn and montelukast are both Pregnancy Category B drugs. Sodium cromolyn is a safe treatment for allergic rhinitis in pregnancy with the previously discussed clinical limitations.⁵⁹⁹, ⁶⁰², ⁶⁰³, ⁶⁰⁴ Montelukast has reassuring animal reproductive studies and unpublished human safety data. A published observational study including 9 patients on LTRAs (specific agent not identified) demonstrated no adverse events.⁶⁰⁵ This drug could be considered if there has been a favorable prepregnancy response.

Intranasal corticosteroids may be used during pregnancy because of their safety and efficacy profile. Clinical and epidemiologic studies on safety in human beings are limited. Although most intranasal corticosteroids are given an FDA Pregnancy Category C rating, gestational risk has not been confirmed in observational human data.⁶⁰³ A recent meta-analysis concluded that the use of intranasal corticosteroids during pregnancy does not increase the risk of major malformations, preterm delivery, low birth weight, and pregnancy-induced hypertension.⁶⁰⁶ The reported safety data on all intranasal corticosteroids have been reassuring, but beclomethasone,¹¹, ⁶⁰², ⁶⁰⁷, ⁶⁰⁸, ⁶⁰⁹ budesonide (Pregnancy Category B),⁶⁰³, ⁶¹⁰ and fluticasone propionate²²⁷, ⁶¹¹ have more accumulated data than triamcinolone,⁶¹², ⁶¹³ mometasone, and flunisolide.⁶¹¹ Because no substantial difference in efficacy and safety has been shown among the available intranasal corticosteroids, it would be reasonable to continue any of the intranasal corticosteroids that have adequately controlled the patient's symptoms before pregnancy.⁶⁰⁹, ⁶¹⁴ If intranasal corticosteroids are started during pregnancy, intranasal budesonide, which is Pregnancy Category B, largely on the basis of extensive human safety data, may be preferred.⁶⁰³, ⁶¹⁰ As with all medication use in pregnancy, intranasal corticosteroids should be administered at the lowest effective dose.

Allergen immunotherapy for allergic rhinitis may be continued during pregnancy if it is effective and not causing significant reactions.⁶¹⁴, ⁶¹⁵ The immunotherapy doses that the patient receives when she becomes pregnant should not be increased and should be adjusted appropriately during pregnancy if necessary to minimize the chance of inducing a systemic reaction. The benefit/risk considerations do not generally favor starting immunotherapy during pregnancy.⁵⁰

Elderly patients [Summary Statement 106] 

Rhinitis in the elderly may be influenced by age-related physiologic changes (eg, cholinergic hyperactivity), anatomic changes, and/or medications taken for other medical conditions. Many of the pathological changes in connective tissue and vasculature associated with aging may predispose to rhinitis symptoms.⁶¹⁶, ⁶¹⁷ These changes can result in dryness of the mucus membranes and increased nasal congestion in some elderly patients. Intranasal corticosteroids may be safely used for treatment of allergic rhinitis in the elderly because they do not cause any clinical or histological atrophic changes in the nasal mucosa.⁶¹⁸

Athletes [Summary Statement 107] 

Athletes with rhinitis can have their performance affected by rhinorrhea and nasal congestion. Endurance athletes, such as long-distance runners or triathletes, may experience rebound nasal congestion after the initial vasoconstriction that naturally occurs with exercise.⁶¹⁹ Prescription of medication for the competitive athlete should be based on 2 important principles¹⁸⁰: (1) no medication given to the athlete should be on any list of doping products and should be approved for use by the USOC (www.wada-ama.org) and IOC (1-800-233-0393)⁵⁵⁰; and (2) no medication should adversely affect the athlete's performance.⁶²⁰ Intranasal corticosteroids and topical decongestants are approved by the USOC, but all oral decongestants are banned. Although antihistamines are approved for use by the USOC, some are banned by the IOC.

Studies have shown that consultation with an allergist/immunologist improves patient outcomes, including QOL, compliance, and satisfaction,⁶²¹, ⁶²², ⁶²³, ⁶²⁴ by providing education on rhinitis and allergen avoidance. Consultation with an allergist/immunologist should be considered when any of the following are present:

Consultation with an allergist/immunologist may be indicated in other situations when there is agreement between the patient and the referring physician that such an approach is in the patient's best interests.

Back to Article Outline

Annotations 

Box 1: Patient presents with symptoms of rhinitis (Fig 6) 

Patients with rhinitis can present with symptoms of rhinorrhea, nasal congestion, sneezing, nasal pruritus, postnasal drainage, and/or associated ocular symptoms. These symptoms can occur with both allergic and nonallergic rhinitis. Symptoms of allergic rhinitis may occur only during specific seasons, may be perennial without seasonal exacerbations, may be perennial with seasonal exacerbations, or may occur episodically after specific aeroallergen exposures. Conjunctival symptoms frequently occur in conjunction with allergic rhinitis. Rhinitis symptoms often worsen during complications, such as otitis media and sinusitis, and frequently coexist with symptoms of other comorbid conditions, such as wheezing, cough, and chest tightness caused by asthma. Patients may be initially evaluated either by a generalist, such as a primary care physician, or by a specialist, such as an allergist/immunologist.

• 
  • View Large Image
  • Download to PowerPoint

• Fig 6. 

  Algorithm.

The history should include (1) the nature of the presenting symptoms, such as rhinorrhea, nasal congestion, sneezing, and associated ocular symptoms; (2) length of symptomatology; (3) the current and past medications used for treatment of rhinitis, including duration, effectiveness, and any associated adverse events; (4) current or past medications taken for other medical conditions and the relationship, if any, with rhinitis symptoms; (5) the degree to which the patient's rhinitis symptoms interfere with the patient's QOL; (6) seasonality of nasal and related symptoms (or lack thereof); (7) occupational exposure; (8) a detailed environmental history; (9) identification of precipitating factors; (10) the presence of other medical conditions; (11) presence of symptoms consistent with complications, such as sinusitis or otitis media, or comorbid conditions, such as asthma; (12) family history of allergic rhinitis, asthma, or atopic dermatitis; and (13) personal or family history of chronic sinus problems or infections, as well as diagnoses that may represent allergic symptoms, such as recurrent bronchitis.

When reviewing the allergic history in children, one may inquire about sniffing, snorting, clearing of the throat, chronic gaping mouth, halitosis, cough, dark circles under the eyes, and eye rubbing. The parents may describe the child as having a poor appetite, learning or attention problems, sleep disturbances, malaise, irritability, and a general sense of not feeling well.

The physical examination should focus on examination of the nose but may include evaluation of the ears, eyes, throat, and lungs. Examination of the nose should focus on the appearance of the nasal mucus membranes, the patency of the nasal passageways, unilaterality or bilaterality of findings, causes for anatomical nasal obstruction, and the quality and quantity of the nasal discharge.

Box 2: Is history and examination suggestive of allergic rhinitis? 

A diagnosis of allergic rhinitis can be confirmed only on the basis of a history of symptoms after exposure to known allergens, which correlates with specific IgE testing. Nonetheless, the history and physical examination alone is often suggestive of either allergic rhinitis or nonallergic rhinitis. Symptoms of pruritus and sneezing are much more common in allergic than nonallergic rhinitis. Seasonal exacerbations are also suggestive of allergic rhinitis. Patients with allergic rhinitis tend to develop the onset of symptoms earlier in life, typically before the age of 20 years, than those with nonallergic rhinitis. In contrast, isolated postnasal drainage is less likely to be a result of allergic rhinitis. Patients with vasomotor rhinitis may have symptoms triggered by strong odors such as perfume or tobacco smoke. A history of isolated rhinorrhea associated with eating is suggestive of gustatory rhinitis. Patients with chronic and frequent use of topical decongestant sprays may have rhinitis medicamentosa. Symptoms that are primarily unilateral suggest a structural problem, such as a nasal polyp, foreign body, septal deformity, or rarely a tumor. Hyposmia or anosmia are often associated with nasal polyposis but may also occur in other forms of rhinitis.

Many typical allergic findings are supportive of but not specific to allergic rhinitis. Mucosal appearance may not distinguish between allergic and nonallergic rhinitis, because nonallergic rhinitis may also present with mucosal pallor, edema, or hyperemia. However, the physical examination can help identify nasal polyps, foreign bodies, or other structural abnormalities.

Box 3: Therapeutic trial for allergic rhinitis symptoms 

Initial treatment of nonsevere rhinitis may include single-agent or combination pharmacologic therapy and avoidance measures.

Oral antihistamines are generally effective in reducing rhinorrhea, sneezing, and itching associated with allergic rhinitis but have little objective effect on nasal congestion. These agents may reduce symptoms of allergic conjunctivitis, which are often associated with allergic rhinitis. Antihistamines have a limited role in treating nonallergic rhinitis syndromes. Although antihistamines can be used on an intermittent basis, such as for episodic allergic rhinitis, it has been shown that continuous treatment for seasonal or perennial allergic rhinitis is more effective,³³¹ primarily because of unavoidable, ongoing allergen exposure. First-generation antihistamines have significant potential to cause sedation, performance impairment (that may not be subjectively perceived by patients), and/or anticholinergic effects (such as dry mouth and urinary retention). Consequently, second-generation antihistamines, which are associated with less risk or no risk for these side effects, are generally preferred over first-generation antihistamines for the treatment of allergic rhinitis. Intranasal antihistamines may be useful alternatives to oral antihistamines but may cause sedation in some patients and/or may be perceived to have a bitter taste.

Oral anti-LT agents, alone or in combination with antihistamines, have proven to be useful in the treatment of allergic rhinitis. There is no significant difference in efficacy between LTRA and antihistamines (with loratadine as the usual comparator), and their concomitant use may be additive,⁴⁰, ⁴², ³⁷⁷ but not all studies with the concomitant administration of an antihistamine and a LTRA have shown an additive effect. Although the concomitant administration of a LTRA and an antihistamine can have an additive effect, in general, this approach is less efficacious than administering intranasal corticosteroids.³⁴⁸, ³⁷⁵, ³⁷⁷, ³⁷⁹

Oral decongestants, such as pseudoephedrine or phenylephrine, help reduce symptoms of nasal congestion in both allergic and nonallergic rhinitis and are beneficial for use in combination with antihistamines. However, they can cause insomnia, loss of appetite, irritability, and palpitations. Elevation of blood pressure after taking an oral decongestant is very rarely noted in normotensive patients and only occasionally in patients with controlled hypertension. However, based on interindividual variation in response, hypertensive patients should be monitored.

Topical decongestants are appropriate to use on a short-term basis for nasal congestion associated with acute bacterial or viral infections, exacerbations of allergic rhinitis, and eustachian tube dysfunction. Intermittent use of topical decongestants may be considered, but efficacy and safety of this approach have not been formally studied. With regular daily use, some patients may develop rhinitis medicamentosa in 3 days, whereas others may not have evidence of rebound congestion after 4 to 6 weeks of use. Given this variability, it would be prudent to instruct patients of the risk of rhinitis medicamentosa when intranasal decongestants are used more than 3 days.

Intranasal corticosteroids are typically the most effective medication class for controlling sneezing, itching, rhinorrhea, and nasal congestion, the 4 major symptoms of allergic rhinitis. They are particularly useful for treatment of more severe allergic rhinitis and may be useful in some forms of nonallergic rhinitis. Intranasal corticosteroids when given in recommended doses are not generally associated with clinically significant systemic side effects. Although local side effects are minimal, if the patient is carefully instructed in the use of this class of drugs, nasal irritation and bleeding may occur. Patients should be instructed to direct sprays away from the nasal septum. The nasal septum should be periodically examined to assure that there are no mucosal erosions. Although nasal septal perforations are rarely caused by intranasal corticosteroids, mucosal erosions may suggest an increased risk for their subsequent development. In children, intranasal corticosteroids should be used at the lowest effective dose. Intranasal corticosteroids may be considered for initial treatment without a previous trial of antihistamines and/or oral decongestants, and they should always be considered before initiating treatment with systemic corticosteroids for the treatment of rhinitis.

A short course (5-7 days) of oral corticosteroids may be appropriate for the treatment of very severe or intractable rhinitis or nasal polyposis. However, single administration of parenteral corticosteroids is discouraged, and recurrent administration of parenteral corticosteroids is contraindicated because of greater potential for long-term corticosteroid side effects.

Nasal cromolyn is less effective than intranasal corticosteroids. It can reduce symptoms of allergic rhinitis in some patients and is most likely to be effective if initiated before symptoms become severe. For maximum efficacy, nasal cromolyn should be administered 4 times a day.

Intranasal anticholinergics may effectively reduce rhinorrhea but have minimal effects on nasal congestion or other nasal symptoms. The combination of intranasal anticholinergics with either antihistamines or intranasal corticosteroids may provide increased efficacy over either drug alone without any increased adverse effects.

Empiric avoidance of suspected inciting factors, such as allergens, irritants, and medications, should be implemented, if possible, even in early treatment of rhinitis. In the management of severe seasonal allergic rhinitis, patients should be advised to follow avoidance measures such as staying inside air-conditioned buildings, whenever possible, with windows and doors closed.

Box 4: Therapeutic trial for nonallergic rhinitis symptoms 

Many of the medications used to treat allergic rhinitis are also used in the management of nonallergic rhinitis. Intranasal corticosteroids and intranasal antihistamines may relieve both congestion and rhinorrhea associated with vasomotor rhinitis. Intranasal anticholinergics are useful in nonallergic rhinitis with predominant rhinorrhea (eg, gustatory rhinitis). Nonsedating oral antihistamines have not been shown to be effective in nonallergic rhinitis. Oral and intranasal decongestants may be considered in patients with nonallergic rhinitis and nasal congestion with similar precautions as discussed. Avoiding aggravating irritants may be helpful, particularly in patients suspected to have vasomotor rhinitis. For patients with rhinitis medicamentosa, discontinuation of nasal decongestant sprays and treatment with either intranasal or systemic corticosteroids may be necessary. Finally, patients suspected of infectious rhinitis should be treated with supportive measures to relieve ostiomeatal obstruction and judicious use of antibiotics for suspected bacterial sinusitis.

Box 5: Does the patient respond? 

In assessing response to therapy, a variety of parameters should be evaluated.

These include nasal symptoms (eg, congestion, itching, and rhinorrhea), physical signs of rhinitis (eg, edema of nasal turbinates), and QOL (eg, affect, ability to sleep, and ability to function effectively at work or school or while driving). In patients who have concomitant conditions that may be aggravated by rhinitis (eg, asthma), an assessment of concomitant conditions should also be made because improved control of rhinitis may be associated with improvement of these conditions. Patients who do not have a good response to treatment should be referred to an allergist/immunologist.

Box 6: Further follow-up, meets consultation criteria? 

If the initial treatment of rhinitis is successful, there is still a need for patient follow-up to assure that there is continued control of symptoms, maintenance of improved QOL, lack of impairment of performance at work or school and in other activities, and absence of medication side effects. Consultation with an allergist/immunologist is appropriate when these conditions are not met. Characteristics that should lead to consideration of consultation with an allergist/immunologist include the following:

Consultation with an allergist/immunologist may be indicated in other situations when there is agreement between the patient and the referring physician that such an approach is in the patient's best interests.

Box 7: Consultation with an allergist/immunologist 

An assessment of rhinitis by a rhinitis specialist requires a detailed history and appropriate physical examination. The history should include all of the components outlined in Box 1 but in more depth. The physical examination should assess the upper airway (nose, oropharynx) and lungs. In addition, rhinoscopy or examination by rigid or flexible rhinolaryngoscopy (endoscope) allows for better visualization of the middle meatus, the posterior septum, the sinus ostia, the nasopharynx, and presence of nasal polyps. Immediate hypersensitivity skin tests or in vitro tests for specific IgE to confirm an underlying allergic basis for the patient's symptoms may be necessary. Nasal cytology may be of value. Rarely, other tests may be indicated such as β- transferrin in nasal secretions (for suspected CNS fluid leakage) or tests of nasal ciliary function. Specific tests may also be necessary for coexisting conditions such as asthma (eg, pulmonary function), nasal polyps (eg, rhinoscopy), or sinusitis (eg, CT scan).

A thorough evaluation is the key component to the development of a long-term management plan. Management may include education regarding environmental avoidance and medication compliance, institution of environmental control measures, changes in medication, and allergen immunotherapy.

Box 8: Does patient have an allergic basis for rhinitis? 

A diagnosis of allergic rhinitis depends on the history of nasal symptoms after exposure to suspected allergens, which are confirmed with positive skin or in vitro tests for specific IgE. Determination of specific IgE, preferably by skin testing, is indicated to provide evidence of an allergic basis for the patient's symptoms, to confirm suspected causes of the patient's symptoms, or to assess the sensitivity to a specific allergen for avoidance measures and/or allergen immunotherapy. The precise sensitivity of specific IgE immunoassays compared with skin prick/puncture tests is approximately 70% to 75%. Skin tests are the preferred tests for the diagnosis of IgE mediated sensitivity. The number of skin tests and the allergens selected for skin testing should be determined on the basis of the patient's age, history, and environment and living situation—for example, area of the country, occupation, and activities. If there is a poor correlation between allergen exposures and symptoms, patients may have nonallergic rhinitis even if skin tests or in vitro tests for specific IgE are positive. For example, a patient with perennial rhinitis with an isolated positive skin test to ragweed would not have ragweed-induced allergic rhinitis as a cause of perennial symptoms and most likely would have nonallergic rhinitis.

A physical examination demonstrating a pale edematous nasal mucosa and the presence of allergic signs (nasal crease, nasal or eye rubbing, dark circles under the eyes) is helpful but does not always differentiate allergic from nonallergic rhinitis. Nasal smears and fiber optic nasal endoscopy are occasionally helpful in making such a differentiation.

Patients who have negative immediate hypersensitivity skin test reactions or negative in vitro tests for specific IgE should be considered nonallergic, especially if there is poor correlation between allergen exposure and symptoms.

Box 9: Management of allergic rhinitis 

Effective management of allergic rhinitis may require combinations of medications, aggressive avoidance measures, management of coexisting conditions, and/or allergen immunotherapy. Avoidance of triggers of rhinitis, such as allergens, irritants, medications, and occupational factors, is fundamental to the successful management of allergic rhinitis. After triggers are identified, the patient or representative should be educated about avoidance. If it is possible to anticipate the onset of symptoms associated with seasonal exposure to pollen or sporadic exposure to other triggers, early administration of medications (eg, before exposure or the development of symptoms) may lessen the impact of such exposures (see Box 3 annotation for a discussion of appropriate medications).

A short course of oral corticosteroids may be appropriate for the treatment of intractable nasal symptoms (see Box 3 annotation) or severe nasal polyposis. The chronic use of oral or parenteral corticosteroids is inappropriate in allergic rhinitis.

Allergen immunotherapy is effective for treatment of allergic rhinitis and allergic rhinoconjunctivitis. Effective immunotherapy has been associated with significant improvement in symptom and medication scores and QOL measures as well as objective parameters such as nasal provocation challenge, immunologic changes in cell markers, and cytokine profiles. Allergen immunotherapy should be considered for patients with allergic rhinitis who have demonstrable evidence of specific IgE antibodies to clinically relevant allergens. The decision to begin allergen immunotherapy depends on the degree to which symptoms can be reduced by avoidance and medication, the amount and type of medication required to control symptoms, and the adverse effects of medications. The severity and duration of symptoms as well as the impact of the patient's symptoms on QOL should also be considered in assessing the need for specific allergen immunotherapy.

Box 10: Management of nonallergic rhinitis 

Nonallergic rhinitis is characterized by sporadic or persistent perennial symptoms of rhinitis that do not result from IgE-mediated immunopathologic events. Examples of nonallergic rhinitis are infectious rhinitis, hormonal rhinitis, vasomotor rhinitis (including gustatory rhinitis), NARES, certain types of occupational rhinitis, and drug-induced rhinitis.

The signs and symptoms suggestive of rhinitis can be produced by anatomic conditions including nasal septal deviation, tumors, adenoidal hypertrophy, and hypertrophy of the nasal turbinates. Examination of the nose should include evaluation of the nasal passageways, secretions, turbinates, septum, and determination of whether nasal polyps are present. In selected cases, fiber optic nasal endoscopy and/or rhinomanometry may be useful. Nasal cytology may aid in differentiating allergic rhinitis and NARES from other forms of rhinitis.

The primary treatments for nonallergic rhinitis syndromes may vary and include (1) avoidance of aggravating irritants that may precipitate symptoms, (2) intranasal corticosteroids, (3) decongestants and exercise to relieve congestion, (4) anticholinergics to relieve rhinorrhea, (5) intranasal corticosteroids and intranasal antihistamines to relieve both congestion and rhinorrhea associated with vasomotor rhinitis, (6) institution of intranasal corticosteroids and discontinuation of nasal decongestant sprays in rhinitis medicamentosa, and (7) antibiotics and supportive measures to relieve ostiomeatal complex obstruction in bacterial rhinosinusitis.

Box 11: Cooperative follow-up 

Cooperative follow-up for allergic rhinitis patients includes the patient, family, and health care providers (ie, the primary care physician, allergist/immunologist, and possibly otolaryngologist). Goals include the reduction of symptoms and improvement in the patient's QOL and ability to function. These goals require cooperative management of exacerbations and complications by optimal use of environmental avoidance measures and medications, and in appropriate patients, use of immunotherapy.

Tapering of medications should always be considered to lessen the risk of adverse reactions. Side effects of medications must be carefully looked for during follow-up of patients. Maximizing compliance with medications and environmental controls can be challenging for the patient and physician, especially if the patient is very young or elderly.

Periodic assessment of the patient's QOL is essential. This includes evaluation of time lost from work or other activities, sleep quality, smell and taste, fatigue level, and general well being.

Patient education is a basic part of the follow-up plan for patients with allergic rhinitis. At each visit, it is important to review preventative measures (eg, environmental controls), medication use, and immunotherapy status with the patient. In addition, the presence of comorbid conditions such as sinusitis, asthma, and otitis media should be ascertained.

Effective follow-up requires awareness of the patient's goals, needs, and concerns. Allergen immunotherapy may be appropriate for patients with allergic rhinitis, especially if the patient is not responding to other therapeutic approaches and symptoms are interfering with the patient's ability to function. Follow-up also requires effective interaction between all health care providers as well as interaction with the patient and often the patient's family.

Although there is no surgical treatment for rhinitis, surgery may be indicated in the management of comorbid conditions, such as nasal obstruction from severe nasal septal deviation or inferior turbinate hypertrophy, adenoidal hypertrophy, or refractory sinusitis and complications thereof. Other reasons for referral to an otolaryngologist include the evaluation of ostiomeatal obstruction, nasal polyp surgery, biopsy of nasal tumors, or other surgical requirements.

Back to Article Outline

Summary statements with discussion 

Definition 

Although the term rhinitis connotes inflammation, and the majority of rhinitides are associated with inflammation, some forms of rhinitis such as vasomotor rhinitis or atrophic rhinitis may not be associated with inflammation of the nasal mucosa. Rhinitis frequently is accompanied by symptoms involving the eyes, ears, and throat.

Differential diagnosis of rhinitis 

Rhinitis is classified as allergic or nonallergic, but not all types of rhinitis can be easily separated into 1 of these categories. For example, occupational rhinitis has been classified separately from allergic and nonallergic because it may have components of both allergic and nonallergic rhinitis. Conditions that mimic symptoms of rhinitis include nasal polyps, cerebrospinal fluid rhinorrhea, ciliary dyskinesia syndrome, and structural/mechanical factors, such as deviated septum and pharyngonasal reflux (see Table I, Table II in the Executive Summary).

Classification of allergic rhinitis 

Recently, an international working group released ARIA recommendations and proposed a revised classification for allergic rhinitis that categorized all patients as either intermittent (<4 days per week or <4 weeks) or persistent (>4 days per week and >4 weeks) and classified severity as mild or moderate-severe.⁹, ¹⁰ This system proposes 4 classes, which include (1) mild intermittent, (2) mild persistent, (3) moderate/severe intermittent, and (4) moderate/severe persistent.¹⁰ This classification system discarded the terms seasonal and perennial, on the basis of several rationales including the observation that an aeroallergen (eg, grass pollen) that occurs seasonally in one region may be detected throughout the year in another geographical area. Demoly et al⁶⁹⁰ reported that 44% of patients traditionally classified as having seasonal rhinitis had persistent rhinitis according to the ARIA classification and that 44% with perennial allergic rhinitis were reclassified as intermittent. Thus, the traditional seasonal/perennial and ARIA schemes define different patient populations.

Treatment guidelines based on the ARIA guidelines have not been adequately studied.¹² However, the ARIA definition of mild rhinitis may be a useful comparative reference point for other severity grading schemes; this states that none of the following items is present: sleep disturbance; impairment of daily activities, leisure and/or sport; impairment of school or work; and symptoms present but not troublesome.⁹ This updated parameter supports the concept that more severe rhinitis is defined as more symptoms or interference with QOL, because data show that it may not be possible to separate patients into moderate and severe categories.¹² A nonvalidated modified 7-point visual analog (graphic rating) scale for grading severity of nasal and nonnasal symptoms of allergic rhinitis and the effects of this disorder on the QOL has been developed and published by the Joint Task Force on Practice Parameters and is included, with minor modification, inFig 1, Fig 2, Fig 3, Fig 4.¹³

In this document, the Joint Task Force retains and uses the terms seasonal and perennial in classifying patients with allergic rhinitis. These traditional descriptive terms are clinically useful and allow for accurate categorization of the vast majority of patients as having seasonal, perennial, or perennial allergic rhinitis with seasonal exacerbations. In addition to seasonal and perennial, episodic is used in this practice parameter to denote allergic nasal symptoms elicited by sporadic exposures to inhalant aeroallergens that are not usually encountered in the patient's indoor or outdoor environment. Although the terms seasonal, perennial, and episodic are clinically useful, therapeutic decisions should also be guided by frequency, duration, and severity of symptoms, and by current and previous responsiveness to medications.¹³

Allergic rhinitis 

Rhinitis is reported to be a very frequent disease, although data regarding the true prevalence of rhinitis are difficult to interpret. Most population surveys rely on physician-diagnosed rhinitis for their data, and this may give rise to a much lower reporting of rhinitis. Some population studies have been performed with questionnaires administered to the subjects, followed in many cases by telephone interviews, to try to make a specific diagnosis of rhinitis. It has been estimated that 25% to 33% of cases of rhinitis are a result of nonallergic rhinitis, and that 44% to 87% of allergic rhinitis has an element of nonallergic rhinitis, referred to as mixed rhinitis.², ⁷ Several studies may reflect a more accurate prevalence of rhinitis but probably still underreport this disease.³, ¹⁴, ¹⁶, ²⁵, ⁶⁹¹, ⁶⁹², ⁶⁹³ Because skin testing or determination of serum specific IgE is rarely assessed in such large epidemiologic studies, allergic causation is uncertain.

The prevalence of allergic rhinitis in various epidemiologic studies ranges from 3% to 19%.⁶⁹⁴ According to the Centers for Disease Control and Prevention, 23.7 million cases of allergic rhinitis were reported in 1996, including 15.9 million cases among persons age 45 years or younger.⁶⁹⁵

Seasonal allergic rhinitis is apparently becoming more common. One study showed that the prevalence of hay fever increased from 4% to 8% in the 10 years from 1971 to 1981.⁶⁹⁶ In another study, atopic skin test reactivity increased from 39% to 50% during an 8-year period of evaluation.⁶⁹⁷ However, a recent study of Swiss children 5 to 7 years old conducted during the last decade suggests that the increasing prevalence of allergic rhinitis may have plateaued in some countries.¹⁰⁹

Studies suggest that seasonal allergic rhinitis (hay fever) is found in approximately 10% to 20% of the population.³, ⁴, ⁵, ⁶ However, 1 study of physician-diagnosed allergic rhinitis showed a prevalence of 42% in 6-year-old children.¹⁶ Overall, allergic rhinitis affects 30 to 60 million individuals in the United States annually.⁶⁹⁸, ⁶⁹⁹, ⁷⁰⁰

In childhood, boys with allergic rhinitis outnumber girls, but the sex ratio becomes approximately equal in adults and may even favor women. Allergic rhinitis develops before age 20 years in 80% of cases. Studies have shown that the frequency of allergic rhinitis increases with age until adulthood and that positive immediate hypersensitivity skin tests are significant risk factors for the development of new symptoms of seasonal allergic rhinitis.⁴, ¹⁴, ¹⁵ There is a greater chance of a child developing allergic rhinitis if both parents have a history of atopy than if only 1 parent is atopic. Children in families with a bilateral family history of allergy generally develop symptoms before puberty; those with a unilateral family history tend to develop their symptoms later in life or not at all.⁶, ²⁵

There tends to be an increased prevalence of allergic rhinitis in nonwhites, in some polluted urban areas, and in individuals with a family history of allergy. Allergic rhinitis is more likely in first-born children. Studies in children in the first years of life have shown that the risk of rhinitis was higher in those youngsters with early introduction of foods or formula, higher serum IgE levels (100 IU/mL before age 6 years), and parental allergic disorders.¹⁶

Over the past few years, several studies supporting the hygiene hypothesis have suggested that early exposure to viral and bacterial infections, such as day care attendance or more siblings, may reduce the incidence of atopic disease by redirecting the immune system away from the allergic T_H2 pattern to the T_H1 pattern.¹⁷, ¹⁸, ¹⁹ One early explanation proposed that the increased incidence of atopy as explained by the hygiene hypothesis is a result of the reduced production of IL-12 and IFNs by cells of the innate immune system that are normally stimulated by bacterial products via their Toll-like receptors.²⁰ More recently, the role of reduced activity of regulatory T cells has been emphasized.²⁰ It is now felt that early infections reinforce the physiological mechanisms of natural dominant tolerance by expanding natural regulatory T cells. It also appears that the proinflammatory ligands of Toll-like receptors on the natural regulatory T cells play a major role in their activation and expansion.²¹ However, some recent studies refute the hygiene hypothesis, demonstrating that increased infections in early life increase allergic disease in childhood and do not contribute to any reduction of atopic disease in adults.²² Animal exposure in early infancy is likewise controversial because some studies have demonstrated that cat exposure in early infancy may reduce atopy and asthma,²³, ²⁴ whereas others have shown either no effect²⁸ or increased allergic disease.⁷⁰¹ Environmental risk factors for rhinitis in early infancy include environmental smoke exposure as well as allergens. Exposure to >20 cigarettes per day has been shown to be associated with an increased risk of developing allergic rhinitis at age 1 year.²⁸ The effect of tobacco smoke on allergic sensitization at age 1 year and the frequency of upper respiratory infections and ear infections in the young child remain controversial.²⁸, ⁷⁰² It has been suggested that the month of birth increases the risk of pollen and dust mite sensitization especially in childhood,⁷⁰³, ⁷⁰⁴ but not all studies agree.⁷⁰⁵

A critical period appears to exist early in infancy in which the genetically programmed individual is at greatest risk of sensitization on exposure to food and aeroallergens.⁷⁰⁶ In infancy, food allergies cause primarily gastrointestinal symptoms and atopic dermatitis and rarely induce nasal symptoms.⁷⁰⁷ Infants born to atopic families are sensitized to pollen aeroallergens more frequently than to indoor aeroallergens in the first year of life.²⁷ Although perennial allergic rhinitis (eg, dust mite and animal dander) may be present at a very early age,²⁸ seasonal allergic rhinitis typically does not develop until the child is 2 to 7 years of age, because 2 seasons of exposure are generally required for sensitization.²⁹, ³⁰ The prevalence of seasonal allergic rhinitis is higher in children and adolescents, whereas perennial allergic rhinitis is higher in adults.³¹

The financial impact on society is tremendous.⁷⁰⁸ The severity of allergic rhinitis ranges from mild to seriously debilitating. The direct cost of treating allergic rhinitis and the indirect cost related to loss of workplace productivity resulting from the disease are substantial. The estimated cost of allergic rhinitis based on direct and indirect costs is $2.7 billion for the year 1995, exclusive of costs for associated medical problems such as sinusitis and asthma. The cost to society has continued to increase. Based on pharmacy and medical care expenditure data, the estimated direct medical cost of allergic rhinitis was $7.3 billion for the year 2002, which was primarily incurred by costs of prescriptions and outpatient clinic visits.⁶⁹⁵ The total direct cost ($7.3 billion) and indirect cost ($4.28 billion) estimates for allergic rhinitis have been estimated to be $11.58 billion for 2002.⁷⁰⁹ This figure included the higher indirect costs associated with increased loss of productivity, which in turn was related to extensive OTC first-generation antihistamine use. Such treatment can cause drowsiness and impair cognitive and motor function.

Rhinitis is also a significant cause of lost school attendance, resulting in more than 2 million absent school days in the United States annually. In children, there is evidence that symptoms of allergic rhinitis can impair cognitive functioning, which can be further impaired by the use of first-generation antihistamines.¹⁷⁶

The nasal mucosa is designed to humidify and clean inspired air. The actions of epithelium, vessels, glands, and nerves are carefully orchestrated to perform these functions.⁷¹⁰ Dysfunction of any of these structures may contribute to the symptoms of allergic and nonallergic rhinitis.

Atopic subjects inherit the tendency to produce specific IgE antibodies and T_H2-directed immune responses. Intermittent or continuous exposure to low concentrations of indoor or outdoor aeroallergens over time may result in sensitization, a process initiated by processing of allergens by dendritic cells expressing CD1a and CD11c,⁷¹¹ in the nasal epithelium mucosa and subsequent presentation of allergenic peptides by MHC II molecules to T-cell receptors on resting CD4⁺ cells in regional lymph nodes. With appropriate costimulatory signals, allergen-stimulated resting T cells proliferate into T_H2-biased cells that produce IL-3, IL-4, IL-13, IL-5, GM-CSF, and other cytokines. T_H2 cytokines promote B-cell isotype switching and allergen specific IgE production by plasma cells, mast cell proliferation and infiltration of airway mucosa, and eosinophilic infiltration into the nasal mucosa and nasal epithelium.

With continued allergen exposure, increasing numbers of IgE-bound mast cells recognize the mucosally deposited allergen and degranulate.⁷¹⁰ Mast cell products include preformed mediators such as histamine, tryptase, chymase, kininogenase, heparin, and other enzymes.⁷¹² Newly formed mediators including prostaglandin D₂⁷¹³ and the cysLTs (LTC₄, LTD₄, and LTE₄) are produced by mast cells, eosinophils, basophils, and macrophages and bind to specific receptors in the nose.⁷¹⁴ These mediators produce edema, watery rhinorrhea, and mucosal hypertrophy; stimulate glands to exocytose their mucoglycoconjugates and antimicrobial substances; and dilate arteriole-venule anastomoses to cause sinusoidal filling and occlusion of nasal air passages. The cysLTs also play an active role in recruitment of inflammatory cells.⁷¹⁴ Sensory nerves are stimulated that convey the sensations of nasal itch and congestion and initiate systemic reflexes such as sneezing paroxysms. Within minutes of allergen exposure, there is release of mast cell mediators and induction of the response. This is known as the early or immediate allergic response. Although most subjects experience sneezing and copious rhinorrhea after allergen exposure, some subjects have sensations of nasal congestion as their predominant symptom. Neuropeptide expression (eg, substance P) has been demonstrated in mucosal nerve fibers of patients with seasonal allergic rhinitis, although the exact roles of sensory neural mediators in the pathogenesis of symptoms of allergic rhinitis are uncertain.⁷¹⁵

The mast cells mediators, including cytokines, are thought to play active roles in generating the late-phase response, which is initiated 4 to 8 hours after allergen exposure. LTC₄ increases both during the early-phase and late-phase nasal responses to allergen.⁷¹⁶ In a study evaluating kinetics of mediators and cytokines in nasal secretions after allergen challenge, histamine was increased in nasal secretions during the early-phase and late-phase nasal responses, and IL-1β and IL-4 were significantly elevated during the late-phase response.⁷¹² In another study that examined nasal mucosal late responses after a single nasal grass allergen exposure, T_H2 cytokines including IL-5 and IL-13 were expressed in association with increased numbers of eosinophils.⁷¹⁷

Local endothelial expression of intercellular adhesion molecule 1, E-selectin, and vascular adhesion molecule 1 have been correlated with increased nasal mucosal eosinophils at 24 hours after nasal allergen provocation, indicating that adhesion molecules are upregulated and facilitate transmigration of activated eosinophils into the nasal mucosa.⁷¹⁸ Chemoattractants, such as IL-5 and eotaxin for eosinophils, as well as chemokines IL-8 and monocyte chemoattractant protein 1 have been detected in nasal secretions during the late-phase response and are thought to enhance infiltration of the superficial lamina propria of the mucosa with neutrophils, eosinophils, and, at later time points, T lymphocytes and macrophages.⁷¹⁶ Eosinophil products such as major basic protein, ECP, hypohalides, LTs, and others are thought to damage the epithelium and other cells, resulting in an inflammatory response that promotes the tissue damage of chronic allergic reactions.³² Pretreatment with glucocorticoids is effective at reducing eosinophils and the release of cytokines (eg, IL-4, IL-5, and IL-13) during the late-phase response.³⁴

When allergen challenges are given repeatedly, the amount of allergen required to induce an immediate response decreases.⁷¹⁹, ⁷²⁰, ⁷²¹ This priming effect is thought to be a result of the influx of inflammatory cells during ongoing, prolonged allergen exposure and repeated late-phase responses. The priming effect demonstrates the importance of knowing the full spectrum of aeroallergens to which a patient responds and seasonal variations in allergic symptoms, and provides the rationale to consider initiating effective anti-inflammatory therapies before the pollen season or before other chronic or repetitive aeroallergen exposures.

Seasonal and perennial allergic rhinitis 

Symptoms of allergic rhinitis may include paroxysms of sneezing, nasal pruritus and congestion, clear rhinorrhea, and palatal itching. The conjunctiva,⁶¹¹ eustachian tubes, middle ear, and paranasal sinuses may also be involved.

Allergic rhinitis is associated with ear fullness and popping, itchy throat, and pressure over the cheeks and forehead. Malaise, weakness, and fatigue may also be present. Allergic rhinitis often begins during childhood and may coincide with or precede development of allergic asthma.⁷²² A positive family history of atopy is associated with development of allergic rhinitis in childhood.⁷²³

When not all the typical rhinitis symptoms are expressed, the diagnosis is more difficult to make. Nasal airflow obstruction, a major symptom of seasonal or perennial allergic rhinitis, is associated with nasal eosinophilic inflammation.⁸⁹ Distinct temporal patterns of symptom production may aid diagnosis. Symptoms of rhinitis that occur whenever the patient is exposed to a furry pet suggest IgE mediated sensitivity to that pet. Patients who are exquisitely sensitive to animal proteins may develop symptoms of rhinitis and asthma when entering a house or laboratory even though the animal is no longer present. Children who own pets can passively transfer cat allergen on their clothing into schools and may contribute to high levels of ambient cat allergen in classrooms.⁷²⁴ Seasonal and perennial forms of allergic rhinitis often coexist in the same individual. Symptoms may be chronic and persistent, and patients may present with secondary complaints of mouth-breathing, snoring, or symptoms of sinusitis.⁷²⁵ Severe allergic rhinitis has been associated with diminished QOL, disordered sleep (in as many as 76% of patients), and impairment in work performance.¹⁰, ¹⁷⁹, ⁷²⁶

Seasonal allergic rhinitis symptoms typically appear during a defined season in which aeroallergens are abundant in the outdoor air. The length of seasonal exposure to these allergens is dependent on geographic location and climactic conditions.⁷²⁷, ⁷²⁸ Familiarity with the pollinating season of the major trees, grasses, and weeds of the locale makes the syndrome easier to diagnose.⁷²⁹, ⁷³⁰, ⁷³¹ Certain outdoor mold spores also display seasonal variation, with highest levels in the summer and fall months.⁷³² Tree (eg, birch, oak, maple, and mountain cedar), grass (eg, timothy and Bermuda), and weed (eg, ragweed) pollens and fungi (eg, Alternaria, Aspergillus, and Cladosporium) are common seasonal allergens.⁷³³ Hyperresponsiveness to irritant triggers such as chlorine is enhanced among patients with seasonal allergic rhinitis.⁶⁷, ⁷³⁴, ⁷³⁵

In studies of seasonal allergic rhinitis, a correlation between the daily pollen count and overall daily symptom score and medication score has been found.⁷³⁶ Nasal sensitivity to seasonal pollen allergens increases as the pollen season progresses because of the priming phenomenon.⁷¹⁹ As a consequence of priming, at the end of the pollen season, nasal symptoms may decline more slowly than the pollen counts.⁷³⁷ Individual host sensitivity to an aeroallergen may influence the intensity of symptoms. The levels of pollen counts that cause symptoms may vary with an individual's degree of sensitivity and with different pollens.⁷³⁸, ⁷³⁹ Indoor allergens responsible for perennial allergic rhinitis are present in the environment throughout the year.⁷⁴⁰, ⁷⁴¹

Both research and clinical experience support the concept that allergic rhinitis and allergic conjunctivitis may exist in rare patients with negative skin tests and/or in vitro tests for specific IgE.²⁴¹, ⁷⁴², ⁷⁴³, ⁷⁴⁴, ⁷⁴⁵ A patient with a compelling history of symptoms after exposure to an allergen can have a positive nasal challenge with that allergen despite negative skin tests and/or in vitro tests for specific IgE antibody. Studies have shown that patients with allergic rhinitis symptoms after exposure to house dust have been found to have local inflammation, nasal IgE production, and a positive response to a nasal allergen provocation test with Dermatophagoides pteronyssinus, despite having negative skin tests and specific IgE to D pteronyssinus.²⁴¹, ⁷⁴², ⁷⁴³ Further research is needed to determine what allergens are capable of producing this type of reaction, the prevalence of this condition, the mechanism responsible for local allergic antibodies, and the optimal treatment for these patients.

Allergic conjunctivitis 

Allergic rhinitis is often accompanied by allergic conjunctivitis (a disease complex sometimes referred to as allergic rhinoconjunctivitis) that produces conjunctival injection and chemosis associated with symptoms of itchy eyes and tearing.⁴³ Estimates of the prevalence and severity of conjunctival symptoms associated with allergic rhinitis vary depending on the aeroallergen, geographic region, and other factors. In 1 seasonal allergic rhinitis study, allergic conjunctivitis symptoms were reported in more than 75% of patients.⁷⁴⁶ Sensitivity to pollens is more frequently associated with rhinoconjunctivitis, whereas sensitivity to house dust mites (D pteronyssinus, Dermatophagoides farinae) is reported to cause less ocular symptoms.⁷³⁹

The Joint Task Force is developing a complete Parameter on Diagnosis and Treatment of Allergic Conjunctivitis that will provide more comprehensive discussion than the more limited statements on allergic conjunctivitis in this Rhinitis Parameter. A complete review of the differential diagnosis of conjunctivitis is beyond the scope of this document. Ocular allergy may include seasonal and perennial allergic conjunctivitis discussed here, but also 2 vision-threatening disorders, atopic keratoconjunctivitis (associated with eczematous lesions of the lids and skin) most commonly seen in older adult patients, and vernal keratoconjunctivitis (chronic inflammation of palpebral conjunctiva), seen most commonly seen in the pediatric and adolescent age groups with a male predominance. In seasonal and perennial allergic conjunctivitis associated with allergic rhinitis, both eyes are typically affected, and itching is usually a prominent symptom.⁷⁴⁷

Oral antihistamines, intranasal antihistamines, oral anti-LT agents, intranasal corticosteroids, and allergen immunotherapy are treatments for allergic rhinitis that have been reported to relieve associated ocular allergy symptoms in controlled trials.³⁷, ³⁸, ³⁹, ⁴⁰, ⁴¹, ⁴², ⁴³, ⁴⁶, ⁴⁷, ⁴⁸, ⁴⁹, ⁵⁰, ⁵¹, ⁵², ⁵³, ⁵⁴ In systematic reviews of randomized controlled studies, intranasal corticosteroids compared with oral antihistamines⁵³, ⁵⁴, ⁷⁴⁸ and intranasal corticosteroids compared with intranasal antihistamines⁴⁶ were not significantly different in relieving eye symptoms. In placebo-controlled studies of adults, fluticasone furoate nasal spray has been demonstrated to reduce significantly ocular symptoms associated with seasonal allergic rhinitis.⁴⁴, ⁴⁵, ⁷⁴⁹

Use of cold compresses and irrigation with saline solution or artificial tears has been advocated to relieve mild symptoms of allergic conjunctivitis. A variety of topical ophthalmic agents are indicated for specific treatment of itching or symptoms of allergic conjunctivitis. These include medications listed in Table XIII and can be summarized by the following categories.

Table XIII. Topical ophthalmic preparations for ocular allergy symptoms

Oral antihistamines are generally less effective in relieving ocular allergy symptoms than topical ophthalmic agents and have slower onset of action.⁷⁵⁰, ⁷⁵¹, ⁷⁵² Although comparative efficacy trials of topical ophthalmic agents in real-life settings are generally lacking, studies performed in environmental challenge chambers or using acute ocular allergen challenges have generally demonstrated that dual action ophthalmic agents are more effective in preventing or treating ocular itching than other ocular agents.⁷⁵³, ⁷⁵⁴, ⁷⁵⁵, ⁷⁵⁶ Oral agents have also been associated with excessive drying of the tear film.

Nonallergic rhinitis 

Vasomotor rhinitis 

Vasomotor rhinitis is unrelated to allergy, infection, structural lesions, systemic disease, or drug abuse. Although the term vasomotor implies increased neural efferent traffic to the blood vessels supplying the nasal mucosa, this has never been proven. Subjects with predominant rhinorrhea (sometimes referred to as cholinergic rhinitis) appear to have enhanced cholinergic glandular secretory activity because atropine effectively reduces their secretions.⁶⁵ Subjects with predominantly nasal congestion and blockage may have nociceptive neurons that have heightened sensitivity to innocuous stimuli.

The term vasomotor rhinitis has been used loosely to describe the condition of patients with perennial rhinitis whose symptoms are intensified by changes in temperature or relative humidity, alcohol, and odors such as bleach, perfume, or solvents. Other triggers include tobacco smoke, dusts, automotive emission fumes, and nonspecific irritant stimuli such as chlorine.⁶⁷ Cold dry air and exercise may also trigger symptoms.⁶⁸, ⁶⁹, ⁷⁵⁷ The symptoms are variable, consisting mainly of nasal obstruction and increased secretion. Sneezing and pruritus are less common. Although the term vasomotor implies increased neural efferent traffic to the blood vessels supplying the nasal mucosa, this has never been proven. A lack of change in nasal compliance after administration of nasal oxymetazoline compared with normal subjects lends support to the hypothesis that vasomotor rhinitis may be attributable to autonomic dysfunction.⁷⁵⁸

Rhinitis from food ingestion 

Foods can provoke rhinitis symptoms by a variety of different mechanisms.⁷⁵⁹, ⁷⁶⁰ Ingested food allergens rarely produce isolated IgE-mediated rhinitis without involvement of other organ systems. Urticarial rash, facial or lip swelling, or bronchospasm strongly suggest an IgE-mediated reaction.⁷⁶¹ In a large group of children undergoing double-blind, placebo-controlled food challenges, nasal symptoms developed in 70% of the positive challenges.⁷⁶², ⁷⁶³ In that study, the most common food allergens confirmed in respiratory tract symptoms included egg, cow's milk, peanut, soy, fish, shellfish, and tree nuts. In contrast, rhinitis may occasionally be reported in unusual food allergens—for example, 2 of 43 patients reporting rhinitis with kiwi allergy.⁷⁶⁴ In another descriptive study that did not include double-blind, placebo-controlled food challenges, rhinitis or conjunctivitis accounted for 5.7% of the total symptoms reported.⁷⁶⁵ In adults, food skin tests may be appropriate in occasional cases if a careful history suggests food-related rhinitis symptoms, particularly if rhinitis symptoms are associated with other systemic symptoms. Although a variety of opinions have been expressed in the literature,²⁵, ⁷⁵⁹, ⁷⁶⁰, ⁷⁶¹, ⁷⁶², ⁷⁶⁶, ⁷⁶⁷, ⁷⁶⁸, ⁷⁶⁹, ⁷⁷⁰ there are few or no credible data available to justify routine performance of food skin tests in the evaluation of rhinitis in adults. In the evaluation of rhinitis in children, in whom the history may be more difficult to interpret and food allergy is more common, there is greater justification to consider performance of limited food skin testing. Beer, wine, and other alcoholic drinks may produce symptoms by nasal vasodilation. Alcohol-induced hypersensitivity symptoms are also more prevalent in persons with allergic rhinitis and asthma.⁷⁰ The syndrome of watery rhinorrhea occurring immediately after ingestion of foods, particularly hot and spicy foods, has been termed gustatory rhinitis and is vagally mediated.⁶⁶

Infectious rhinitis 

Acute rhinitis is usually associated with a viral upper respiratory infection and frequently presents with rhinorrhea, nasal obstruction, and fever. Initially, viral rhinitis is characterized by clear, watery rhinorrhea that is accompanied by sneezing and nasal obstruction. Edema of the nasal mucosa produces occlusion of the sinus ostia with resulting facial pain or of the eustachian tube with resulting ear fullness. The nasal drainage may become cellular and cloudy due to the presence of organisms, white blood cells, and desquamated epithelium. Responsible viruses include rhinoviruses, respiratory syncytial virus, parainfluenza, influenza, and adenoviruses. Unless there is bacterial superinfection (<2% of the time),⁷⁵, ⁷⁶ the condition is self-limiting and usually resolves within 7 to 10 days. Acute bacterial rhinosinusitis may occur de novo or may follow viral rhinitis. Nasal obstruction, cloudy drainage, vestibular crusting, and facial pain occur. Not all patients report fever. Bacteria frequently recovered from nasal or sinus cultures include Streptococcus pneumoniae, Moraxella catarrhalis, and Haemophilus influenzae.⁷⁷¹

Prominent symptoms reported by patients with chronic rhinosinusitis include nasal congestion, sinus congestion, nasal discharge, headache, fatigue, and change in olfaction.⁷⁷² Although nearly 50% of patients diagnosed with chronic rhinosinusitis exhibit no growth on culture, in sinus puncture studies the most frequently isolated organisms are H influenzae, Staphylococcus aureus, and Pseudomonas aeruginosa.⁷⁷³ In patients with immunodeficiency, HIV positivity, or AIDS, mycobacterial, fungal, and other opportunistic organisms may be involved.

The symptoms of allergic rhinitis are frequently confused with infectious rhinitis when patients complain of a constant cold. Purulent nasal drainage may be present in either infectious or noninfectious rhinitis. Symptoms persisting longer than 2 weeks should prompt a search for causes other than infection. Foreign body rhinitis should be considered in the differential diagnosis, especially in children. Symptoms may be acute or chronic, unilateral or bilateral, and the nasal discharge may be bloodstained or foul smelling.

Exacerbations of rhinitis symptoms with predominant clear rhinorrhea in patients with a known history of allergic rhinitis may prove to be a diagnostic challenge. The distinction between active infection and allergy should be made. When the history or physical examination is not diagnostic, a nasal smear may be obtained to aid in differentiation. Early in rhinovirus infections, there is an increase in vascular permeability that is likely a result of bradykinin. Later, there may be an increase in glandular secretion, particularly of locally synthesized secretory IgA.⁷⁷⁴ Neutrophilic infiltrates may be present in rhinoviral and other viral rhinitis syndromes.

Physical examination findings in both acute and chronic sinusitis may include sinus tenderness on palpation, mucosal erythema, purulent nasal secretions, increased pharyngeal secretions, and periorbital edema. Furthermore, because these symptoms tend to overlap with those of perennial rhinitis, there is a frequent need to perform imaging studies to assist in the differential diagnosis. Nasal cytology may be useful, but the clinical value is limited by low specificity and sensitivity. Although the absence of neutrophils argues against infection, neutrophils may be present in both acute and chronic sinusitis and may be noted alongside eosinophils in allergic rhinitis during acute sinusitis (see “The Diagnosis and Management of Sinusitis: A Practice Parameter Update”⁷⁷ for more detail).

Allergy, mucociliary disturbance, and immune deficiency may predispose certain individuals to the development of more frequent acute⁷⁷⁵ or chronic infections. Mucociliary abnormalities may be congenital (eg, PCD, Young syndrome, CF) or secondary to infection.⁷⁷⁶, ⁷⁷⁷

Infectious rhinitis in children 

Viral rhinitis, starting in the neonatal period, averages about 3 to 8 episodes per year in children and accounts for the majority of infectious rhinitis.⁷⁷, ⁷⁷⁸ The progression from viral rhinitis to secondary bacterial rhinitis occurs in approximately 10% of children and adults.⁷², ⁷³, ⁷⁴ These bacterial infections may progress to acute sinusitis and otitis media.⁷⁷⁹ Although it is generally accepted that atopic-prone infants and young children compared with their lower-risk cohorts appear to experience more episodes of otitis media and sinusitis,⁷⁷ not all research supports this conclusion.⁸⁵, ⁸⁶ Primary bacterial rhinitis, although uncommon, may occur in the newborn because of congenital syphilis with characteristic rhinorrhea followed by ulceration. Primary localized bacterial rhinitis may also occur during β-hemolytic streptococcal infections, particularly when scarlet fever is present (50% prevalence).⁹³ Secondary bacterial rhinitis with or without sinusitis occurs more frequently in children with antibody, complement, and leukocyte deficiency disorders; hyper-IgE syndrome; structural defects (eg, cleft palate and osteopetrosis); and CF. In CF, S aureus and P aeruginosa are important pathogens in infectious rhinitis. Children with normal immunity may also develop secondary bacterial rhinitis with S aureus infection manifesting as impetigo of the anterior nares with characteristic crusting and irritation. Purulent rhinorrhea, especially if unilateral, persistent, bloody, or malodorous, may suggest an intranasal foreign body.⁹³ Culturing the nasal pharynx of normal children without visualization is of limited value because pathogenic bacteria within the nasal pharynx have been recovered in as many as 92% of asymptomatic healthy children.⁹³ However, a recent meta-analysis as well as individual clinical studies have demonstrated that endoscopically directed middle meatus cultures is a highly sensitive and accurate culture method for acute bacterial rhinitis/sinusitis in adults and might be considered in the older child.⁹⁴, ⁹⁵, ⁹⁶, ⁹⁷

Differentiating allergic rhinitis from infectious rhinosinusitis or adenoiditis may be difficult especially in children, because the symptoms overlap and even purulent nasal drainage may be present in noninfectious rhinosinusitis. Careful consideration of the need for antimicrobial use is increasingly important because antibiotic use has been causally related to the development of bacterial drug resistance.⁷⁸, ⁷⁹, ⁸⁰, ⁸¹, ⁸² Furthermore, the administration of antimicrobials increases the carriage of antimicrobial-resistant strains of certain bacterial pathogens, such as S pneumoniae, especially in children.⁷⁸, ⁷⁹, ⁸³, ⁸⁴

NARES 

In NARES, individuals experience perennial symptoms of sneezing paroxysms, profuse watery rhinorrhea, nasal pruritus, and occasional loss of smell.¹⁰¹, ⁷⁸⁰ Patients with NARES are at risk for development of obstructive sleep apnea.¹⁰⁴ They are typically middle-age and have a characteristic perennial course but with paroxysmal episodes. NARES occurs extremely infrequently in childhood and probably accounts for less than 2% of children with nasal eosinophilia.⁷⁸¹ The prevalence of this syndrome in the general population is unknown.

The etiology of the syndrome is obscure but may be an early stage of nasal polyposis and aspirin sensitivity.¹⁰³ NARES is characterized by large numbers (inconsistently defined as >5% to >20%) of eosinophils on nasal smear.⁹⁸, ⁹⁹, ¹⁰⁰, ¹⁰², ⁷⁸² Similar to findings in patients with allergic rhinitis, mast cells with bound IgE and elevated tryptase have been detected in nasal mucosal biopsies of patients with NARES.⁷⁸³ Patients commonly lack evidence of allergic disease as determined by skin testing and/or determination of in vitro aeroallergen specific IgE assays.

Occupational rhinitis 

Occupational rhinitis may be defined as inflammation of the nasal mucosa resulting in nasal symptoms caused by exposures in the workplace. The concept of “the united airway” is likely applicable to occupational rhinitis in which the respiratory mucosa forms a continuum from the nose to the lower airways,⁷⁸⁴ whereby nasal inflammatory responses triggered by exposure to occupational sensitizers are associated with parallel inflammatory responses in the lower airways.¹¹² Occupational rhinitis may be caused by direct effects of respiratory irritants or via immunologic mechanisms. Irritant exposures encountered in the workplace to agents such as grain dust constituents (eg, endotoxin), flour dust, fuel oil ash, and ozone elicit neutrophilic inflammation of the nasal mucosa.¹⁰⁷, ¹⁰⁸, ¹⁰⁹ Alternatively, IgE-mediated sensitization and rhinoconjunctival symptoms may result from occupational exposure to protein allergens including flour, laboratory animals (rats, mice, guinea pigs, and so forth), animal products, coffee beans, natural rubber latex, storage mites, mold spores, pollen, psyllium, enzymes, and many other substances.¹⁰⁵, ¹⁰⁶ In workers with IgE-dependent sensitization to proteins (eg, flour, laboratory animals, and natural rubber latex), eosinophils, basophils, ECP, and tryptase are significantly increased in nasal lavage after nasal allergen challenge.¹¹¹, ¹¹², ¹¹³ Some chemicals such as acid anhydrides, platinum salts, and chloramine may cause IgE-mediated occupational rhinitis.¹¹⁴, ⁷⁸⁵ After nasal challenge with hexahydrophthalic anhydride, an acid anhydride, increased eosinophils and neutrophils have been identified in nasal lavage fluid.¹¹⁴ Immunologic mechanisms may be important for other chemical sensitizers (eg, glutaraldehyde and diisocyanates) that cause occupational rhinitis and OA even though specific IgE is not detected consistently.⁷⁸⁶, ⁷⁸⁷

The incidence of occupational rhinitis attributable to specific substances may depend entirely on the nature of industrial exposures encountered in a given geographical region. For example, the relative risk of occupational rhinitis in Finland, which has many agricultural industries, was highest among furriers, bakers, and livestock breeders.⁷⁸⁸ The prevalence of occupational rhinitis is essentially 100% among workers with OA who are sensitized to high-molecular-weight protein allergens, whereas only 50% of those with OA caused by chemicals have been identified with work-related rhinitis.¹¹⁰ The prevalence of work-related rhinoconjunctival symptoms is frequently reported by laboratory animal handlers (24%), although concomitant SPT reactivity to laboratory animal allergens is demonstrated in only a minority (9.6%) of symptomatic workers,¹⁰⁶, ⁷⁸⁹ suggesting that nonallergic factors may also be important. Airborne exposure to endotoxin is commonly detected in animal housing facilities and has been considered as a potential cause of occupational rhinitis, although current evidence is lacking to support effects in animal workers.⁷⁸⁹ Occupational rhinitis may precede or accompany the development of OA. Atopy and intensity of exposure are risk factors for developing occupational rhinitis.¹¹⁵

Symptoms may occur acutely at work after intermittent exposure or more chronically at work after continuous exposure. Occupational rhinitis should be suspected in patients with nasal symptoms, which are temporally related to exposure at work and often improve away from the workplace. An asymptomatic latency period of exposure lasting weeks to years often precedes work-related symptoms caused by occupational respiratory sensitizers.¹⁰⁵, ¹¹⁶ Skin prick testing may confirm sensitization if appropriate and if suitable reagents are available. Occupational rhinitis has been evaluated with nasal allergen challenge methods that measure prechallenge and postchallenge symptoms scores, nasal lavage cells, and mediators as well as nasal airflow; however, their diagnostic validity has not been evaluated.¹¹², ¹¹⁴

Irritant-induced rhinitis in an occupational setting, referred to as reactive upper-airways dysfunction syndrome (RUDS), is a chronic rhinitis syndrome triggered acutely by high-level exposure to irritants. Chronic RUDS has been reported among fire fighters exposed to complex mixtures of airborne pollutants during the World Trade Center disaster.⁷⁹⁰, ⁷⁹¹ Exposed workers present acutely with nasal burning, hypersecretion of mucus, and nasal congestion.⁷⁹² Because there is insufficient information regarding the natural history and diagnosis of RUDS, the condition is poorly defined, and further study is required.

Optimal management of occupational rhinitis is avoidance of the occupational trigger by modifying the workplace, using filtering masks, or removing the patient from the adverse exposure. Pharmacologic therapy as discussed in earlier sections can be instituted, recognizing that chronic use of medication will probably be required. Strategies to prevent or reduce symptoms may include the daily use of intranasal corticosteroids or the administration of antihistamines and/or intranasal cromolyn immediately before allergen exposure. It is also important to institute avoidance measures for nonoccupational (and occupational) allergens that may contribute to rhinitis symptoms. Specific immunotherapy (SIT) is a possible treatment option for IgE-dependent occupational rhinitis to occupational protein allergen. Immunotherapy could be considered when 1 or a few allergens have been linked clinically to disease, avoidance of the triggering allergens is impossible, a commercial allergen extract is available, and efficacy and safety have been demonstrated to the treatment allergens. For example, SIT with pollen extracts may benefit outdoor workers with seasonal allergic rhinitis, and SIT with standardized cat allergen extract may decrease occupational symptoms among sensitized animal workers.⁵⁰³, ⁷⁹³ Trials of subcutaneous SIT have been conducted in workers with natural rubber latex allergy but failed clearly to demonstrate acceptable safety and/or efficacy.¹¹⁷ Immunotherapy is not appropriate to treat occupational rhinitis caused by low-molecular-weight chemical antigens.

Hormonal-induced rhinitis 

Rhinitis symptoms are common during pregnancy.⁵⁹⁵, ⁵⁹⁶, ⁶⁰⁴, ⁶⁰⁹, ⁶¹⁴, ⁶⁸⁷, ⁷⁹⁴ The most common causes of nasal symptoms during pregnancy are allergic rhinitis, sinusitis, rhinitis medicamentosa, and vasomotor rhinitis of pregnancy. Allergic rhinitis worsens in approximately 1/3 of pregnant patients.¹¹⁸ Sinusitis has been reported to be 6 times more common in pregnant than nonpregnant women.⁷⁹⁵ Nasal vascular pooling caused by vasodilation and increased blood volume may account for worsening allergic rhinitis and increased sinusitis during pregnancy.¹¹⁹ The development of a type of rhinitis unique to the pregnant patient is referred to as vasomotor rhinitis of pregnancy or pregnancy rhinitis. It has been suggested that pregnancy rhinitis be defined as rhinitis without an infectious, allergic, or medication-related cause that starts before the last 6 weeks of pregnancy, persists until delivery, and resolves completely within 2 weeks after delivery.¹²⁰ It has been suggested that when pregnancy rhinitis causes snoring, it may even be a factor in the development of pre-eclampsia.¹²¹ Elevated progesterone, estrogen, prolactin, vasoactive intestinal peptide, and/or placental growth hormone levels during pregnancy have been associated with a number of secondary phenomena. They include nasal mucosal swelling caused by vascular pooling of blood and vascular leaking of plasma into the stroma as well as the increase in glandular secretion and nasal vascular smooth muscle relaxation.¹²⁰, ⁶⁰⁹, ⁷⁹⁶ However, there is no convincing evidence that any of these hormones contribute directly to pregnancy rhinitis.¹²⁰ Pregnancy rhinitis may respond in milder cases to exercise, head of bed elevation, nasal alar dilatation, and saline rinses. Although there is no research on the safety of short-term topical decongestants combined with intranasal corticosteroids in pregnancy, these have been suggested for management of pregnancy rhinitis when the measures discussed are not effective.¹²⁰, ⁷⁹⁷

During the menstrual cycle, nasal congestion has been shown to concur with ovulation and rise in serum estrogens, although additional evidence supporting this relationship is lacking.¹²²

Drug-induced rhinitis 

Medications may induce symptoms of nasal congestion and/or rhinorrhea. In the past, antihypertensive medications (eg, reserpine and guanethidine) were frequently incriminated, but they are no longer commonly used. Currently, ACE inhibitors⁷⁹⁸ and β-blockers⁷⁹⁹ occasionally elicit rhinitis symptoms.¹²³ Rhinitis symptoms are often caused by α-receptor antagonists used in treatment of benign prostatic hypertrophy (eg, prazosin, terazosin).¹²⁴ Phosphodiesterase-5–selective inhibitors used for treatment of erectile dysfunction can cause nasal congestion.¹²⁵ Phentolamine mesylate, an α-1 and α-2–selective adrenergic receptor antagonist, has been reported to cause rhinitis symptoms in 7.7% of patients treated for erectile dysfunction.⁸⁰⁰

Although oral contraceptives have long been implicated as causes of nasal symptoms, a recent study found no nasal physiologic effects on female patients receiving a modern combined oral contraceptive pill.¹²⁶ Aspirin and NSAIDs may produce rhinorrhea as an isolated symptom or as part of a symptom complex of rhinosinusitis, nasal polyposis, and asthma.¹²⁷, ¹²⁸

Prolonged usage of α-adrenergic decongestants may lead to a hypertrophy of the nasal mucosa termed rhinitis medicamentosa. The repetitive and prolonged use of topical α-adrenergic nasal decongestant sprays may induce rebound nasal congestion on withdrawal. These agents include OTC products containing oxymetazoline or phenylephrine. Benzalkonium chloride in vasoconstrictor spray products may augment local pathologic effects.⁸⁰¹ Also, patients may develop tachyphylaxis because of the need for more frequent doses to provide adequate decongestion. The nasal mucosa is often beefy red, appears inflamed, and shows areas of punctate bleeding and scant mucus. There is loss of ciliated epithelial cells leading to reduced mucociliary clearance.¹³³ Nasal septal perforation is a rare complication.¹³⁴ Similar consequences may occur with prolonged use of other vasoconstrictor agents such as cocaine.

Atrophic rhinitis 

Primary (idiopathic) atrophic rhinitis, more prevalent in developing countries with warm climates,¹³⁶, ⁸⁰² is a chronic condition characterized by progressive atrophy of the nasal mucosa, nasal crusting, nasal dryness (caused by atrophy of glandular cells), and fetor.¹³⁶, ¹³⁷ The nasal cavities appear abnormally wide on examination, and squamous metaplasia, atrophy of glandular cells, and loss of pseudostratified epithelium have been detected in nasal biopsies.⁸⁰³ The sinus CT shows the characteristic resorption of underlying bone and the absence of identifiable turbinates, a finding referred to as the “empty nose syndrome.”¹³⁸ The dryness and reduction of nasal mucosal tissue with the resultant resistance to airflow are, paradoxically, perceived by patients as severe nasal congestion. The etiology of primary atrophic rhinitis has not yet been established. Klebsiella ozaenae and other bacteria including S aureus, Proteus mirabilis, and Escherichia coli may be causative, although it is also plausible that these secondarily infect previously damaged nasal mucosa.¹³⁸ A genetic association has also been suggested⁸⁰⁴ but needs further confirmation.

Primary atrophic rhinitis should be separated from secondary atrophic rhinitis, which develops as a direct result of other primary conditions, such as chronic granulomatous disorders, chronic sinusitis, excessive surgery to the nasal turbinates, trauma, and irradiation.¹³⁸ Although secondary atrophic rhinitis may be less severe and progressive, treatment of primary and secondary atrophic rhinitis is aimed at reducing crusting and alleviating the foul odor. There are no controlled trials evaluating therapies for atrophic rhinitis. Although even the published observational data are limited, the mainstay of treatment is continuous nasal hygiene—for instance, intranasal irrigations¹³⁹ with saline or sodium bicarbonate solution, and periodic debridement of the crusts, if necessary. As used for recalcitrant rhinitis and sinusitis,¹⁴⁰ adding antibiotics such as mupirocin to the lavage solution has been suggested for purulent secretions. Systemic antibiotics are indicated when an acute infection is present.

Nasal polyps 

Nasal polyposis is an inflammatory condition of the nasal and sinus mucosa and usually presents as persistent nasal obstruction. Nasal polyps have a prevalence of 2% to 4%¹⁴¹, ¹⁴², ¹⁴³ in the general as well as the allergic population¹⁴³ and usually occur after age 40 years.¹⁴³ Although previous studies showed a 2:1 male to female prevalence of nasal polyps,¹⁴², ¹⁴⁴, ¹⁴⁵ a recent large population study showed no sex preference.¹⁴³ Frequently reported symptoms are rhinorrhea (39%), nasal congestion (31%), and anosmia (29%).⁸⁰⁵ Chronic nasal polyposis has been associated with reduced QOL and greater risk of sleep disturbances.⁸⁰⁶

Nasal polyps may occur in as many as 50% of children with CF, in immotile cilia syndrome, and in 7% to 15% of adults with asthma.⁸⁰⁷, ⁸⁰⁸, ⁸⁰⁹ Nasal polyps coupled with AERD are rarely noted before the adolescent years. The profile of inflammatory mediators (eg, myeloperoxidase and IL-8) and prominent numbers of neutrophils found in nasal polyps of patients with CF differ from increased eosinophils and associated mediators (eg, IL-5, eotaxin, ECP) detected in adults with non-CF polyps, suggesting that these are different disorders.⁸⁰³, ⁸¹⁰ AERD is recognized in 13% of patients with nasal polyposis.⁸⁰⁹ In adult patients without CF, the pathogenesis of nasal polyposis is uncertain. Infiltrates of eosinophils, T cells, plasma cells, and mast cells are consistent findings in nasal polyp tissue and may explain why corticosteroids are therapeutically effective.¹²⁸ When associated with asthma, patients with nasal polyposis hyperexcrete urinary LTE₄,¹⁴⁸ suggesting that overproduction of cysLTs may play a pathogenetic role. Reduced apoptosis of eosinophils in nasal polyp tissue has been demonstrated, which could enhance tissue inflammation and growth of nasal polyps.⁸¹¹ Allergy does not appear to predispose to polyp formation. Between 10% and 15% of patients with allergic rhinitis also have nasal polyps.⁶⁹⁸ The noses and sinuses of patients with chronic rhinosinusitis and nasal polyps are frequently colonized with fungi (principally Aspergillus and Penicillium).⁸¹² Allergic fungal sinusitis is a distinct pathologic entity defined by specific IgE for Aspergillus, Bipolaris, or other mold antigens; chronic sinusitis with nasal polyposis; radiographic sinus opacification and eosinophilic mucin material containing eosinophilic debris; and fungal hyphae in tissue resected from the sinuses.⁸¹³, ⁸¹⁴ Proinflammatory mediators including eosinophilic major basic protein and neutrophil elastase have been identified in allergic mucin.⁸¹⁵ The efficacy of local or systemic antifungal therapy in treating allergic fungal sinusitis has not been established.⁸¹²

The treatment and control of nasal polyps is challenging. Sinus disease and nasal polyps are more difficult to control in patients with asthma and AERD.⁸⁰⁹ Intranasal corticosteroids are effective in improving sense of smell and reducing nasal congestion, and effects are optimized with twice-daily versus once-daily dosing.⁸¹⁶ For severe nasal polyposis, a short course of oral prednisone is effective in reducing symptoms and polyp size and improving nasal flow. The beneficial effects are then maintained by subsequent administration of maintenance intranasal corticosteroids.¹⁴⁹, ¹⁵⁰, ¹⁵¹ Subjective improvement in nasal polyp symptoms has been observed in patients administered the LT modifiers montelukast, zafirlukast, and zileuton as add-on therapy to intranasal corticosteroids.¹⁵², ¹⁵³ After sphenoidal ethmoidectomy, recurrence rates and rescue medication requirements in patients treated with montelukast were equivalent to those observed in patients receiving postoperative nasal beclomethasone.¹⁵⁴ In recent years, functional endoscopic sinus surgery has been used extensively for treating rhinosinusitis associated with nasal polyposis. Patients with AERD and nasal polyps have worse outcomes with functional endoscopic sinus surgery than aspirin-tolerant patients.⁸¹⁷ In patients with nasal polyposis and AERD, aspirin desensitization followed by long-term daily aspirin treatment may be considered. Long-term studies of patients with AERD suggest that maintenance aspirin therapy may reduce nasal symptoms, frequency of sinus infections, requirement for nasal polypectomies, and need for systemic corticosteroids.¹⁵⁵, ¹⁵⁶ The numbers of nasal mucosal leukocytes expressing cysLT receptors (cysLT1), which are increased in nasal mucosa of patients with AERD, decrease after aspirin desensitization.¹⁵⁷

Other conditions that may be confused with rhinitis 

Nasal obstruction may be caused by congenital or acquired anatomic abnormalities, which may mimic symptoms of rhinitis. Reduced airflow through the nasal passages in infants may be a result of congenital choanal atresia. Nasal septal deviation and nasal turbinate or adenoidal hypertrophy many block flow of nasal secretions, leading to rhinorrhea or postnasal drip, as well as causing nasal blockage.

Although comparatively rare, both benign and malignant tumors may cause rhinitis symptoms.¹⁵⁸, ¹⁵⁹ Lesions generally cause unilateral occlusion of the nasal airway. Rapidly growing nasal malignancies may cause nasal obstruction early in the disease. Lesions arising in the maxillary sinus present with nasal symptoms in the late stages of the disease, usually after the tumor has penetrated the medial wall of the antrum. These tumors may present with bleeding, hyposmia or anosmia, pain, and/or otalgia. Prolonged occupational exposure to chemicals such as nickel and chrome have been associated with carcinoma.⁸¹⁸

Systemic immunologic and nonimmunologic diseases may affect the nose. These include Wegener granulomatosis, sarcoidosis, relapsing polychondritis, and midline granuloma.⁸¹⁹, ⁸²⁰ Patients with uremia develop thinning of the nasal epithelium.⁸²¹ At times, the systemic symptoms may be absent or undetected when patients present with nasal complaints. Infections such as tuberculosis, syphilis, leprosy, sporotrichosis, blastomycosis, histoplasmosis, and coccidiomycosis also may cause granulomatous nasal lesions. These are usually ulcerative, and crust formation may lead to nasal obstruction or bleeding. Rhinoscleroma is a rare chronic infectious granulomatous disease caused by Klebsiella rhinoscleromatis that presents as a polypoid mass with symptoms of epistaxis and nasal obstruction.⁸²² Rhinoscleroma is endemic in tropical and subtropical regions of America, Asia, and Africa.

Complete or partial nasal obstruction in the infant below 2 to 6 months of age can lead to fatal airway obstruction, because many neonates are obligate nasal breathers. In the newborn, the nasal passages may contribute to 50% of the total airway resistance.⁹³, ¹⁶¹ Thus, any minor increase of congestion, such as a URI, can create near total obstruction. Although food allergy, such as, milk, is often considered to contribute to nasal symptoms including congestion, 1 large prospective study demonstrated that only .3% of food hypersensitivity in children and adolescents is associated with rhinitis symptoms.⁷⁰⁷ Cinematoradiographic findings have implicated a causal relationship of nasal obstruction and sudden infant death syndrome.⁸²³

The most common acquired anatomic cause of nasal obstruction in infants and children is adenoidal hypertrophy. Enlarged adenoids commonly result in mouth breathing, nasal speech, and snoring. The main indication for adenoidectomy, a common outpatient surgical procedure in children, is sleep apnea caused by adenotonsillar hypertrophy, chronic adenoiditis, and chronic sinusitis. Nasal symptoms, such as congestion, are also common in infants and children with pharyngonasal reflux resulting from prematurity, neuromuscular disease, dysautonomia, velopharyngeal incoordination, or cleft palate.¹⁶¹ This is a result of inflammation and narrowing of the posterior choanae because of acid inflammation.¹⁶¹ When gastroesophageal reflux involves the upper esophagus, larynx, and/or pharyngeal area, it is often referred to as laryngopharyngeal reflux. Infants with laryngopharyngeal reflux experience frequent choking, apneic spells, recurrent pneumonia (because of concomitant gastroesophageal reflux and/or tracheal aspiration), and aspiration of formula leading to secondary chemical/infectious rhinitis. Although diagnosis of laryngopharyngeal reflux can usually be made with nasopharyngoscopy, milk scintography or a pH probe study may be required in select cases.¹⁶¹ Thickened feedings, positioning upright after feeding, and the use of histamine-2 receptor antagonists or proton pump inhibitors have become the mainstay of treatment.¹⁶¹, ⁸²⁴ Of some concern is a recent pediatric prospective study showing that therapy with gastric acidity inhibitors, both protein pump inhibitors and H2 blockers, may increase the risk of acute gastroenteritis and community acquired pneumonia,⁸²⁵ a finding that has also been described in adults.

Cerebral spinal fluid rhinorrhea should be differentiated from the rhinorrhea found in patients with chronic rhinitis. Refractory clear rhinorrhea may be a result of CSF leak even in the absence of trauma or recent surgery, although these remain the most common causes of CSF leak.¹⁶⁰ Benign intracranial hypertension or pseudotumor cerebri, which typically presents in middle-age women with chronic headaches, has been implicated as a cause of spontaneous, nontraumatic CSF rhinorrhea.⁸²⁶, ⁸²⁷ Although detection of glucose historically has been used as an indication for its presence,⁸²⁸ β-2-transferrin protein is a more sensitive and specific indicator because it is found in cerebral spinal fluid and inner ear perilymph, but not in blood, nasal, or ear secretions.²⁵⁵, ²⁵⁶

Defective ciliary function in the airway may be described as ciliary immotility (no movement), ciliary dyskinesia (abnormal movement), or ciliary aplasia (absence of cilia). Screening diagnostic techniques for upper airway disease include measures of mucociliary clearance with saccharin or Teflon particles tagged with the short-lived isotope technetium 99. An absence of mucociliary clearance is a sign of immotility, dysmotility, or aplasia that may be congenital or acquired.

Primary ciliary dyskinesia, also known as immotile-cilia syndrome, is a rare genetic defect (1/20,000 to 1/60,000)¹⁶² caused by a genetically, functionally, and ultrastructurally diverse or heterogenous disease involving a defect in ciliary function. Defective epithelial ciliary clearance of secretions from the upper airway compartments including eustachian tubes and sinuses as well as lower airways produces chronic inflammatory injury to these areas.⁷⁷⁷, ⁸²⁹ Approximately 50% of subjects with PCD are affected by situs inversus (Kartagener syndrome). The majority have an autosomal-recessive form of PCD, but autosomal-dominant and X-linked cases have been reported.

The clinical history is usually that of respiratory disease in the newborn or recurrent upper and lower respiratory disease including recurrent sinusitis, otitis, otosalpingitis, rhinitis, chronic cough, and nasal polyposis. It may also be associated with difficult-to-control asthma and/or cylindrical or saccular bronchiectasis demonstrated on a chest radiograph or chest CT. Additional clinical findings include situs inversus, agenesis of the frontal sinuses, hydrocephalus, heterotaxy, and infertility. Spirometry reveals mild to moderate obstruction with a positive response to a bronchodilator. Any of these clinical findings in combination with a positive family history of diagnosed or probable PCD warrant a full investigation.¹⁶⁵

Secondary ciliary defects are certainly more common than PCD. Natural as well as experimentally induced viral upper respiratory infections have been associated with prolonged mucociliary clearance as measured by radiolabeled resin beads or dyed saccharin.¹⁶³, ⁸³⁰ This effect is maximum at 3 days, persists up to 11 days, and is found in a higher proportion of patients with versus without allergy.¹⁶³, ⁸³⁰ Acute viral infections may also cause cytopathic epithelial damage that may take a number of weeks to resolve.¹⁷¹, ¹⁷² Tobacco smoking of 1 or more cigarettes in an in vitro frog palate model results in a reduction of mucus clearance and disruption and defoliation of the ciliated epithelium.⁸³¹ Although it is often assumed that similar effects occur in human beings, 1 study using saccharin clearance time demonstrated normal mucociliary clearance in healthy smokers, although the average clearance time was longer than in nonsmokers.¹⁷³ Likewise, there was no significant difference in mean nasal ciliary beat frequency when comparing healthy smokers with nonsmokers.¹⁷³ It has been suggested that tobacco smoking leads to the dysfunction of the normal metachronal waves that drive mucus over nonciliated areas and that prolonged, sustained exposure to cigarettes may produce loss of ciliated epithelium secondary to activation of matrix metalloproteinases.⁸³¹ However, even this ciliary dysfunction shows at least partial recovery within 30 minutes of cigarette smoke avoidance in pure air.¹⁷⁴

Evaluation of rhinitis 

An appropriate general medical history and a thorough allergic history are usually the best diagnostic tools available. If a structured allergy history questionnaire⁸³², ⁸³³, ⁸³⁴ is used, the physician should review this with the patient during the initial evaluation. When obtaining an allergic history, it is important to ask about chief concerns and symptoms, including the patient's perception of what is causing the allergic symptoms or the patient's self-diagnosis (although this may be misleading) as well as directed questions relating to nasal symptoms. For example, questions relating symptoms to exposure to pollen and animals may have positive predictive value for diagnosing allergic rhinitis.¹⁷⁵ Each complaint or symptom should be separately evaluated for date of onset including (1) related or resolved symptoms from infancy or childhood; (2) frequency (eg, continual or episodic); (3) characteristics (eg, color and tenacity of nasal secretions); (4) pattern (eg, seasonal, perennial, or a combination); (5) severity, both past and present; (6) triggers that precipitate or worsen the complaint, including allergens, irritants, hormonal influences, exercise, eating, medications, and weather changes; (7) timing after exposure to trigger (eg, immediate or delayed onset); (8) association with geographical and environmental (eg, home vs work vs day care) location or relationship with a particular activity or event (eg, dusting or raking leaves); (9) previous medical evaluation and treatment results, including specific pharmacologic success or failure; and (10) severity (an estimate of effect of the allergic symptoms on QOL, including work or school performance and sleep quality). When a likely allergen is identified by history, a directed question regarding willingness to modify the exposure, such as house pet or occupational allergen, can be asked of the patient and family/care givers. In addition, preferences for the treatment of allergic symptom control including delivery method (eg, oral or nasal) of pharmacologic therapy or a long-term treatment approach with allergy immunotherapy may be explored with the patient and/or others involved in this decision.

Each patient concern or symptom should be evaluated and documented. This could include (1) nasal congestion, sneezing, and rhinorrhea; (2) throat symptoms of soreness, dryness, and PND; (3) cough; (4) ocular redness, tearing, and itching; (5) voice changes; (6) snoring; (7) sinus pain or pressure; (8) ear pain, blockage, or reduced hearing; and (9) itching of nose, ears, or throat. Hyposmia and anosmia are most often associated with severe obstructive upper airway disease, frequently caused by the presence of nasal polyps. It may be helpful to question the patient about symptoms of fatigue, irritability, poor quality sleep, absenteeism and presenteeism at work and/or school, and general QOL problems during their symptomatic periods.¹⁷⁶, ¹⁷⁷, ¹⁷⁸

When reviewing the allergic history in children, one may inquire about sniffing, snorting, clearing of the throat, chronic gaping mouth, halitosis, cough, dark circles under the eyes, and eye rubbing.⁸³⁵ The parents may describe the child as having a poor appetite, learning or attention problems, sleep disturbances, malaise, irritability, and a general sense of not feeling well.¹⁸⁰ When allergic symptoms are recurrent but nonseasonal, the presenting complaint may be recurrent URIs, because the parent cannot differentiate a URI in a young child attending day care from allergic rhinitis. Further complicating this differentiation is the increased responsiveness of the nasal mucosa to allergens and irritants after a viral URI.⁸³⁶

The history for rhinitis generally includes the family history of allergic rhinitis, asthma, atopic dermatitis, chronic sinus problems or infections, diagnoses that may represent allergic symptoms such as recurrent bronchitis, and all major nonallergic medical diagnoses. Although a positive family history makes it more likely that the patient's nasal symptoms are a result of allergic rhinitis, a negative family history by no means rules out the diagnosis of allergic rhinitis. Important components of the initial interview include the past medical history, previous trauma or surgery to the nose and sinuses, and established allergic and nonallergic medical diagnoses. Response to previous therapeutic interventions, such as pharmacotherapy or surgery, should be discussed. Documentation of all current medications or herbal preparations, physician-prescribed or OTC, is recommended. An environmental survey should be conducted exploring potential sources for indoor and outdoor allergens in the patient's home and the homes of close relatives, friends, and caretakers, as well as school and work settings. Questions relating to the indoor environment will usually include items such as the presence of pets and insects, carpet, curtains, and upholstered furniture; age and composition of mattress, pillows, and bed coverings; and the cleaning methods in use. One should inquire about the air conditioning and heating sources and their customary use patterns. It is also important to determine the presence of active or passive tobacco smoke exposure.

At any age, allergic rhinitis can compromise QOL.¹⁷⁸ In adults, this often manifests as sleep disorders, impairment at work, limitations of activities, or impairment of social functioning. Recent findings that the sexual QOL is affected by seasonal allergic rhinitis and that appropriate treatment brings the patient's sexual functioning back toward normal emphasizes that allergic rhinitis is an underappreciated disease with systemic effects.¹⁸¹ As evidence of the disparities 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 underrecognized and inadequately treated by the patient's physician. ¹⁸² Understanding the impact of allergic rhinitis on the patient's QOL represents the cornerstone of therapy.

There are definitely some significant consequences of untreated allergic rhinitis in children. Unrecognized or uncontrolled allergic rhinitis can lead to structural complications and permanent disfigurement such as increased facial length, a high arched palate, class II dental malocclusions, and retrognathic maxilla and mandible.¹⁸⁰ Allergic rhinitis that is poorly controlled can result in poor sleep, school absenteeism, learning impairment, inability to integrate with peers, anxiety, and family dysfunction.¹⁷⁷, ⁵⁵⁰ After effective treatment of perennial allergic rhinitis, improvement in school attendance, school work concentration, and sleep can be demonstrated.⁴⁴⁸ Furthermore, chronic nasal congestion and secondary sleep apnea and disordered sleep can lead to systemic symptoms of headache, fatigue, irritability, poor growth, and reduced QOL. The psychological ramifications of untreated allergic rhinitis can lead to low self-esteem, shyness, depression, anxiety, and fearfulness.¹⁸⁰

The effect of rhinitis on QOL has been measured using both generic and disease-specific questionnaires (Table III, Table IV). The advantage of using a generic questionnaire is that the burden of rhinitis can be compared with other diseases, such as asthma. In fact, in adults, moderate-to-severe perennial rhinitis and moderate-to-severe asthma have equal functional impairment.¹⁸³, ¹⁸⁴ On the other hand, disease-specific QOL questionnaires describe disease-associated problems more accurately and seem to be more responsive to measuring the change with therapeutic interventions. Adult generic questionnaires include the Sickness Impact Profile, the Duke Health Profile, the Nottingham Health Profile, and the Medical Outcome Survey Short Form 36 (Table III). The Short Form 36 has been used to evaluate the effects of a nonsedating H1-antihistamine on QOL.⁸³⁷ Generic QOL questionnaires in children, such as the Child Health Questionnaire–Parental Form 50, Pediatric Quality of Life Inventory, and SF-10 (Table III), are used at times for comparing different allergic diseases. Disease-specific rhinitis QOL questionnaires have been adapted to different age groups. For example, when studying rhinitis in children the Juniper Pediatric Rhinoconjunctivitis Quality of Life Questionnaire (RQLQ),⁶⁵¹ can be used for ages 6 to 12 years and Juniper Adolescent RQLQ⁶⁵² for ages 12 to 20 years (Table IV). Although both the generic and disease-specific QOL questionnaires are often used in research trials for the evaluation of a study group, their sensitivity and precision for use with individual patients has been questioned, especially because QOL and clinical measurements may not be fully interchangeable and distortion, masking, or faking can occur.¹⁸⁵, ¹⁸⁶ For example, there are studies documenting a clear clinical improvement after antihistamines or bronchodilators, but these are not accompanied by detectable changes in the health-related quality of life.¹⁸⁷, ¹⁸⁸ In contrast, in other studies, the clinical evaluation did not discriminate between 2 different treatments, whereas a difference was noted with QOL assessment.¹⁸⁹, ¹⁹⁰ Use of generic QOL measurements in individual patients when studied in other areas of medicine has not led to changes in practice style and has not improved patients' health outcomes.⁸³⁸ While we await the development of a tool that will be valid and useful for following the individual patient, the clinician may find the current QOL questionnaires of benefit in select clinical settings and in clinical trials. The use of a modified visual analog (graphic rating) scale for assessing the severity of allergic rhinitis has been recommended for the clinician when assessing the individual patient for nasal and nonnasal symptom severity, global nasal and nonnasal severity, and QOL assessment of rhinitis severity¹³ (see Fig 1, Fig 2, Fig 3, Fig 4). We are also starting to see the development of rhinitis instruments, such as the Multiattribute Rhinitis Symptom Utility index,⁶⁵⁰ to assist in comparing the cost effectiveness of various medical treatments of rhinitis.

The elements of the physical examination of the patient with rhinitis with emphasis on the nasal passages are described in Table V. The examiner should carefully look for any signs of accompanying otitis,¹⁹¹ eustachian tube dysfunction,¹⁹² acute or chronic sinusitis, allergic conjunctivitis, asthma,¹⁹³ and atopic dermatitis in addition to findings compatible with rhinitis. In children, findings of dental malocclusion, a high-arched palate, and upper lip elevation may suggest early-onset and/or longstanding disease.⁸³⁹ On the other hand, if the patient is asymptomatic at the time of the physical examination, there may be minimal or no findings even with a history suggestive of rhinitis.

The nasal examination should note the patency of the nasal valve and any alar collapse. If there is improvement in breathing when performing the Cottle maneuver—pulling the patient's cheek laterally to open the nasal valve angle—this may suggest nasal valve pathology. A deviated/deformed nose may suggest previous trauma, whereas a saddle nose deformity may indicate previous trauma, previous surgery, cocaine abuse, or an inflammatory process.

The nasal and nasopharyngeal examination is accomplished with a nasal speculum with appropriate lighting, otoscope with nasal adapter, indirect mirror, and/or rigid or flexible nasopharyngoscope, based on the expertise of the examiner and the assessment needs.¹⁹⁴ The anterior rhinoscopy examination will reveal any caudal septal deformity or inferior turbinate hypertrophy. If there is significant caudal septal deflection, the inferior turbinate on the side opposite the deviation is often enlarged. If after applying a topical decongestant there is a reduction of turbinate mucosal edema, this may assist in delineating mucosal versus bony hypertrophy.

The use of the nasopharyngoscope allows for better visualization of the middle meatus, the posterior septum, the sinus ostia, posterior choanae, the nasopharynx, and the presence of nasal polyps. The presence of mucopurulent material in this region is suggestive of sinusitis. The use of a mirror or the nasopharyngoscope is necessary to complete a posterior rhinoscopy examination. A pneumatic otoscope is used to assess tympanic membrane mobility. At times, the impedance tympanometer is also needed to assess the tympanic membrane mobility and the presence or absence of fluid, especially in children.

Many typical allergic findings are supportive but not specific to allergic rhinitis. Mucosal appearance may not distinguish between allergic and nonallergic rhinitis, because nonallergic rhinitis may also present with mucosal pallor, edema, or hyperemia. The mucosa is usually reddened in acute infections and with overuse of topical decongestant sprays. Occasionally, the mucosa can be hyperemic with allergic rhinitis. Dennie-Morgan lines, often noted in patients with atopic dermatitis, are symmetrical, prominent folds extending from the medial aspect of the lower lid. These are usually present at birth, or appear shortly thereafter, and persist for life. Dennie-Morgan lines (noted in 60% to 80% of atopic children¹⁹⁵) are very similar to the folds seen in patients with Down syndrome. They may have an ethnic variation and are characteristically but not exclusively present in patients with allergy. Allergic shiners, asymptomatic, symmetrical, blue-grey discolorations of the periorbital skin, are most apparent below the orbit and are attributed to venous stasis. They are reported to occur in as many as 60% of atopic patients and in 38% of nonatopic individuals.¹⁹⁶ Their presence is usually associated with nasal congestion.¹⁹⁶ These do tend to fade with increasing age and are often found in atopic family members.¹⁹⁶

The quantity and quality of nasal secretions should be noted. With allergic rhinitis, there may be watery mucus on the epithelial surface or on the floor of the nasal passage. With abnormal mucociliary clearance or total nasal obstruction, thick secretions can be seen pooling in the floor of the nose. Unlike the nasal turbinates, with which they are often confused, polyps appear glistening, mobile, and opaque and are insensitive to touch.⁸⁴⁰ Nasal polyps may be differentiated from severely edematous mucosa by applying a small amount of a topical vasoconstrictor such as phenylephrine to the mucosa and re-examining the mucosa 5 to 10 minutes later. Nasal polyps will not shrink in size after topical vasoconstrictor has been applied, unlike edematous mucosa.⁸⁴¹ Crusting on an inflamed mucosa may suggest atrophic rhinitis or a systemic disease such as sarcoidosis. The presence of a septal perforation should raise the possibility of intranasal narcotic abuse,⁸⁴², ⁸⁴³ adverse effects of other topical preparations,⁸⁴³, ⁸⁴⁴, ⁸⁴⁵ previous surgery, or systemic granulomatous diseases.

Skin testing 

In vitro assays for specific IgE 

Demonstration of specific IgE antibodies to known allergens by skin testing or in vitro tests¹⁹⁷, ¹⁹⁸ helps determine whether the patient has allergic rhinitis and the specific allergens for avoidance measures and/or allergen immunotherapy. Skin test reactivity alone does not define clinical sensitivity. Skin test positivity must be combined with reported symptoms, increased symptom scores, or physical signs during a known pollen season, controlled laboratory, or environmental exposure unit challenges.²¹⁰, ²¹¹

A careful history is the most important step toward the diagnosis of allergic disease. Skin testing to allergens is indicated to provide evidence of an allergic basis for the patient's symptoms, to confirm suspected causes of the patient's symptoms, or to assess the sensitivity to a specific allergen. The simplicity, ease, and rapidity of performance, low cost, and high sensitivity make skin tests highly favorable for use in patients with rhinitis.

Quality control measures and proper performance of skin testing are vital to produce accurate and reproducible results. It is important to recognize that there is a variable wheal and flare response with the different devices used for skin testing.⁸⁴⁶ The number of skin tests performed may vary depending on the age, potential allergen exposures, and area of the country. It is essential to know which aeroallergens are present locally, are clinically important, and have cross-reactivity with botanically related species to interpret skin tests or in vitro tests for specific IgE properly.

In vitro specific-IgE tests (eg, RAST) are an alternative to skin testing. The precise sensitivity of specific IgE immunoassays compared with skin prick/puncture tests has been reported to range from less than 50% to greater than 90%, with the average being around 70% to 75% for most studies.¹⁹⁹, ²⁰⁰, ²⁰¹, ²⁰², ²⁰³, ²⁰⁴, ²⁰⁵, ²⁰⁶, ²⁰⁷, ²⁰⁸, ²⁰⁹ Skin tests are therefore the preferred tests for the diagnosis of IgE-mediated sensitivity. Interpretation of specific IgE tests may be confounded by variables such as potency of allergens bound to solid support systems, cross-reactive proteins and glycoepitopes, specific IgG antibodies in the test serum, and high total IgE (see “Allergy Diagnostic Testing: An Updated Practice Parameter” for more detail⁹).

Specific IgE immunoassays may be preferable to skin testing under special clinical conditions such as widespread skin disease (ie, severe eczema or dermatographism), skin test suppressive therapy in use, an uncooperative patient, or a history suggesting an unusually high risk of anaphylaxis from skin testing.

Although history and routine physical examination are usually sufficient for a diagnosis of allergic rhinitis, special techniques may be useful in selected patients. Furthermore, patients with nonallergic upper airway pathology may initially report symptoms suggestive of rhinitis.

Upper airway endoscopy 

Endoscopy may be especially useful for the evaluation of rhinitis when symptoms or physical findings are atypical, complications are noted, therapeutic response is suboptimal, or conditions other than rhinitis are suspected. Without endoscopy, it is not possible to view many of the important recessed structures of the upper airway. Either the rigid or a flexible fiber optic endoscope can be used for this examination.

Upper airway endoscopy (rhinolaryngoscopy) is the most useful diagnostic procedure in an evaluation for anatomic factors causing upper airway symptoms. Endoscopy provides a clear view of the nasal cavity and allows detailed examination of the middle meatus, superior meatus, sphenoethmoidal recess, posterior choanae, and nasopharynx, as well as the structures of the oropharynx and larynx.²¹², ²¹³ The procedure is usually performed in the office after decongestion and topical anesthesia. Analysis of videotaped fiber optic upper airway endoscopy has also been used as a research technique to measure cross-sectional area of the nasal cavity.²¹⁴

Imaging techniques 

The primary goals of radiologic imaging of the upper airway are to provide an accurate reproduction of the regional anatomy and to establish the presence and extent of anatomic disease. This information may assist in planning medical therapy and provide an anatomic guide to facilitate subsequent surgical treatment.²¹⁴

Radiologic imaging techniques, such as plain films, CT, and MRI, have no use in the evaluation of patients with uncomplicated rhinitis. However, imaging may be merited when rhinitis with complications or comorbidities such as nasal polyposis and concomitant sinusitis are present.

CT and MRI 

Computerized tomographic scanning and MRI using coronal sections for imaging of sinuses frequently identify turbinate congestion, concha bullosa, nasal polyps, and septal deviation as causes of nasal airway obstruction. Although CT and MRI have been used to validate acoustic rhinometry as a diagnostic technique, they are expensive and may not correlate well with functional obstruction when used for this purpose.

High-resolution CT can demonstrate disease that is not shown on routine x-ray films. It can also delineate pathologic variations and demonstrate anatomic structures inaccessible by physical examination or endoscopy. Because of its superb contrast resolution, CT is an excellent method for examining the complex anatomy of the upper airway, particularly the ostiomeatal complex. The capability of CT to display bone, soft tissue, and air facilitates accurate definition of regional anatomy of the nose and paranasal sinuses. The main indications for the CT are chronic sinusitis not responding to appropriate medical therapy, acute recurrent sinusitis, abnormal diagnostic nasal endoscopic examination, and persistent facial pain.²¹⁵

Magnetic resonance imaging provides better imaging of soft tissue than CT, but it is less suited to imaging the bony anatomy of this region. MRI is useful in the evaluation of upper airway malignancies.⁹

Aerodynamic methods for estimation of nasal airway obstruction 

Resistance to airflow through the nose (or conductance, the inverse of resistance) may be measured by rhinomanometry. Rhinomanometry objectively measures functional obstruction to airflow in the upper airway, although the technique has not been fully standardized. Subjective perception of nasal stuffiness may correlate only loosely with measured nasal airway resistance,²³⁵, ⁸⁴⁷, ⁸⁴⁸ and rhinomanometry may be used in the assessment of the severity of symptoms. In addition, rhinomanometry may provide objective information on the results of therapeutic interventions. The objective information obtained from rhinomanometry may be particularly important when it is suspected that occupational exposure results in nasal symptoms, including nasal congestion. Rhinomanometry is not a substitute for careful endoscopy of the nose because significant pathology in the nose can occur with nasal airway resistance values in the normal range.

Rhinomanometry may be used to assess the severity of anatomical abnormalities that are causing airway obstruction in the nose, including nasal valve abnormalities, septal deviation, and polyposis. This application requires measurements before and after a potent intranasal decongestant. Other indications for rhinomanometry include the evaluation of patients with obstructive sleep apnea.²¹⁷

Acoustic rhinometry 

Acoustic rhinometry depends on reflection of acoustic signals from structures in the nasal cavity.²¹⁸, ²¹⁹, ²²⁰ It is currently not a technique used in the routine evaluation of patients with rhinitis. It produces an image that represents variations in the cross-sectional dimensions of the nasal cavity and closely approximates nasal cavity volume and minimal cross-sectional area. It also allows identification of the distance of the minimal cross-sectional area of the nasal cavity from the naris. Changes in nasal geometry measured by acoustic rhinometry during histamine challenge testing have been documented,⁸⁴⁹, ⁸⁵⁰ and the results of parallel determinations by acoustic rhinometry and rhinomanometry are comparable.⁸⁵⁰ However, nasal airway resistance cannot be easily computed from the acoustic rhinometry data.

Acoustic rhinometry is a safe, rapid, and noninvasive technique that requires minimal patient cooperation and effort and no patient training.⁸⁵¹ It may be used in the evaluation of infants, children, and adults. It can be performed on a severely congested nose because it does not require nasal flow. Measurements by acoustic rhinometry have been validated by comparison with CT and MRI.²²¹ Although there is high correlation for the anterior 2/3 of the nasal cavity, the posterior nasal cavity shows more variance.²²², ²²³, ²²⁴, ²²⁵ Compared with CT and MRI, acoustic rhinometry is more rapid, may be performed at the bedside, and, unlike CT, does not expose the patient to radiation. Acoustic rhinometry and rhinomanometry have similar reproducibility²³¹ and compare favorably in challenge studies²³² but measure different changes and are best viewed as complementary.²³³, ²³⁴, ²³⁵ Clinically, acoustic rhinometry is used to help diagnose rhinitis, evaluate nasal pharyngeal surgical outcome, and monitor response and adherence to medical therapy such as intranasal corticosteroids.²²⁶, ²²⁷ It is a logical choice for the objective measurement of area and volume in diseases of the nose. A number of factors lead to measurement variation when the procedure is used. Common reasons for measurement inaccuracy are an air leak between the nosepiece and the nose and the presence of nasal secretions.²²⁸ Studies have shown that patient perception of nasal obstruction does not correlate with actual compromised nasal airflow.²³⁵

Nasal provocation testing 

Identification of sensitivity of the nose to a particular aeroallergen usually can be based on a history of symptoms of allergic rhinitis provoked by exposure to the allergen and confirmed by skin testing. Nasal provocation testing with allergen is unnecessary unless criteria that are more stringent are needed to incriminate the suspected allergen. For example, nasal provocation testing with allergen may be required for confirmation of sensitivity to allergens in the workplace. Testing of sensitivity to allergens requires that responses to incremental doses of allergens be assessed.²³⁶ Single-dose allergen provocation measures nasal reactivity to allergens, not sensitivity. Because nasal reactions to instillation of placebo materials may occur, response to diluent must be measured before provocation with allergens.

Nasal sensitivity/hyperresponsiveness to histamine and methacholine has been found in allergic rhinitis²³⁷, ²³⁸, ²³⁹ and vasomotor rhinitis.²⁴⁰ Although this measurement may be a marker for these diseases, the clinical utility of nasal provocation testing with histamine or methacholine may be limited; there is a considerable overlap between patients with and without allergy in their sensitivity to these agents. However, these provocation tests may be useful during clinical trials to determine the efficacy of drugs and allergen immunotherapy in reducing nasal irritability.

Nasal smears for eosinophils are usually considered elevated when 10% of cells are eosinophils.⁹⁰ The presence of eosinophils has been associated with loss of epithelial integrity in patients with both allergic and nonallergic rhinitis.⁸⁵² When taking nasal smears, both nostrils should be sampled because the findings from 1 nostril are not reliably representative of the total cell distribution in both nostrils.²⁴² Samples collected by blowing mucus into transparent wrap contain less cellular material than when a cytology brush, probe or ultrasonic nebulization of hypertonic saline are used, but are adequate for detecting eosinophils and neutrophils.⁸⁵³, ⁸⁵⁴, ⁸⁵⁵ Once collected, the nasal secretions are transferred to a slide, fixed, and then treated with Hansel stain, which highlights eosinophil granular contents.⁸⁵⁶ Although nasal smears are generally adequate for assessment of nasal eosinophilia, there is some evidence that nasal biopsy for eosinophils is more accurate.⁸⁵⁷ Many studies have shown a high correlation of nasal eosinophilia and allergic rhinitis; however, it is questionable how much this benefits the clinician in making the diagnosis of allergic rhinitis.⁸⁷, ⁸⁸, ⁸⁹ In a study of adolescents and adults, adding nasal smears for eosinophils to an expert's clinical evaluation in establishing a diagnosis of allergic rhinitis contributed very little to the final diagnosis and was considered clinically irrelevant.⁹⁰ When eosinophils in nasal smears are present, there is only a 71% correlation with SPTs and a 69% correlation with nasal challenge tests, suggesting that routine use of the nasal smear may not be beneficial.⁹¹ In clinical trials, nasal eosinophils have been used to evaluate anti-inflammatory effects of intranasal corticosteroids and may be associated with improved nasal symptom scores.³⁷⁶, ³⁸⁰

As many as 4.7% of patients with a history very suggestive of allergy will have negative prick tests but a positive nasal challenge and a positive nasal smear for eosinophils,⁹¹ and may have nasal specific IgE,²⁴¹ supporting the diagnosis of allergic rhinitis.⁹¹, ²⁴¹ Under special circumstances, when faced with a convincing history, negative SPT, and elevated nasal eosinophils, the clinician may wish to conduct a nasal or conjunctival challenge test. On the other hand, as many as 6% of patients with a similar history suggestive of allergy will have negative prick skin test and nasal challenge but will have nasal eosinophilia, establishing the diagnosis of nonallergic rhinitis with eosinophilia.⁹¹ When both SPTs and nasal smears for eosinophils are negative in patients with rhinitis, a less favorable response to medical therapy can be anticipated.

Additional research is needed to establish whether nasal smears for eosinophils are useful for predicting the onset, course, and progression of allergic disease. In 1 pediatric study, nasal eosinophilia was found to predict prolonged or subsequent allergic rhinitis symptoms.⁸⁵⁸ In addition, the nasal eosinophil count has been shown to correlate with the severity of perennial allergic rhinitis in children.⁸⁵⁹ Recognizing that many patients with allergic rhinitis have increased airway reactivity and will subsequently develop asthma, the nasal smear for eosinophils may help predict the progression of disease; in adult patients with allergic rhinitis as the only allergic diagnosis, it has been shown that the number of nasal eosinophils correlates with the methacholine response.⁸⁹, ⁸⁶⁰

The absence of eosinophils and the presence of large numbers of polymorphonuclear neutrophils especially when intracellular bacteria are noted suggest an infectious rhinitis or sinuitis.⁹² On the basis of sinus aspirates, the number of polymorphonuclear cells varies with the infecting organism, because H influenzae is associated with significantly fewer leukocytes than Streptococcus pyogenes.⁸⁶¹ A viral infection is usually associated with fewer polymorphonuclear cells than a bacterial process.²⁴³ However, the mere presence of neutrophilia cannot be diagnostic of an infectious process because as many as 79% of school children and 97% of infants have neutrophils in their nasal secretions.⁸⁸

The saccharin test (with saccharine or a substitute dye marker) may be used by the clinician as a screening test for primary or secondary ciliary dysfunction. The test requires a cooperative subject but is quite noninvasive. The saccharin test involves placement of a 1-mm to 2-mm particle of saccharin on the inferior nasal turbinate 1 cm from the anterior border. The subject then sits with the head bent forward and the test is completed when either the patient tastes the saccharin or the clinician visualizes the presence of the dye marker in the posterior pharynx. If the time is beyond 1 hour or the subject is unable to taste the saccharin or detect the dye, mucociliary clearance is considered impaired. When an abnormal study is obtained, additional studies are required before a firm diagnosis can be established,¹⁶⁶ because the saccharin test has too many false-positives and false-negatives.

Nasal biopsies are used to determine if a suspicious lesion is neoplastic or granulomatous and to evaluate suspected ciliary dysfunction. Biopsies to determine ciliary structure and function can be obtained endoscopically from bronchi or the nasopharynx and by curette or brush from the inferior concha. The cilia can be viewed by video or examined in cross-section by electron microscopy for specific defects or usual ultrastructure.²⁴⁴, ²⁴⁵ Combining electron microscopy with computer-based image processing algorithms can improve the visualization of ultrastructural defects.¹⁶⁵, ¹⁶⁷, ¹⁶⁸, ¹⁶⁹, ⁸⁶² Depending on the results of the nasal biopsy evaluation of ciliary function, a tracheal biopsy may be required for confirmation of ciliary dyskinesia. Electrophoresis, genetic analysis using a dynein gene probe, and decreased exhaled nitric oxide are additional diagnostic procedures under investigation for the evaluation of ciliary function.¹⁶⁵

Measurement of total IgE in cord blood or in children has been proposed as means of predicting the risk of allergic disease; however, recent studies have found that cord blood is not a reliable predictor for atopic disease.²⁴⁶ The total serum IgE has low sensitivity (43.9%) as well as low positive and negative predictive values when evaluating a patient for allergic rhinitis and therefore is of limited clinical benefit.²⁴⁷, ²⁴⁸

In recent research, the presence of specific immunoglobulin responses of the IgG subclasses has been suggested to be a risk factor for allergic disease.⁸⁶³ Furthermore, measurement of nonspecific and specific IgG₄ and/or of other subclasses has been advocated as a diagnostic test for clinical allergy. In general, scientific evidence supporting its use has been controversial and inconclusive.²⁴⁹, ²⁵⁰, ²⁵¹, ²⁵², ²⁵³, ²⁵⁴ The routine measurement of IgG₄ should not be part of the diagnosis evaluation of patients with allergic nasal disease.

Special testing considerations in children 

In children with rhinitis, select tests that may be indicated on an individual basis include quantitative immunoglobulins, complement studies, ciliary functional and morphologic studies (as described in Summary Statements 44, 45), and the sweat test and/or genetic typing for CF when disorders such as immunodeficiency, ciliary dyskinesia, and CF are suspected (see “Allergy Diagnostic Testing: An Updated Practice Parameter”⁹ and “Practice Parameter for the Diagnosis and Management of Primary Immunodeficiency”⁸⁶⁴).

There is ongoing controversy on the usefulness of plain sinus radiography in children for the diagnosis of acute bacterial sinusitis.⁷⁷, ⁸⁶⁵, ⁸⁶⁶ Although the diagnosis of acute bacterial sinusitis in children can usually be made by clinical assessment, plain radiography may be considered for confirmation in children 6 years and older with persistent symptoms and for all children (regardless of age) with severe or worsening symptoms.⁸⁶⁷, ⁸⁶⁸ In children, as in adults, CT scans of the sinuses are more sensitive than plain radiography and should be considered for potential complications of acute bacterial sinusitis, such as orbital or intracranial complications, for patients who fail to improve with appropriate medical therapy, or for the diagnosis of chronic sinusitis.⁸⁶⁶, ⁸⁶⁹ A lateral nasopharyngeal radiograph may help to exclude adenoid hypertrophy in children with mouth breathing, snoring, sleep apneic episodes, and nasal obstruction. When available, dynamic video rhinoscopy is more accurate at assessing adenoid hypertrophy and percent airway occlusion than lateral neck radiography.²¹⁶ Overnight polysomnography may be necessary to confirm the diagnosis of OSAS, noted in 1% to 3% of children, before surgical removal of enlarged adenoids and tonsils.⁸⁷⁰

Atopy has been associated with habitual snoring in infants.²⁵⁷ In children, the presence of rhinitis is a strong predictor of habitual snoring.²⁵⁸ Children who are African American, have upper respiratory disease, and have a family history of sleep apnea are at enhanced risk for sleep-disordered breathing.²⁵⁹ Thus, formal evaluation for OSAS may be considered in children presenting with chronic rhinitis and other risk factors associated with sleep-disordered breathing.

In snoring adults with rhinitis and sleep apnea symptoms, increased nasal airway resistance has been associated with apnea and hypopnea.²⁶⁰, ²⁶¹ Obstructive sleep apnea episodes determined by polysomnography were more frequent in patients with ragweed allergy during symptomatic periods when nasal resistance was increased than during asymptomatic periods.⁸⁷¹ Intranasal corticosteroids reduce nasal airway resistance and apnea-hypopnea frequency in patients with OSAS and rhinitis and may be of benefit in the management of some patients with OSAS.²⁶¹

Rhinitis and asthma are linked by common epidemiologic, physiologic, and pathologic mechanisms, as well as common comorbidities and therapeutic approaches, leading to the concept of “one airway, one disease.”²⁶², ²⁶³, ²⁶⁴, ²⁶⁵ This concept has been popularized by a publication of the ARIA workshop group, where it is stated in the introduction, “…patients with persistent allergic rhinitis should therefore be evaluated for asthma and patients with asthma should be evaluated for rhinitis.”¹¹ Thus, pulmonary function tests should be considered in patients with rhinitis to assess the possibility that asthma might be present. The presence of asthma may not be apparent because such patients (1) may have difficulty in recognizing their symptoms, (2) may have variable symptoms throughout the day, (3) may have a physical examination of the respiratory system that appears normal, and (4) may present with symptoms that are atypical. Furthermore, the physical examination of the lower respiratory systems may be normal during the medical evaluation of rhinitis.

Management of rhinitis 

Environmental triggers for rhinitis can be divided into 2 general categories: allergens and irritants. Ideally, the management of rhinitis includes identification of these triggers when possible and implementation of avoidance measures when practical.

Allergens are substances that trigger rhinitis through an IgE-dependent mechanism. The most common allergic triggers for rhinitis include pollens, fungi, dust mites, furry animals, and insect emanations. The ideal way for patients to manage allergic rhinitis is with complete avoidance of all relevant allergens. Because this generally is not possible, patients should be counseled to reduce their exposure to as many relevant allergens as is practical. This may improve their ability to tolerate exposure to unavoidable aeroallergens. With the development of sensitive immunochemical techniques, direct measurement of indoor allergen concentrations to confirm that exposure reduction has occurred is now possible.²⁹³ Even so, the effectiveness of environmental control measures should be judged primarily by clinical parameters such as reduction in patient symptoms and medication scores.²⁶⁶

Pollen that triggers allergic rhinitis principally comes from plants that are wind-pollinated (anemophilous). This includes many trees, grasses, and weeds, although exposure to pollen from insect-pollinated (entomophilous) plants may produce symptoms if sufficient concentrations are encountered.⁸⁷² Allergens are quickly eluted from pollen grains on contact with ocular or respiratory mucosa. In addition, similar allergens may be found on fragments derived from other portions of the plant. Pollen allergens, forming an allergenic bio aerosol, can be detected in the outdoor environment even when intact pollen grains are not present.²⁶⁷, ²⁶⁸, ²⁶⁹

The types of pollen responsible for symptoms vary widely with locale, climate, and introduced plantings.⁸⁷³, ⁸⁷⁴ In temperate regions of North America, tree pollen generally predominates in early to mid-spring, grasses in late spring and early summer, and weeds from late summer until early fall.⁸⁷⁵ The dose of pollen allergen that is able to elicit symptoms depends on the degree of allergic sensitization and on nasal mucosal inflammation that already is present, often referred to as “priming.”⁷²¹, ⁸⁷⁶, ⁸⁷⁷

Indoor pollen exposure increases when windows are open or attic fans are in use during pollen season. Therefore, to reduce indoor exposure, windows and doors should be kept closed. If air conditioning is used to keep the home or vehicle comfortable, any outdoor vents should remain closed.⁸⁷⁸ It may be helpful to take a shower or bath following outdoor activity, thereby reducing indoor pollen contamination. Because pets also can be vectors for pollen intrusion, it may be beneficial to wash furry animals after they have been outdoors. Although it is not practical to remain indoors all of the time, it is helpful to limit outdoor exposure during periods with high pollen counts.⁸⁷⁹ For example, because ragweed pollen concentrations tend to peak at noon or in the early afternoon, it may help to plan outdoor activities for the early morning or late evening.⁸⁸⁰ Highly sensitive patients whose symptoms are triggered by very low pollen levels may need to limit their outdoor activities.²⁷⁷ Having such individuals wear a facemask during outdoor activities should be considered.²⁷⁷ Activities involving extended time outdoors, such as camping trips, may need to be avoided during certain pollen seasons. Because pollen counts tend to be higher on sunny, windy days with low humidity, it may help to limit outdoor activities when those weather conditions are present. In contrast, outdoor activities may be well tolerated after a gentle, sustained rain when pollen counts tend to be low. Because the interplay of different weather factors (eg, wind, temperature, rain, humidity) is complex, it is not reliably possible to predict levels of outdoor aeroallergens on the basis of the influence of a single weather factor.²⁷⁰, ²⁷¹, ²⁷²

Fungi are ubiquitous organisms, many of which produce clinically important allergens.⁸⁸¹, ⁸⁸², ⁸⁸³, ⁸⁸⁴, ⁸⁸⁵, ⁸⁸⁶ They exist in great numbers outdoors but also may contaminate indoor environments. Most fungal allergens are encountered through inhalation of spores, although fragments of hyphae also may be important. Fungi are present in the air throughout the year except during periods of snow cover. In the Northern United States, spore concentrations tend to increase in late spring and again during late summer, whereas in the southern United States, they tend to remain elevated year-round. Most fungi are found in soil and tend to release spores when the earth is disturbed (eg, during plowing, excavation, and so forth). Outdoor fungi grow on both viable and decaying vegetation and are particularly abundant during harvesting activities in agricultural regions.

Because there is a temporal association between exposure to spores and development of allergic symptoms in sensitive individuals, it is important for patients to be aware of conditions that are associated with elevated spore concentrations.⁸⁸⁷ Spore concentrations are strongly influenced by local conditions such as moisture, temperature, wind, rain, and humidity.²⁷⁴, ²⁷⁵, ²⁷⁶ Some fungi require moist conditions for spore release, leading to elevated levels of these spores during rainy weather and with dew formation at night.²⁷³ Such hydrophilic fungi include Fusarium, Phoma, most ascospores, and basidiospores (mushrooms). Other common allergenic fungi, such as Alternaria and Cladosporium, are more abundant during dry, windy weather. Rain or high humidity can induce spore release, particularly when the rainy period ends. Thunderstorms have even been associated with spore plumes.⁸⁸⁸

Avoidance of outdoor fungi may require the patient to remain indoors as much as is practical. As with pollen avoidance, air conditioning units, if necessary for comfort, should be used with the outdoor vents closed. Because air conditioning units at home, at work, and in automobiles may become contaminated with fungi, they should be inspected regularly and maintained according to the manufacturer's instructions. Other situations associated with increased fungus exposure include plant-disturbing activities such as mowing, threshing, or raking leaves and proximity to compost, silage, or dry soil. Use of face masks may be helpful for reducing exposure during such outdoor activities.²⁷⁷, ²⁷⁸

Many factors influence growth of indoor fungi, including the age and construction of the residence; the presence of a basement or crawl space; the type of heating, ventilation, and air conditioning system; and the use of humidifiers. Fungi require oxygen, a source of carbohydrate, and moisture for optimal growth. Moisture becomes available to fungi through entry into the building by intrusion from outside, leakage from pipes, or condensation onto cold surfaces with temperatures that are below the dew point of air. Therefore, environments most likely to become contaminated with fungi include homes with elevated humidity (above 50%), basements with water intrusion, and cold surfaces. Other locations often providing favorable conditions for fungal growth include window moldings, sinks, shower stalls, nonrefrigerated vegetable storage areas, and garbage pails.

Reduction of fungal exposure consists of eliminating the source of moisture. Fungicides may kill or at least retard fungal growth. Products containing a dilute bleach solution with a detergent have been shown to denature fungal allergens and in many cases to prevent regrowth by killing the mycelia. These are effective when used on nonporous surfaces or when contamination is limited to a small area. Applications that treat the surfaces only are unlikely to remediate fungally contaminated porous materials such as wallboard because mycelia can penetrate these surfaces. It may therefore be necessary to remove and replace such materials. Unfortunately, such chemical and physical measures to control indoor fungi will usually fail in the presence of elevated relative humidity and condensation.

Because cool mist humidifiers may be reservoirs for bacteria and fungi, they are best avoided.⁸⁸⁹, ⁸⁹⁰, ⁸⁹¹, ⁸⁹², ⁸⁹³, ⁸⁹⁴ If they are used, they need to be cleaned regularly. Because central humidifiers operate through evaporation, they are less likely to produce particles containing fungi and therefore are preferable. Homes constructed with a crawl space should have a plastic vapor barrier over exposed soil, and foundation vents should be kept open to provide ventilation. Spores also are present in carpeting, bedding, and upholstered furniture and are reduced by the same measures used for dust mite avoidance. Carpeting and upholstered furnishings therefore should be avoided in damp areas or in locations that tend to flood. A dehumidifier should be used and standing water removed as quickly as possible in such locations.

A major source of allergen in house dust is the fecal residue of dust mites belonging to the genus Dermatophagoides.⁸⁹⁵ A principal food source of dust mites consists of exfoliated human skin cells. Consequently, mites are most abundant in locations where skin cells are shed such as bedding, fabric covered furniture, soft toys, and carpeting.⁸⁹⁶, ⁸⁹⁷ In addition to the availability of this food source, the other major factors influencing mite growth are temperature and humidity. To reproduce, dust mites generally require a relative humidity of 50% or greater.²⁸¹ Recent changes in home construction and housecleaning methods have created environments conducive to dust mite proliferation. These include enhanced energy efficiency in buildings leading to reduced ventilation and increased humidity, wall-to-wall carpeting, furnished basements, and use of water for laundry that is not hot enough to kill mites.

To reduce mite allergen exposure, humidity should be maintained between 35% and 50%, reservoirs in which they reside should be minimized, and barriers should be created between the mites and the building's occupants. Humidity can be reduced with air conditioning or a dehumidifier and can easily be measured with an inexpensive hygrometer. Common reservoirs to be avoided include upholstered furniture, carpeting, bedding, and stuffed toys. Dust mite fecal pellets easily become airborne when their reservoir is disturbed, although they rapidly settle once the disturbance stops. Ordinary vacuuming and dusting therefore have little effect on mite allergen concentrations because the mites themselves are not removed and the pellets easily pass through low-efficiency vacuum bags, becoming widely dispersed throughout the room.²⁸⁰ Carpeting therefore is best removed from the bedroom and replaced with smooth finish wood, tile, or vinyl flooring.²⁸² If this is impractical, one may consider treating carpets with an acaricide (benzyl benzoate) that kills mites.²⁷⁹, ²⁸⁶, ²⁸⁷, ²⁸⁸ Carpeting installed over a concrete slab will inevitably become contaminated with both mites and fungi because of condensation and is best avoided if possible. If carpeting is present, vacuum cleaners with HEPA filtration or central vacuums that remove the air to a distant location should be used. Ideally, housecleaning should be performed when the allergic person is not at home, although patients who do their own cleaning may benefit from wearing a face mask.