Allergic Rhinitis

Eric J. Czech, MSBS, PA-Ca,b,*, Andrew Overholser, MSBS, PA-C

a,b
,
Paul Schultz, MDb

KEYWORDS
 Allergic rhinitis  Histamine  Seasonal allergies  Allergen  Antihistamine
 Intranasal corticosteroids  Immunotherapy  Decongestant

KEY POINTS
 Allergic rhinitis is a common condition that can impact quality of life.
 Diagnosis of allergic rhinitis is largely based on history and physical examination.
 First-line treatment for allergic rhinitis is intranasal glucocorticosteroids.
 Allergen testing and desensitization immunotherapy (allergy shots) may be used for pa-
tients with chronic moderate-severe disease recalcitrant to first-line therapies.
 First-line therapies are available over the counter (eg, intranasal steroid sprays, antihista-
mines).

INTRODUCTION

Rhinitis is a common complaint in primary care, characterized by rhinorrhea, sneezing,

congestion, cough, and nasal pruritus. Allergens are one of many rhinitis causes.
Nonallergic rhinitis can occur from several mechanisms, including gustatory, vaso-
motor, irritants, medications, or various systemic diseases. Differentiating allergic
versus nonallergic rhinitis is an essential skill for health care providers. Appropriate,
accurate diagnosis and management can lead to increased quality of life and patient
satisfaction.

EPIDEMIOLOGY

Approximately 10% to 20% of Americans are affected by allergic rhinitis, costing the
US health care system $4.9 billion annually. Indirect costs can double this burden via
lost work time, missed diagnosis, overprescribing, or secondary effects. This must be

This article originally appeared in Primary Care: Clinics in Office Practice, Volume 50 Issue 2,
June 2023.
a
Division of Physician Assistant Studies, Department of Family Medicine, The University of
Toledo College of Medicine and Life Sciences, 3333 Glendale Avenue, Toledo, OH 43614, USA;
b
Department of Family Medicine, The University of Toledo College of Medicine and Life Sci-
ences, 3333 Glendale Avenue, Toledo, OH 43614, USA
* Corresponding author.
E-mail address: eric.czech@utoledo.edu

Med Clin N Am 108 (2024) 609–628

https://doi.org/10.1016/j.mcna.2023.08.013 medical.theclinics.com
0025-7125/24/ª 2023 Elsevier Inc. All rights reserved.

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610 Czech et al

taken with a degree of skepticism, as while allergic rhinitis is a clinical diagnosis,

further diagnostic options influence the data reported in several epidemiological
studies.1

PATHOPHYSIOLOGY

Upper airway allergic reactions occur primarily through a sequence of events in which
allergens bind to specific receptors, prompting production of immunoglobulin E (IgE)
and activating mast cells and basophils. Individuals must first become sensitized to an
allergen before IgE is present. Histamine, prostaglandins, and leukotrienes play a role
in the early phase response via activation of H1 receptors leading to pruritus, rhinor-
rhea, and sneezing. Prostaglandin and leukotrienes trigger release of vascular endo-
thelial growth factors, contributing to increased vascular permeability and
subsequent nasal congestion.2 Late-phase responses include continued rhinorrhea
and discharge of the nasal mucosa. The late phase response may continue and pro-
mote an influx of inflammatory cells, with an increased significance and duration.2

CLINICAL PRESENTATION

Allergic rhinitis is characterized by nasal congestion, nasal discharge, or rhinorrhea, with

episodic, paroxysmal sneezing. Patients may also experience coughing, postnasal drip,
nasal pruritus, conjunctival inflammation, and congestion of the upper airway, primarily
in the nasal passages and maxillary and frontal sinuses.3 Allergic rhinitis may be sea-
sonal or perennial, mild, moderate, or severe. Allergic rhinitis is considered to be persis-
tent when symptoms are present for greater than 4 times weekly over a period of longer
than 4 weeks; conversely, allergic rhinitis with symptoms that occur less than 4 times
weekly and last fewer than 4 weeks is considered intermittent.4
Variation in seasonal allergens causes differences between patients and the presen-
tation of symptoms, with the need for management varying throughout the year. Inves-
tigations into pollen burden by region demonstrate changes in peak concentration and
season duration and a variation of plant species between regions (Table 1). These fac-
tors influence the varied presentation of symptoms between geographic locations and
individual patients.5
Patients with allergic rhinitis may also experience adverse effects on quality of life
and cognitive performance. These primarily stem from altered breathing patterns lead-
ing to decreased sleep quality.6 Sequelae of this phenomenon adversely affect cogni-
tive performance and focus, resulting in general fatigue and daytime somnolence.
Sequelae of allergic rhinitis have been linked to either the manifestation or exacerba-
tion of attention deficit hyperactivity disorder in children and adolescents.7
Common associations with allergic rhinitis include atopic dermatitis, asthma, and
food allergies. Thirty-eight percent of patients with allergic rhinitis are also afflicted
with asthma.8 Evidence suggests that symptoms of asthma can be exacerbated by
allergic rhinitis itself, further complicating care. Comorbidities associated with allergic
rhinitis include sinusitis, sleep pattern aberration, migraines, and gastroesophageal
reflux.9

DIAGNOSTICS

Allergic rhinitis is a clinical diagnosis, rooted firmly in history and objective examination
findings. Diagnosis is supported by classic symptoms of rhinorrhea, nasal congestion,
sneezing paroxysms, nasal pruritus, cough, postnasal drip, and conjunctival inflam-
mation. Presence of other atopic conditions supports the diagnosis. A thorough

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Table 1
Average season start and length for common allergens in the United States

Allergens Peak Season Start Dates Season Length

Oak Spring Northeast Late April Northeast 14–21 days
Southeast Early March Southeast 35–45 days
Midwest Mid-April Midwest 19–30 days
Southwest March-April Southwest 27–45 days
Northwest Late April Northwest 14–30 days
Birch (Betula) Spring Northeast Late April Northeast 29–35 days
Southeast Mid-February - early March Southeast 35–40 days
Midwest Late March - late April Midwest 29–36 days
Southwest – Southwest –
Northwest Late April Northwest 27–34 days
Grass Early summer Northeast Mid-April – mid-June Northeast 37–91 days
Southeast Early March - mid April Southeast 110–217 days
Midwest Mid-April - late May Midwest 56–127 days
Southwest Mid-March - late May Southwest 56–199 days
Northwest Mid-May – mid-June Northwest 37–91 days
Ragweed Late summer, autumn Northeast Late July - early August Northeast 32–41 days
Southeast Late August – mid-September Southeast 36–50 days
Midwest Late July – mid-August Midwest 32–44 days
Southwest Mid-August – mid-September Southwest 42–56 days
Northwest Late July - early August Northwest 32–41 days
Mugwort Late summer, autumn Northeast Early - late August Northeast 39–46 days
Southeast Late August - late September Southeast 29–46 days
Midwest Mid July - late August Midwest 29–46 days

Allergic Rhinitis
Southwest Late August - late September Southwest 24–46 days
Northwest Mid July - early September Northwest 8–43 days

Adapted from Zhang Y, Bielory L, Cai T, Mi Z, Georgopoulos P. Predicting onset and duration of airborne allergenic pollen season in the United States. Atmos En-
viron (1994). 2015;103:297-306.

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612 Czech et al

history should focus on symptom frequency and duration, specific symptoms and in-
tensity, with previous therapies and their efficacy. Clinicians should assess at what
time during the year allergic rhinitis symptoms are most prominent, if there are any
known exacerbating triggers such as occupational exposures or pet dander, and if
previously trialed treatments were effective.10
Physical examination of the patient with allergic rhinitis should include an assess-
ment of the eyes, ears, nose, and throat. Pale, boggy, edematous nasal mucosa are
common in allergic rhinitis, with a 67% sensitivity and 37% specificity. Nasal turbinate
hypertrophy carries a 90% sensitivity but only a 2.3% specificity.11 Examination of the
eyes may reveal lacrimation and inflamed conjunctiva, while the oropharynx may
demonstrate postnasal drip or a cobblestone appearance.10
Patients may demonstrate various physical findings of allergic rhinitis, including
morning Dennie-Morgan lines (creases or folds inferior to the lower eyelids), infraorbi-
tal edema and darkening known as allergic shiners, or nasal polyps.10 Nasal polyps
carry a 95% specificity but only a 12% sensitivity.11
Qualifying allergic rhinitis into severity categories influences therapeutic intensity.
Classic categories are mild or moderate-severe. Mild allergic rhinitis is associated
with absence of alteration in daily activities, sleep, performance in work or school-
type environments, and a lack of overall troubling symptoms. The diagnosis of
moderate-severe allergic rhinitis can be established with aberrations in normal sleep
patterns, daily routines or activities, adverse effects on cognitive performance, or
overall troublesome symptoms.10 Symptoms and severity of allergic rhinitis can prog-
ress over time. Patients may move between mild or moderate-severe allergic rhinitis
throughout the disease process.
Additional laboratory testing is available to confirm and specify responsible aller-
gens. To identify allergen triggers, serum IgE levels to environmental allergens can
be assessed in primary care. Skin prick testing can be done in an allergist’s office.
The more specific diagnosis of local allergic rhinitis can be confirmed with the pres-
ence of IgE in nasal secretions, although this is rarely done.12

MANAGEMENT/THERAPEUTICS

Allergic rhinitis usually requires pharmacological therapy to control symptoms. Often,

patients can only minimally change or control their environment. Many pharmacolog-
ical therapies for allergic rhinitis are available over the counter, and patients tend to try
their own therapies (Table 2). This can cause overuse of first-generation antihista-
mines and the underuse of intranasal corticosteroids. Some concerns leading to un-
derutilization of intranasal corticosteroids include safety and efficacy, confusing
intranasal corticosteroids with decongestants, cost, undesirable feelings of intranasal
use, and inability to feel a result quickly.13

Allergen Avoidance
The best method to control allergic rhinitis is prevention by avoiding allergens. If prac-
tical, the patient and provider should develop avoidance strategies to minimize or
eliminate exposure to causative agents. Patients frequently have multiple environ-
mental allergens, making meaningful avoidance difficult to achieve. A summary of
avoidance strategies is presented in Fig. 1.14

Allergen Immunotherapy
Once specific triggering allergens are determined, under the treatment of an allergist,
a patient can have desensitizing immunotherapy to reduce symptoms and the need for

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Table 2
Summary of medical therapy for allergic rhinitis
Therapy Changing Other
Class and Adverse/Side Prescription Generic Mechanisms Use in
Receptors Effected Generic Name Brand Name Effects Required? Available? Pediatric Dosing Adult Dosing of Action? Pregnancy? Other
First Generation Beclomethasone Beconase AQ Potential for Yes No Age 6–11 y: Start 1–2 sprays Yes
Intra-Nasal dipropionate nasal (42 mg/spray) hypercortisicm 1 spray each nostril each nostril
Corticosteroids twice daily. May twice daily
(Bioavailability increase to 1 to 2
10%–50%) sprays each nostril
twice daily
Age >12 y: 1 to
2 sprays each
nostril twice daily
Qnasl Childrens Potential for Yes No 4–11 y: 1 spray each Yes
(40 mg/spray) hypercortisicm nostril daily
Qnasl Potential for Yes No >12 y: 2 sprays each 2 sprays each Yes
(80 mg/spray) hypercortisicm nostril daily nostril daily
Budesonide nasal Rhinocort Allergy Potential for No Yes Age 6–11 y: Start 1–2 sprays each Yes,
(32 mg/spray) hypercortisicm 1 spray each nostril nostril daily preferred
once daily. May agent
increase to 1 to
2 sprays each
nostril once daily
Age >12 y: 1 to
2 sprays each
nostril once daily
Flunisolide nasal Nasarel Potential for Yes Yes Age 6–14 y: 2 sprays 2 sprays each Yes
(25 mg/spray) hypercortisicm each nostril twice nostril 2–3 times
daily daily
Age >15 y: 2 sprays
each nostril
two-three
times daily
Triamcinolone nasal Nasacort Allergy Potential for No Yes Age 2-5 y: 1 spray 2 sprays each Yes
24 h (55 mg/spray) hypercortisicm each nostril nostril once
once daily daily

Allergic Rhinitis
Age 6–11 y: Start
1 spray each nostril
once daily. May
increase to 1 to 2
sprays each nostril
once daily
Age >12 y: 1–2 sprays
each nostril
once daily

(continued on next page)

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Table 2

Czech et al
(continued )
Therapy Changing Other
Class and Adverse/Side Prescription Generic Mechanisms Use in
Receptors Effected Generic Name Brand Name Effects Required? Available? Pediatric Dosing Adult Dosing of Action? Pregnancy? Other
Second-generation Ciclesonide nasal Omnaris Lower theoretical Yes No Age 2–11 y: 1 to 2 sprays each Yes
intranasal (50 mg/spray) potential for 2 sprays each nostril daily
corticosteroids hypercortisicm as nostril once daily
(Bioavailability compared to first Age >12 y: 2 sprays
<1%) generation each nostril
once daily
Zetonna Lower theoretical Yes No Age >12 y: 1 spray 1 spray each Yes
(37 mg/spray) potential for each nostril nostril daily
hypercortisicm as once daily
compared to first
generation
Fluticasone Xhance Lower theoretical Yes No 1–2 sprays each Yes
propionate nasal (93 mg/spray) potential for nostril twice daily
hypercortisicm as
compared to first
generation
Flonase Lower theoretical No Yes Age 4–11 y: 1 spray 1–2 sprays each Yes
(50 mg/spray) potential for each nostril nostril daily
hypercortisicm as once daily
compared to first Age >12 y: 2 sprays
generation each nostril
once daily
Fluticasone Flonase Sensimist Lower theoretical No No Age 2–11 y: 1 spray 2 sprays each Yes Taking with
furoate nasal (27.5 mg/spray) potential for each nostril nostril daily a CYP3A4
hypercortisicm as once daily inhibitor
compared to first Age >12 y: 1–2 sprays will increase
generation each nostril fluticasone
once daily blood levels
Momentasone nasal Nasonex Lower theoretical No Yes Age 2–11 y: 1 spray 2 sprays each Yes
*50 mg/spray) potential for each nostril once nostril daily
hypercortisicm as daily
compared to first Age >12 y: 1–2 sprays
generation each nostril once
daily
 second-generation Loratadine Claratin Low potential for No Yes Age 2-5 y: 5 mg by 10 mg once daily Yes
antihistimines sedation mouth daily
(histimine-1 Age >6 y: 10 mg
peripheral by mouth daily
receptor Desloratadine Clarinex Low potential for Yes No Age 6–11 mo: 1 mg 5mg once daily Yes
antagonist) sedation by mouth daily
Age 1-5 y: 1.25 mg
by mouth daily
Age 6–11 y: 2.5 mg
by mouth daily
Age >12 y: 5 mg
by mouth daily
Cetirizine Zytec Higher risk of No Yes Age 6–11 mo: 10 mg once daily Yes
sedation as 2.5 mg by Age > 65 y: 5 mg
compared mouth daily by mouth daily
to other Age 12–23 mo:
second gen 2.5 mg by mouth
antihistamines daily or twice daily
(10% of patients) Age 2-5 y: 5 mg by
mouth daily. Start
2.5 mg by mouth
daily.
Age >6 y: 5–10 mg
by mouth daily
Levocetirizine Xyzal Low potential for Yes No Age 6–11 y: 2.5 mg 2.5-5 mg once Yes
sedation by mouth nightly daily at bedtime
Age >12 y: 2.5-5 mg
by mouth nightly
Children’s Xyzal Low potential for Yes No Age 2-5 y: 2.5 mL Yes
(2.5 mg/5 mL sedation by mouth nightly
solution) Age 6–11 y: 5 mL
by mouth nightly
Age 12–18 y: 5–10 mL
by mouth nightly
Age >65 y: 5 mL by
mouth nightly
Third-generation Fexofenadine Allegra No Yes Age 2–11 y: 30 mg 180 mg once daily Yes Taking with
antihistimines by mouth daily juice (fruit
(histimine-1 Age >12 y: 180 mg juice) will
peripheral by mouth daily lower blood
receptor levels
antagonist)

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Allergic Rhinitis

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Czech et al
Table 2
(continued )
Therapy Changing Other
Class and Adverse/Side Prescription Generic Mechanisms Use in
Receptors Effected Generic Name Brand Name Effects Required? Available? Pediatric Dosing Adult Dosing of Action? Pregnancy? Other
Intranasal Olopatadine nasal Patanase Yes No Age 6–11 y: 1 spray 2 sprays each Antihistmine, Yes
antihistimines (660 mg/spray) each nostril twice nostri twice Mast cell
(histimine-1 0.6% daily daily stabilizer,
peripheral/central Age >12 y: 1–2 sprays and anti-
nervous system each nostril twice inflammatory
[CNS] receptor daily effects
antagonst) Azelastine nasal Astepro No No Age 6–11 y: 1 spray 1–2 sprays each Antihistimine Yes
(205.5 mg/spray) each nostril twice nostril daily and anti-
0.15% daily inflammatory
Age >12 y: 1–2 sprays effects
each nostril twice
daily
Intranasal mast Cromolyn sodium Nasalcrom No No Age 2 years and 1 sprays each Yes Limited efficacy.
cell stabilizer 5.2 mg/spray older: 1 sprays each nostril three-four May be tried.
nostril three-four times daily. Max Very safe to
times daily. Max 1 1 spray each use
spray each nostril nostril six times
six times daily daily
Antileukotriene Montelukast Singulair Serious Yes Yes Age 6–23 mo: 4 mg 10 mg by mouth Probably Can use if
agents neuropsychiatric by mouthevery day daily not other agents
(leukotriene effects seen. Age 2–5 y: 4 mg by do not work.
receptor Alternative mouth every day
antagonist) therapies now Age 6–14 y: 5 mg by
recommended mouth every day
based on benefit/ Age >15 y: 10 mg by
risk ratio mouth everyday
Systemic Prednisone Deltasone Higher potential for Yes Yes 0.05–2 mg/kg/day by 5–60 mg by mouth Yes Not
corticosteroids hypercortisicm mouth divided daily recommended
(ie, prednisone) as compared to once-four times for mild/
topical daily moderate cases.
preparations Use for shortest
duration
Methylprednisolone Medrol Higher potential for Yes Yes 0.5–1.7 mg/kg/day 4–48 mg/day by Yes Not
hypercortisicm as by mouth divided mouth divided recommended
compared to every 6–12h once-four times for mild/
topical daily moderate cases.
preparations Use for shortest
duration
 Intranasal Ipratropium Atrovent Nasal Anticholinergic Yes Yes Age 5 years and 2 sprays each Yes May help with
anticholinergics bromide (21g/spray) 0.06% older: 2 sprays nostril four rhinorrhea if
(muscarinic each nostril four times daily uncontrolled
receptor times daily on other agents
antagonist) (topical
glucocorticoids)
First-generation Diphenhydramine Benadryl Sedation, No Yes Age 2-5 y: 6.25 mg 25–50 mg by Intracellar Yes Age 2–11 y: For
antihistimines anticholinergic by mouth every mouth every sodium channel severe symptoms:
(histimine-1 4-6 h. Max 37.5 mg 2–6 h. Max blocker (Can 1-2 mg/kg/dose
peripheral/CNS daily 300 mg daily produce local every 6 h as
receptor Age 6–11 y: Limit use >65 y anesthesia) needed. Max
antagonist, 12.5–25 mg by old patients 50 mg/dose and
muscarinic mouth every 4-6 h. 300 mg daily
receptor Max 150 mg daily.
antagonist) Age >12 y: 25–50 mg
every 2-6 h. Max
300 mg daily.
Dimenhydrinate Dramamine Sedation, No Yes Age 2-5 y: 50–100 mg by Intracellar Yes 8-chlorotheophylline
(diphenhydramine/ anticholinergic 12.5–25 mg by mouth every sodium channel is a xanthine
8- mouth every 6-8 h. 4-6 h. Max blocker (Can derivative, such
chlorotheophylline) Max 75 mg daily. 600 mg daily. produce local as caffeine. It is
Age 6–11 y: Limit use >65 y anesthesia) combined with
25–50 mg by old patients diphenhydramine
mouth every 6-8 h. in an attempt to
Max 150 mg daily. counteract the
Age >12 y: sedative effects
50–100 mg every
4-6 h. Max 600 mg
daily.
Doxylamine Vick’s ZzzQuil Ultra Sedation, No Yes Age >12 y: 12.5 mg 12.5 mg by Yes
Unisom Sleep Tabs anticholinergic by mouth every mouth every
4-6 h. Max 75 mg 4-6 h. Max
daily 75 mg daily
Limit use >65 y
old patients
Chlorpheniramine Aller-Chlor Sedation, No Yes Age 6–11 y: 2 mg 4mg by mouth Yes
anticholinergic by mouth every every 4-6 h.
6-8 h. Max 12 mg Max 24 mg daily
daily. Limit use >65 y
Age >12 y: 4 mg old patients
every 4-6 h. Max
24 mg daily.

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Allergic Rhinitis

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Table 2

Czech et al
(continued )
Therapy Changing Other
Class and Adverse/Side Prescription Generic Mechanisms Use in
Receptors Effected Generic Name Brand Name Effects Required? Available? Pediatric Dosing Adult Dosing of Action? Pregnancy? Other
Brompheniramine Children’s Dimetapp Sedation, No No Age 6–11 y: 10 mL No Only available
(Brompheniramine/ anticholinergic by mouth every in combination
Phenylephrine 4 h. Max 60 mL with
2 mg-5 mg/10 mL) daily. phenylephrine.
Age >12 y: 10 mL
every 4 h. Max
120 mL daily.
Promethazine Phenergan Sedation, Yes Yes Age 2 years and 6.25–25 mg by Dopamine-2 Proabably
anticholinergic, older: 0.1 mg/kg/ mouth three-four Receptor not. Risk
extrapyramidal dose times daily. Max Antagonist, of fetal
symptoms, by mouth every 6 h. 100 mg daily. Alpha-1 respiratory
orthostatic Max 12.5 mg/dose Limit use >65 y Adrenergic depression
hypotension during day, old patients Receptor
25 mg/dose at night, Antagonist
100 mg daily.
Hydroxyzine Atarax Sedation, less Yes Yes Age <6 y: 2 mg/kg/day 25 mg by mouth Weak Proabably Less
anticholinergic by mouth divided every 6-8 h. antagonist at anti-cholinergic
every 6-8 h Limit use >65 y Serotonin action than
Age 6–12 y: old patients 5-HT2a, diphenhydramine
2 mg/kg/day by Dopamine
mouth divided D2, and
every 6-8 h alpha-1
Age >12 y: 25 mg by adrenergic
mouth every 6-8 h. receptors.
Carbinoxamine Karbinal ER Sedation, Yes Yes Age 2-3 y: 6–16 mg by mouth Yes
anticholinergic 0.2–0.4 mg/kg/day every 12 h.
by mouth divided Limit use >65 y
every 12 h old patients
Age 4-5 y:
0.2–0.4 mg/kg/day
by mouth divided
every 12 h
Age 6–11 y:
0.2–0.4 mg/kg/day
by mouth divided
every 12 h
 Age >12 y: 6–16 mg
by mouth every 12 h.
Clemastine Sedation, No Yes Age 6–11 y: 0.5–1 mg 1-2 mg by mouth Yes
anticholinergic by mouth twice daily. Max
twice-three 6 mg daily
times daily. Max Limit use >65 y
3 mg daily. old patients
Age >12 y: 1–2 mg by
mouth twice-three
times daily. Max
6 mg daily.
Cyproheptadine Periactin Sedation, Yes Yes Age 6–11 y: 2 mg by 4mg by mouth Serotonin 5-HT1 Yes
anticholinergic mouth every 8–12h. three times antagonist,
Max 3 mg daily. daily. Max 5-HT2
Age 7–14 y: 4 mg by 0.5 mg/kg/day antagonist,
mouth every 8–12h Limit use >65 y possible
Max 6 mg daily. old patients antiandrogenic.
Triprolidine Histex Sedation, No Yes Age 6–11 y: 1.25 mg No
anticholinergic by mouth every
4-6 h. Max 5 mg
daily
Age >12 y: 2.5 mg by
mouth every 4-6 h.
Max 10 mg daily
Decongestants, Phenylephrine Sudafed-PE Hypertension, No Yes Age >12 y: 10 mg by 10 mg by mouth No Not
oral (alpha-1 insomnia, mouth every 4-6 h. every 4-6 h. Max recommended
adrenergic irritability, Max 60 mg daily 60 mg daily monotherapy.
agonists) headache, Do not use
rebound nasal longer than
congestion 3 days
Pseudoephedrine Sudafed Hypertension, No Yes Age 2-3 y: 15 mg by 60 mg by mouth No Not
insomnia, mouth every 4-6 hr. every 4-6 h. Max recommended
irritability, Max 60 mg daily 240 mg daily monotherapy.
headache, Age 4-5 y: 15 mg by Do not use
rebound nasal mouth every 4-6 hr. longer than
congestion Max 60 mg daily 3 days
Age 6–11 y: 30 mg
by mouth every
4-6 hr. Max 120 mg
daily
Age >12 y: 60 mg by
mouth every 4-6 h.
Max 240 mg daily

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Czech et al
Table 2
(continued )
Therapy Changing Other
Class and Adverse/Side Prescription Generic Mechanisms Use in
Receptors Effected Generic Name Brand Name Effects Required? Available? Pediatric Dosing Adult Dosing of Action? Pregnancy? Other
Intranasal Oxymetazoline Afrin Nasal Hypertension, No Yes Age >6 y: 2–3 sprays 2–3 sprays in each Yes Not
decongestants Spray 0.05% insomnia, in each nostril nostril q10–12 h recommended
(alpha-1 irritability, q10–12 h monotherapy.
Adrenergic headache, Do not use
agonists) rebound nasal longer than
congestion 3 days
Phenylephrine Neo-synephrine Hypertension, No Yes 2–3 sprays in each Proabably Not
Nasal Spray 1% insomnia, nostril every 4 h not recommended
irritability, monotherapy.
headache, Do not use
rebound nasal longer than
congestion 3 days
 Allergic Rhinitis 621

Fig. 1. Common indoor allergens and allergen avoidance strategies. (Adapted from Platts-
Mills TA. Allergen avoidance in the treatment of asthma and allergic rhinitis.
Uptodate.com, 2021, Available at: https://www.uptodate.com/contents/allergen-avoidance-
in-the-treatment-of-asthma-and-allergic-rhinitis?search5Allergen%20avoidance%20in
%20the%20treatment%20of%20asthma%20and%20allergic%20rhinitis&source5search_
result&selectedTitle51w150&usage_type5default&display_rank51, Accessed September
27, 2022.)

chronic medication. Immunotherapy is usually deployed with either subcutaneous

immunotherapy (SCIT) or sublingual immunotherapy (SLIT). Only a few allergens
have been standardized with dosing and extracts, as discussed in Table 2.1 Using
SLIT may provide a less invasive route of administration and increase patient compli-
ance, but current data suggest that SCIT may be more efficacious than SLIT. Head-to-
head trials are lacking, however, and further research is needed.15

Nasal Saline
Irrigation with sterile saline can aid in cleansing the nasal cavity of allergens. This is
generally recommended for mild allergic rhinitis. Administration of nasal saline can
be through over-the-counter bottles, Nettie Potts, syringes, or electronic devices. It
is important to use sterile saline and not tap water or another nonsterile solution to pre-
vent entry of foreign microbes and material into the nasal cavity. Isotonic nasal saline
irrigation is an effective adjunctive or monotherapy for mild allergic rhinitis when
compared with intranasal corticosteroids.16

Glucocorticoid Nasal Sprays

Glucocorticoid nasal sprays are the most effective monotherapy agent and are the
mainstay of treatment for allergic rhinitis, with adverse effects at recommended
doses.17,18

Agent Selection
Specific agents are listed in Table 2. Studies fail to demonstrate any significant differ-
ences in efficacy of one agent over another. Therefore, when prescribing these med-
ications, care should be taken regarding comorbidities and bioavailability of the

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622 Czech et al

corticosteroid. First-generation corticosteroids have significantly higher systemic

bioavailability than second-generation; however, the risk of systemic adverse effects
for first-generation or second-generation formulations is low. A potential worrisome
side effect would be hypercorticism, which can lead to hypothalamic pituitary adrenal
axis suppression. Fortunately, multiple studies with first- and second-generation cor-
ticosteroids have shown hypothalamic pituitary adrenal axis suppression does not
occur with long-term use.19,20 Other major concerns related to intranasal use of glu-
cocorticosteroids include slow growth in children, promotion of osteopenia, osteopo-
rosis, glaucoma, and cataracts. A 2020 practice guideline review on allergic rhinitis
and multiple studies failed to show any significant adverse effects of long-term intra-
nasal corticosteroid use in children and adults.5,21–24 Class-wide adverse effects
including taste change, burning, dryness, and epistaxis are less concerning for
long-term harm but may lead to patient intolerance and treatment cessation. Perfora-
tion of the nasal septum has been a reported complication, but incidence is low.20
Epistaxis with intranasal corticosteroid use is seen in 5% to 10% of patients, most
likely the result of mucosal irritation and minor trauma. Trace blood in mucosal secre-
tions should be expected. Stopping treatment for a couple of days can mitigate these
symptoms. In patients with persistent and/or severe epistaxis, workup for other
causes should ensue, and stopping therapy may be warranted with transition to other
alternatives.25
Most of the onset of action is within a few hours; maximal effect occurs within 2 days
to 3 weeks.26 Patients may believe the medication is not working, because effects are
not immediate. Proper education on onset of action and use of these medications is
important for compliance.27 It is recommended to start therapy at the highest dose
based on age, tapering down to the lowest effective dose after symptom control.

Administration of Intranasal Corticosteroids

Proper administration of intranasal corticosteroids depends on patients’ ability to self-
administer. The head should be pointed downward while spraying, preventing excess
corticosteroids from draining down the throat; patients should spray away from the
nasal septum. If the patient has significant congestion preventing effective administra-
tion and coating of the mucosa, temporary use of a decongestant spray before intra-
nasal corticosteroid administration can increase corticosteroid penetrance.28,29

Antihistamines
When comparing the efficacy of oral antihistamines against intranasal corticosteroids,
intranasal corticosteroids are significantly more efficacious than antihistamines,
reducing total nasal symptom score by 25% more than the control, whereas antihis-
tamines have. decreased total nasal symptoms by up to 10%.30,31 A 2020 practice
parameter update recommends starting therapy for intermittent allergic rhinitis with
either an intranasal corticosteroid or oral antihistamine. Patients with persistent symp-
tomatically mild allergic rhinitis should start with an intranasal corticosteroid and use
an oral antihistamine if symptoms are not controlled. Adding oral antihistamines to
intranasal glucocorticoids provides no additional benefit.5

First-Generation Antihistamines
First-generation antihistamines are widely available; however, potential adverse ef-
fects limit their use. These drugs can cross the blood-brain barrier and antagonize
central nervous system histamine-1 receptors, causing sedative side effects.5 In addi-
tion, they have a varying affinity for antagonizing peripheral and central muscarinic re-
ceptors, leading to significant anticholinergic side effects.5 This is particularly

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 Allergic Rhinitis 623

important when using antihistamines in older patients who may have a higher risk of
falls or dizziness associated with central antagonism of histamine.5 Furthermore, anti-
cholinergic side effects in older patients can include urinary retention, constipation,
delirium, tachycardia, and increased intraocular pressure.32 A 2015 study also corre-
lated the risk of chronic anticholinergic use with dementia.33 First-generation antihis-
tamines are not recommended for allergic rhinitis in favor of second and third-
generation nonsedating antihistamines.5

Second- and Third-Generation Antihistamines

Second-generation and third-generation antihistamines are more lipophobic than
first-generation antihistamines, decreasing their adverse effects. Although second-
generation antihistamines are less sedating, cetirizine can be sedating in up to 10%
of patients.34 Also, there can be varying levels of anticholinergic adverse effects in
some patients, although they tend to be less than first-generation antihistamines.35
Although not superior to intranasal glucocorticoids, second- and third-generation an-
tihistamines are recommended for use in allergic rhinitis.5 There is no evidence to sug-
gest that tolerance develops with antihistamines, allowing for chronic use.36

Intranasal Antihistamines
Intranasal antihistamines have significant clinical benefits in allergic rhinitis along with
anti-inflammatory effects.37 Olopatadine is shown to have antihistamine, mast cell sta-
bilizing, and anti-inflammatory properties.38 Benefits of intranasal antihistamines may
include an onset of action within 15 minutes, although maximum efficacy occurs in 2 to
3 days.39 When comparing the efficacy of intranasal antihistamines and intranasal cor-
ticosteroids, many studies favor corticosteroids.40 Some studies suggest intranasal
antihistamines have comparable efficacy to intranasal corticosteroids.41,42 There is
no statistical benefit of choosing an intranasal antihistamine over an oral antihistamine
other than choosing targeted versus systemic therapy.43

Intranasal Mast Cell Stabilizer

Cromolyn sodium is the only intranasal mast cell stabilizer available in the United
States and reduces mast cell histamine release. Use is limited because of low efficacy
and is relegated to an adjunctive role in some cases of mild allergic rhinitis.44

Antileukotriene agents
Leukotriene receptor antagonists like montelukast are moderately effective in treating
allergic rhinitis and are similar in efficacy to oral antihistamines.45,46 Other studies sug-
gest that leukotriene receptor antagonists are moderately less effective than oral an-
tihistamines,47,48 and are far less efficacious than intranasal corticosteroids.48,49
Previously, montelukast was widely used in combination with oral antihistamines to
provide additional benefit for allergic rhinitis. This is not favorable because of
increased neuropsychiatric adverse effects.50,51 The US Food and Drug Administra-
tion (FDA) released a black box warning for montelukast because of increases in these
adverse effects in pediatric, adolescent, and adult patients. Adverse effects can
include vivid dreams, depression with suicidal thoughts, insomnia, disorientation,
aggression, hallucinations, obsessive-compulsive symptoms, tics, and memory
impairment.52 When considering this medication for allergic rhinitis, shared decision
making regarding the risks and benefits of treatment is advised. Antileukotriene agents
can benefit patients with concurrent asthma that is not well controlled. Leukotriene re-
ceptor antagonists are not recommended for initial treatment of allergic rhinitis. They

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624 Czech et al

are best reserved as adjunctive treatment in combination therapy based on careful

risk-benefit analysis.52

Systemic Corticosteroids
Systemic corticosteroids may be used for a short treatment course of severe and/or
intractable allergic rhinitis over 5 to 7 days. This allows time for other agents to take
effect. The recommendation is to use the lowest dose for the shortest amount of
time because of potential adverse effects.53

Oral and Intranasal Decongestants

Oral decongestants such as phenylephrine and pseudoephedrine act as peripheral
alpha-adrenergic agonists, relieving nasal congestion and rhinorrhea through vaso-
constriction.54 Unfortunately, oral phenylephrine is ineffective at treating nasal
congestion at doses up to 40 mg when compared with placebo.54 Class adverse ef-
fects include elevated blood pressure, insomnia, appetite suppression, irritability,
and palpitations. Cautious consideration of these agents in those with cardiac comor-
bidities, thyroid disease, glaucoma, benign prostatic hyperplasia, psychiatric condi-
tions, and cerebrovascular disease is advised.54
Many topical nasal decongestants are available with vasoconstrictive activity. They
are effective for nasal congestion. Use is limited for symptom relief to 3 days because
of the risk of rhinitis medicamentosa. Proper use of topical nasal decongestants com-
bined with topical corticosteroids can more effectively treat the symptoms of rhinitis
and nasal congestion without the risk of rhinitis medicamentosa.53

Intranasal Anticholinergics
Ipratropium bromide is the only available anticholinergic nasal spray and can be effec-
tive in decreasing rhinorrhea. It is significantly less efficacious than intranasal cortico-
steroids for sneezing, pruritus, and nasal congestion.44 It is not recommended as a
first-line treatment for allergic rhinitis because of limited efficacy compared with other
agents. This agent should only be used in those with allergic rhinitis where rhinorrhea
is not controlled with first-line agents.44

SUMMARY

Allergic rhinitis is common in primary care, affecting up to 20% of Americans. It can

have a variable presentation with IgE-mediated symptoms including runny nose,
congestion, sneezing, mucosal pruritus, postnasal drip, and conjunctival inflamma-
tion. Diagnosis is typically made on history and physical examination. At this initial
stage, laboratory and/or imaging studies are not generally needed. Ruling out other
etiologies with similar presentations is often challenging. Reassessment of alternative
diagnoses is important when treatments are ineffective. When allergic rhinitis is mild,
properly performed nasal saline rinses provide significant relief. In both mild and
moderate-severe allergic rhinitis, first-line treatment with intranasal glucocorticoid
sprays can provide symptom improvement. Educating patients in proper technique
to administer nasal spray can optimize drug efficacy. An alternative treatment shown
to provide benefit either as monotherapy or in combination with steroid nasal spray is a
second- or third-generation antihistamine. First-generation antihistamines are not
first-line options because of potential side effects of sedation and urinary retention.
Leukotriene receptor antagonists can reduce the inflammatory response in nasal
and respiratory mucosa. These continue to be an option for adjunctive therapy in pa-
tients with associated asthma. When nasal steroid sprays and/or second-generation

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 Allergic Rhinitis 625

antihistamines are insufficient, and symptoms are at a level to create secondary ef-
fects (eg, fatigue, cognitive impairment, sleep disruption), allergen testing can be per-
formed. Once triggering allergens are identified, desensitizing immunotherapy (allergy
shots) can reduce symptom burden. At initiation of treatment, use of temporary symp-
tom relief measures such as intranasal or systemic decongestants can provide benefit
while waiting for intranasal glucocorticoids to become effective. In more severe pre-
sentations, a short, 5- to 7-day course of oral corticosteroids can be considered while
waiting for first-line treatments to become therapeutic. A shared decision-making
approach incorporating a risk-benefit discussion and patient education is advisable.

CLINICS CARE POINTS

 Allergic rhinitis is an IgE-mediated immune response to environmental allergens.

 Diagnosis is achieved through history and physical examination; testing is not usually
needed.
 Other conditions can overlap with allergic rhinitis. If first-line therapies are not effective,
reconsider the differential diagnoses.
 For known allergens, avoidance measures can provide a cost-effective, low-risk benefit.
 Recommend nasal saline rinses, as these reduce symptoms.
 Intranasal corticosteroid sprays are the most efficacious first-line therapy.
 Educate patients to spray up toward the sinuses, away from the nasal septum, while
performing a coordinated subtle sniff to ensure medication will be delivered to the nasal
mucosa.
 Second- or third-generation antihistamines are also effective either in monotherapy or in
combination with nasal steroid sprays.
 Although many options are available over the counter, patients may fail to optimize these
medications. Patient education on treatment options, mechanisms of action, and
treatment goals is essential.
 First-generation antihistamines can provide symptom relief but are best avoided, particularly
in the geriatric population, because of increased adverse effect potential.
 Allergen testing and desensitizing immunotherapy are best reserved for those recalcitrant to
first-line therapy options and/or those who have moderate-severe symptoms impacting
quality of life.

DISCLOSURE

The authors have nothing to disclose.

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