Practice Essentials

Rhinitis, which occurs most commonly as allergic rhinitis, is an inflammation of the nasal
membranes that is characterized by sneezing, nasal congestion, nasal itching, and rhinorrhea, in
any combination. [1] Although allergic rhinitis itself is not life-threatening (unless accompanied
by severe asthma or anaphylaxis), morbidity from the condition can be significant.

Background
Rhinitis is defined as inflammation of the nasal membranes [2] and is characterized by a symptom
complex that consists of any combination of the following: sneezing, nasal congestion, nasal
itching, and rhinorrhea. [1] The eyes, ears, sinuses, and throat can also be involved. Allergic
rhinitis is the most common cause of rhinitis. It is an extremely common condition, affecting
approximately 20% of the population.

Although allergic rhinitis is not a life-threatening condition, complications can occur and the
condition can significantly impair quality of life, [3, 4] which leads to a number of indirect costs.
The total direct and indirect cost of allergic rhinitis was recently estimated to be $5.3 billion per
year. [5] A 2011 analysis determined that patients with allergic rhinitis averaged 3 additional
office visits, 9 more prescriptions filled, and $1500 in incremental healthcare costs in 1 year than
similar patients without allergic rhinitis. [6]

Pathophysiology
Allergic rhinitis involves inflammation of the mucous membranes of the nose, eyes, eustachian
tubes, middle ear, sinuses, and pharynx. The nose invariably is involved, and the other organs are
affected in certain individuals. Inflammation of the mucous membranes is characterized by a
complex interaction of inflammatory mediators but ultimately is triggered by an immunoglobulin
E (IgE)–mediated response to an extrinsic protein. [7]

The tendency to develop allergic, or IgE-mediated, reactions to extrinsic allergens (proteins

capable of causing an allergic reaction) has a genetic component. In susceptible individuals,
exposure to certain foreign proteins leads to allergic sensitization, which is characterized by the
production of specific IgE directed against these proteins. This specific IgE coats the surface of
mast cells, which are present in the nasal mucosa. When the specific protein (eg, a specific
pollen grain) is inhaled into the nose, it can bind to the IgE on the mast cells, leading to
immediate and delayed release of a number of mediators. [7, 8, 9]

The mediators that are immediately released include histamine, tryptase, chymase, kinins, and
heparin. [8, 9] The mast cells quickly synthesize other mediators, including leukotrienes and
prostaglandin D2. [10, 11, 12] These mediators, via various interactions, ultimately lead to the
symptoms of rhinorrhea (ie, nasal congestion, sneezing, itching, redness, tearing, swelling, ear
pressure, postnasal drip). Mucous glands are stimulated, leading to increased secretions.
Vascular permeability is increased, leading to plasma exudation. Vasodilation occurs, leading to
congestion and pressure. Sensory nerves are stimulated, leading to sneezing and itching. All of
these events can occur in minutes; hence, this reaction is called the early, or immediate, phase of
the reaction.

Over 4-8 hours, these mediators, through a complex interplay of events, lead to the recruitment
of other inflammatory cells to the mucosa, such as neutrophils, eosinophils, lymphocytes, and
macrophages. [13] This results in continued inflammation, termed the late-phase response. The
symptoms of the late-phase response are similar to those of the early phase, but less sneezing and
itching and more congestion and mucus production tend to occur. [13] The late phase may persist
for hours or days.

Systemic effects, including fatigue, sleepiness, and malaise, can occur from the inflammatory
response. These symptoms often contribute to impaired quality of life.

Epidemiology
Frequency

United States

The prevalence of allergic rhinitis in the United States ranges from 3% to 19%, and 30 to 60
million people are affected each year. The development of allergic rhinitis before 20 years of age
occurs in 80% of cases. [14] In 2012, 9% of children younger than 18 years and 7.5% of adults
reported allergic rhinitis in the past 12 months. [15]

International

Throughout the world, the prevalence of allergic rhinitis has slightly escalated. [16] Currently,
approximately 10 to 30% of adults and 40% of children are affected. [14] The European
Community Resporatory Health survey recorded a prevalence of 10 to 41% in adults with
allergic rhinitis. [17] Scandinavian studies have demonstrated a cumulative prevalence rate of 15%
in men and 14% in women. [18] The prevalence of allergic rhinitis may vary within and among
countries. [19, 20, 21, 22] Highest prevalence of severe allergic rhinitis symptoms in children were
observed in Africa and Latin America. [23] This may be due to geographic differences in the types
and potency of different allergens and the overall aeroallergen burden.

Mortality/Morbidity

While allergic rhinitis itself is not life-threatening (unless accompanied by severe asthma or
anaphylaxis), morbidity from the condition can be significant. Allergic rhinitis often coexists
with other disorders, such as asthma, and may be associated with asthma exacerbations. [24, 25, 26]

Allergic rhinitis is also associated with otitis media, eustachian tube dysfunction, sinusitis, nasal
polyps, allergic conjunctivitis, and atopic dermatitis. [2, 1, 27] It may also contribute to learning
difficulties, sleep disorders, and fatigue. [28, 29, 30]
  Numerous complications that can lead to increased morbidity or even mortality can occur
secondary to allergic rhinitis. Possible complications include otitis media, eustachian tube
dysfunction, acute sinusitis, and chronic sinusitis.
 Allergic rhinitis can be associated with a number of comorbid conditions, including
asthma, atopic dermatitis, and nasal polyps. Evidence now suggests that uncontrolled
allergic rhinitis can actually worsen the inflammation associated with asthma [24, 25, 26] or
atopic dermatitis. [27] This could lead to further morbidity and even mortality.
 Allergic rhinitis can frequently lead to significant impairment of quality of life.
Symptoms such as fatigue, drowsiness (due to the disease or to medications), and malaise
can lead to impaired work and school performance, missed school or work days, and
traffic accidents. Cost of allergic rhinitis have increased substantially in the United States.
In 1996, the overall cost (direct and indirect) of allergic rhinitis was estimated to be $5.3
billion per year. [5] In 2002, total costs including indirect costs were estimated at $11.58
billion. [14]

Race

Allergic rhinitis occurs in persons of all races. Prevalence of allergic rhinitis seems to vary
among different populations and cultures, which may be due to genetic differences, geographic
factors or environmental differences, or other population-based factors.

Sex

In childhood, allergic rhinitis is more common in boys than in girls, but in adulthood, the
prevalence is approximately equal between men and women.

Age

Onset of allergic rhinitis is common in childhood, adolescence, and early adult years, with a
mean age of onset 8-11 years, but allergic rhinitis may occur in persons of any age. In 80% of
cases, allergic rhinitis develops by age 20 years. [31] The prevalence of allergic rhinitis has been
reported to be as high as 40% in children, subsequently decreasing with age. [32, 33] In the geriatric
population, rhinitis is less commonly allergic in nature.

History
Obtaining a detailed history is important in the evaluation of allergic rhinitis. Important elements
include an evaluation of the nature, duration, and time course of symptoms; possible triggers for
symptoms; response to medications; comorbid conditions; family history of allergic diseases;
environmental exposures; occupational exposures; and effects on quality of life. A thorough
history may help identify specific triggers, suggesting an allergic etiology for the rhinitis.

Symptoms that can be associated with allergic rhinitis include sneezing, itching (of nose, eyes,
ears, palate), rhinorrhea, postnasal drip, congestion, anosmia, headache, earache, tearing, red
eyes, eye swelling, fatigue, drowsiness, and malaise. [1]
Symptoms and chronicity

Determine the age of onset of symptoms and whether symptoms have been present continuously
since onset. While the onset of allergic rhinitis can occur well into adulthood, most patients
develop symptoms by age 20 years. [31]

Determine the time pattern of symptoms and whether symptoms occur at a consistent level
throughout the year (ie, perennial rhinitis), only occur in specific seasons (ie, seasonal rhinitis),
or a combination of the two. Determine whether the symptoms are present all day or only at
specific times during the day. This information can help suggest the diagnosis and determine
possible triggers.

According to the Allergic Rhinits and its Impact on Asthma (ARIA) study, allergic rhinitis is
classified by frequency and severity of symptoms. A patient has intermittent allergic rhinitis if
symptoms occur less than 4 days a week or 4 weeks of the year. Persistent allergic rhinitis is
labeled if symptoms occur more than 4 days per week and more than 4 weeks of the year.
Symptoms are classified as mild when quality of life is not affected. Symptoms are moderate to
severe if patients have at least one of the following: sleep disturbance, impairment of daily
activities, sports, or leisure, impairment of school or work, or troublesome symptoms. [34]

Determine which organ systems are affected and the specific symptoms. Some patients have
exclusive involvement of the nose, while others have involvement of multiple organs. Some
patients primarily have sneezing, itching, tearing, and watery rhinorrhea (the classic hayfever
presentation), while others may only complain of congestion. Significant complaints of
congestion, particularly if unilateral, might suggest the possibility of structural obstruction, such
as a polyp, foreign body, or deviated septum.

Trigger factors

Determine whether symptoms are related temporally to specific trigger factors. This might
include exposure to pollens outdoors, mold spores while doing yard work, specific animals, or
dust while cleaning the house.

Irritant triggers such as smoke, pollution, and strong smells can aggravate symptoms in a patient
with allergic rhinitis. These are also common triggers of vasomotor rhinitis. Many patients have
both allergic rhinitis and vasomotor rhinitis.

Other patients may describe year-round symptoms that do not appear to be associated with
specific triggers. This could be consistent with nonallergic rhinitis, but perennial allergens, such
as dust mite or animal exposure, should also be considered in this situation. With chronic
exposure and chronic symptoms, the patient may not be able to associate symptoms with a
particular trigger.

Response to treatment
Response to treatment with antihistamines supports the diagnosis of allergic rhinitis, although
sneezing, itching, and rhinorrhea associated with nonallergic rhinitis can also improve with
antihistamines. [35]

Response to intranasal corticosteroids supports the diagnosis of allergic rhinitis, although some
cases of nonallergic rhinitis (particularly the nonallergic rhinitis with eosinophils syndrome
[NARES]) also improve with nasal steroids.

Comorbid conditions

Patients with allergic rhinitis may have other atopic conditions such as asthma [24, 25] or atopic
dermatitis. [27] Of patients with allergic rhinitis, 20% also have symptoms of asthma.
Uncontrolled allergic rhinitis may cause worsening of asthma [26] or even atopic dermatitis. [27]
Explore this possibility when obtaining the patient history.

Look for conditions that can occur as complications of allergic rhinitis. Sinusitis occurs quite
frequently. Other possible complications include otitis media, sleep disturbance or apnea, dental
problems (overbite), and palatal abnormalities. [36] The treatment plan might be different if one of
these complications is present. Nasal polyps occur in association with allergic rhinitis, although
whether allergic rhinitis actually causes polyps remains unclear. Polyps may not respond to
medical treatment and might predispose a patient to sinusitis or sleep disturbance (due to
congestion).

Allergic rhinitis is a risk factor for obstructive sleep apnea (OSA) syndrome. [37] Patients who
have allergic rhinitis have increased nighttime awakenings and daytime sleepiness. [38] Nasal
airway resistance is increased in those with allergic rhinitis and it is intesified in the supine
position compared to the upright position. [39]

Investigate past medical history, including other current medical conditions. Diseases such as
hypothyroidism or sarcoidosis can cause nonallergic rhinitis. Concomitant medical conditions
might influence the choice of medication.

A population-based, case-control study found a strong association between atopic diseases (AD)
and attention-deficit/hyperactivity disorder (ADHD) in children. The results of the study, which
included 4692 children with ADHD and 18,768 randomly selected controls, showed that children
with ADHD had a higher rate of allergic disease than controls, particularly allergic rhinitis and
allergic conjunctivitis. [40]

Family history

Because allergic rhinitis has a significant genetic component, [41] a positive family history for
atopy makes the diagnosis more likely.

In fact, a greater risk of allergic rhinitis exists if both parents are atopic than if one parent is
atopic. However, the cause of allergic rhinitis appears to be multifactorial, and a person with no
family history of allergic rhinitis can develop allergic rhinitis.
Environmental and occupational exposure

A thorough history of environmental exposures helps to identify specific allergic triggers. This
should include investigation of risk factors for exposure to perennial allergens (eg, dust mites,
mold, pets). [42, 43] Risk factors for dust mite exposure include carpeting, heat, humidity, and
bedding that does not have dust mite–proof covers. Chronic dampness in the home is a risk
factor for mold exposure. A history of hobbies and recreational activities helps determine risk
and a time pattern of pollen exposure.

Ask about the environment of the workplace or school. This might include exposure to ordinary
perennial allergens (eg, mites, mold, pet dander) or unique occupational allergens (eg, laboratory
animals, animal products, grains and organic materials, wood dust, latex, enzymes).

Effects on quality of life

An accurate assessment of the morbidity of allergic rhinitis cannot be obtained without asking
about the effects on the patient's quality of life. Specific validated questionnaires are available to
help determine effects on quality of life. [3, 4]

Determine the presence of symptoms such as fatigue, malaise, drowsiness (which may or may
not be related to medication), and headache.

Investigate sleep quality and ability to function at work.

Physical
The physical examination should focus on the nose, but examination of facial features, eyes,
ears, oropharynx, neck, lungs, and skin is also important. Look for physical findings that may be
consistent with a systemic disease that is associated with rhinitis.

General facial features

"Allergic shiners" are dark circles around the eyes and are related to vasodilation or nasal
congestion. [1, 44]

"Nasal crease" is a horizontal crease across the lower half of the bridge of the nose that is caused
by repeated upward rubbing of the tip of the nose by the palm of the hand (ie, the "allergic
salute"). [1, 44]

Nose

The nasal examination is best accomplished with a nasal speculum or an otoscope with nasal
adapter. In the specialist's office, a rigid or flexible rhinolaryngoscope may be used.
The mucosa of the nasal turbinates may be swollen (boggy) and have a pale, bluish-gray color.
Some patients may have predominant erythema of the mucosa, which can also be observed with
rhinitis medicamentosa, infection, or vasomotor rhinitis. While pale, boggy, blue-gray mucosa is
typical for allergic rhinitis, mucosal examination findings cannot definitively distinguish
between allergic and nonallergic causes of rhinitis.

Assess the character and quantity of nasal mucus. Thin and watery secretions are frequently
associated with allergic rhinitis, while thick and purulent secretions are usually associated with
sinusitis; however, thicker, purulent, colored mucus can also occur with allergic rhinitis.

Examine the nasal septum to look for any deviation or septal perforation, which may be present
due to chronic rhinitis, granulomatous disease, cocaine abuse, prior surgery, topical decongestant
abuse, or, rarely, topical steroid overuse.

Examine the nasal cavity for other masses such as polyps or tumors. Polyps are firm gray masses
that are often attached by a stalk, which may not be visible. After spraying a topical
decongestant, polyps do not shrink, while the surrounding nasal mucosa does shrink.

Ears, eyes, and oropharynx

Perform otoscopy to look for tympanic membrane retraction, air-fluid levels, or bubbles.
Performing pneumatic otoscopy can be considered to look for abnormal tympanic membrane
mobility. These findings can be associated with allergic rhinitis, particularly if eustachian tube
dysfunction or secondary otitis media is present.

Ocular examination may reveal findings of injection and swelling of the palpebral conjunctivae,
with excess tear production. Dennie-Morgan lines (prominent creases below the inferior eyelid)
are associated with allergic rhinitis. [45]

The term "cobblestoning" is used to describe streaks of lymphoid tissue on the posterior pharynx,
which is commonly observed with allergic rhinitis. Tonsillar hypertrophy can also be observed.
Malocclusion (overbite) and a high-arched palate can be observed in patients who breathe from
their mouths excessively. [46]

Neck

Look for evidence of lymphadenopathy or thyroid disease.

Lungs

Look for the characteristic findings of asthma.

Skin

Evaluate for possible atopic dermatitis.

Other

Look for any evidence of systemic diseases that may cause rhinitis (eg, sarcoidosis,
hypothyroidism, immunodeficiency, ciliary dyskinesia syndrome, other connective tissue
diseases).

Causes
The causes of allergic rhinitis may differ depending on whether the symptoms are seasonal,
perennial, or sporadic/episodic. Some patients are sensitive to multiple allergens and can have
perennial allergic rhinitis with seasonal exacerbations. While food allergy can cause rhinitis,
particularly in children, it is rarely a cause of allergic rhinitis in the absence of gastrointestinal or
skin symptoms.

Seasonal allergic rhinitis is commonly caused by allergy to seasonal pollens and outdoor molds.

Pollens (tree, grass, and weed)

Tree pollens, which vary by geographic location, are typically present in high counts during the
spring, although some species produce their pollens in the fall. Common tree families associated
with allergic rhinitis include birch, oak, maple, cedar, olive, and elm.

Grass pollens also vary by geographic location. Most of the common grass species are associated
with allergic rhinitis, including Kentucky bluegrass, orchard, redtop, timothy, vernal, meadow
fescue, Bermuda, and perennial rye. A number of these grasses are cross-reactive, meaning that
they have similar antigenic structures (ie, proteins recognized by specific IgE in allergic
sensitization). Consequently, a person who is allergic to one species is also likely to be sensitive
to a number of other species. The grass pollens are most prominent from the late spring through
the fall but can be present year-round in warmer climates.

Weed pollens also vary geographically. Many of the weeds, such as short ragweed, which is a
common cause of allergic rhinitis in much of the United States, are most prominent in the late
summer and fall. Other weed pollens are present year-round, particularly in warmer climates.
Common weeds associated with allergic rhinitis include short ragweed, western ragweed,
pigweed, sage, mugwort, yellow dock, sheep sorrel, English plantain, lamb's quarters, and
Russian thistle.

Outdoor molds

Atmospheric conditions can affect the growth and dispersion of a number of molds; therefore,
their airborne prevalence may vary depending on climate and season.

For example, Alternaria and Cladosporium are particularly prevalent in the dry and windy
conditions of the Great Plains states, where they grow on grasses and grains. Their dispersion
often peaks on sunny afternoons. They are virtually absent when snow is on the ground in winter,
and they peak in the summer months and early fall.

Aspergillus and Penicillium can be found both outdoors and indoors (particularly in humid
households), with variable growth depending on the season or climate. Their spores can also be
dispersed in dry conditions.

Perennial allergic rhinitis is typically caused by allergens within the home but can also be caused
by outdoor allergens that are present year-round. [47] In warmer climates, grass pollens can be
present throughout the year. In some climates, individuals may be symptomatic due to trees and
grasses in the warmer months and molds and weeds in the winter.

House dust mites

In the United States, 2 major house dust mite species are associated with allergic rhinitis. These
are Dermatophagoides farinae and Dermatophagoides pteronyssinus. [42]

These mites feed on organic material in households, particularly the skin that is shed from
humans and pets. They can be found in carpets, upholstered furniture, pillows, mattresses,
comforters, and stuffed toys.

While they thrive in warmer temperatures and high humidity, they can be found year-round in
many households. On the other hand, dust mites are rare in arid climates.

Pets

Allergy to indoor pets is a common cause of perennial allergic rhinitis. [42, 43]

Cat and dog allergies are encountered most commonly in allergy practice, although allergy has
been reported to occur with most of the furry animals and birds that are kept as indoor pets.

Cockroaches

While cockroach allergy is most frequently considered a cause of asthma, particularly in the
inner city, it can also cause perennial allergic rhinitis in infested households. [48, 49]

Rodents

Rodent infestation may be associated with allergic sensitization. [50, 51, 52]

Sporadic allergic rhinitis causes

Sporadic allergic rhinitis, intermittent brief episodes of allergic rhinitis, is caused by intermittent
exposure to an allergen. Often, this is due to pets or animals to which a person is not usually
exposed. Sporadic allergic rhinitis can also be due to pollens, molds, or indoor allergens to which
a person is not usually exposed. While allergy to specific foods can cause rhinitis, an individual
affected by food allergy also usually has some combination of gastrointestinal, skin, and lung
involvement. In this situation, the history findings usually suggest an association with a
particular food. Watery rhinorrhea occurring shortly after eating may be vasomotor (and not
allergic) in nature, mediated via the vagus nerve. This often is called gustatory rhinitis.

Occupational allergic rhinitis

Occupational allergic rhinitis, which is caused by exposure to allergens in the workplace, can be
sporadic, seasonal, or perennial. People who work near animals (eg, veterinarians, laboratory
researchers, farm workers) might have episodic symptoms when exposed to certain animals,
daily symptoms while at the workplace, or even continual symptoms (which can persist in the
evenings and weekends with severe sensitivity due to persistent late-phase inflammation). Some
workers who may have seasonal symptoms include farmers, agricultural workers (exposure to
pollens, animals, mold spores, and grains), and other outdoor workers. Other significant
occupational allergens that may cause allergic rhinitis include wood dust, latex (due to inhalation
of powder from gloves), acid anhydrides, glues, and psyllium (eg, nursing home workers who
administer it as medication).

Diagnostic Considerations
Vasomotor rhinitis or nonallergic rhinitis

Gustatory rhinitis (vagally mediated)

Rhinitis medicamentosa (eg, due to topical decongestants, antihypertensives, cocaine abuse)

Hormonal rhinitis (eg, related to pregnancy, hypothyroidism, oral contraceptive use)

Anatomic rhinitis (eg, deviated septum, choanal atresia, adenoid hypertrophy, foreign body,
nasal tumor)

NARES

Immotile cilia syndrome (ciliary dyskinesis)

Cerebrospinal fluid leak

Nasal polyps

Granulomatous rhinitis (eg, Wegener granulomatosis, sarcoidosis)

Differential Diagnoses
 Acute Sinusitis
 Chronic Sinusitis
Laboratory Studies
Testing for reaction to specific allergens can be helpful to confirm the diagnosis of allergic
rhinitis and to determine specific allergic triggers. If specific allergic triggers are known, then
appropriate avoidance measures can be recommended. It is essential to know which allergens a
patient is sensitive to in order to perform allergen immunotherapy (desensitization treatment). To
an extent, allergy testing provides knowledge of the degree of sensitivity to a particular allergen.
The most commonly used methods of determining allergy to a particular substance are allergy
skin testing (testing for immediate hypersensitivity reactions) and in vitro diagnostic tests, such
as the fluorescence enzyme immunoassay (FEIA), for example ImmunoCAP, which indirectly
measures the quantity of specific IgE to a particular antigen.

Allergy skin tests (immediate hypersensitivity testing) are an in vivo method of determining
immediate (IgE-mediated) hypersensitivity to specific allergens. Sensitivity to virtually all of the
allergens that cause allergic rhinitis (see Causes) can be determined with skin testing.

By introducing an extract of a suspected allergen percutaneously, an immediate (early-phase)

wheal-and-flare reaction can be produced. Percutaneous introduction can be accomplished by
placing a drop of extract on the skin and scratching or pricking a needle through the epidermis
under the drop. Depending on the exact technique used, this testing is referred to as scratch,
prick, or puncture testing.

The antigen in the extract binds to IgE on skin mast cells, leading to the early-phase (immediate-
type) reaction, which results in the release of mediators such as histamine (see Pathophysiology).
This generally occurs within 15-20 minutes. The released histamine causes the wheal-and-flare
reaction (A central wheal is produced by infiltrating fluid, and surrounding erythema is produced
due to vasodilation, with concomitant itching.). The size of the wheal-and-flare reaction roughly
correlates with the degree of sensitivity to the allergen.

The extract can also be introduced intradermally (ie, injected into the dermis with an intradermal
[TB] needle). With this technique, the extract is allowed to contact the underlying dermal tissues,
including skin mast cells. Intradermal testing is approximately 1000-fold more sensitive than
percutaneous testing. This should be performed with care by qualified specialists. The rate of
false-positive results may be high.

In vitro allergy tests, ie, FEIA, allow measurement of the amount of specific IgE to individual
allergens in a sample of blood. The amount of specific IgE produced to a particular allergen
approximately correlates with the allergic sensitivity to that substance. These tests allow
determination of specific IgE to a number of different allergens from one blood sample, but the
sensitivity and specificity are not always as good as accurate skin testing (depending on the
laboratory and assay used for the FEIA). As with skin testing, virtually all of the allergens that
cause allergic rhinitis (see Causes) can be determined using the in vitro specific IgE, although
testing for some allergens is less well established compared to others.

Testing every patient for sensitivity to every allergen known is not practical. Therefore, select a
limited number of allergens for testing (this applies to both skin testing and in vitro specific IgE).
When selecting allergens, select from among the allergens that are present locally and are known
to cause clinically significant allergic disease. A clinician who is specifically trained in allergy
testing should select allergens for testing.

Total serum IgE

This is a measurement of the total level of IgE in the blood (regardless of specificity). While
patients with allergic rhinitis are more likely to have an elevated total IgE level than the normal
population, this test is neither sensitive nor specific for allergic rhinitis. As many as 50% of
patients with allergic rhinitis have normal levels of total IgE, while 20% of nonaffected
individuals can have elevated total IgE levels. Therefore, this test is generally not used alone to
establish the diagnosis of allergic rhinitis, but the results can be helpful in some cases when
combined with other factors.

Total blood eosinophil count

As with the total serum IgE, an elevated eosinophil count supports the diagnosis of allergic
rhinitis, but it is neither sensitive nor specific for the diagnosis. The results can sometimes be
helpful when combined with other factors.

Signs and Symptoms

History

Signs and symptoms of allergic rhinitis include the following:

 Sneezing
 Itching: Nose, eyes, ears, palate
 Rhinorrhea
 Postnasal drip
 Congestion
 Anosmia
 Headache
 Earache
 Tearing
 Red eyes
 Eye swelling
 Fatigue
 Drowsiness
 Malaise

Complications of this allergic rhinitis include the following:

 Acute or chronic sinusitis

  Otitis media
 Sleep disturbance or apnea
 Dental problems (overbite): Caused by excessive breathing through the mouth
 Palatal abnormalities
 Eustachian tube dysfunction

Physical examination

Nasal features of allergic rhinitis can include the following:

 Nasal crease: A horizontal crease across the lower half of the bridge of the nose; caused
by repeated upward rubbing of the tip of the nose by the palm of the hand
 Thin, watery nasal secretions
 Deviation or perforation of the nasal septum: May be associated with chronic rhinitis,
although there can be other, unrelated causes

Manifestations of allergic rhinitis affecting the ears, eyes, and oropharynx include the following:

 Ears: Retraction and abnormal flexibility of the tympanic membrane

 Eyes: Injection and swelling of the palpebral conjunctivae, with excess tear production;
Dennie-Morgan lines (prominent creases below the inferior eyelid); and dark circles
around the eyes (“allergic shiners”), which are related to vasodilation or nasal congestion
 Oropharynx: "Cobblestoning," that is, streaks of lymphoid tissue on the posterior
pharynx; tonsillar hypertrophy; and malocclusion (overbite) and a high-arched palate

See Clinical Presentation for more detail.

Diagnosis

Laboratory tests used in the diagnosis of allergic rhinitis include the following:

 Allergy skin tests (immediate hypersensitivity testing): An in vivo method of determining

immediate (IgE-mediated) hypersensitivity to specific allergens
 Fluorescence enzyme immunoassay (FEIA): Indirectly measures the quantity of
immunoglobulin E (IgE) serving as an antibody to a particular antigen
 Total serum IgE: Neither sensitive nor specific for allergic rhinitis, but the results can be
helpful in some cases when combined with other factors
 Total blood eosinophil count: Neither sensitive nor specific for the diagnosis, but, as with
total serum IgE, can sometimes be helpful when combined with other factors

Imaging studies used in the diagnosis and evaluation of allergic rhinitis include the following:

 Radiography: Can be helpful for evaluating possible structural abnormalities or to help

detect complications or comorbid conditions, such as sinusitis or adenoid hypertrophy
 Computed tomography scanning: Can be very helpful for evaluating acute or chronic
sinusitis
  Magnetic resonance imaging: Also can be helpful for evaluating sinusitis

See Workup for more detail.

Management

The management of allergic rhinitis consists of the following 3 major treatment strategies:

 Environmental control measures and allergen avoidance: These include keeping exposure
to allergens such as pollen, dust mites, and mold to a minimum
 Pharmacologic management: Patients are often successfully treated with oral
antihistamines, decongestants, or both; regular use of an intranasal steroid spray may be
more appropriate for patients with chronic symptoms
 Immunotherapy: This treatment may be considered more strongly with severe disease,
poor response to other management options, and the presence of comorbid conditions or
complications; immunotherapy is often combined with pharmacotherapy and
environmental control

See Treatment and Medication for more detail.