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Allergic Rhinitis Clinical Presentation

  • Author: Javed Sheikh, MD; Chief Editor: Michael A Kaliner, MD  more...
 
Updated: Feb 16, 2015
 

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.[2]

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.[30]

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. During periods of exacerbation, determine whether symptoms occur on a daily basis or only on an episodic basis. 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.

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.[31]

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[23, 24] or atopic dermatitis.[26] Of patients with allergic rhinitis, 20% also have symptoms of asthma. Uncontrolled allergic rhinitis may cause worsening of asthma[25] or even atopic dermatitis.[26] 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.[32] 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).

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 AD than controls, particularly allergic rhinitis and allergic conjunctivitis.[33]

Family history

Because allergic rhinitis has a significant genetic component,[34] 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).[35, 36] 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.

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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.[2, 37]

"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").[2, 37]

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.[38]

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.[39]

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).

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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.[40] 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.[35]

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.[35, 36]

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.[41, 42]

Rodents

Rodent infestation may be associated with allergic sensitization.[43, 44, 45]

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).

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Contributor Information and Disclosures
Author

Javed Sheikh, MD Assistant Professor of Medicine, Harvard Medical School; Clinical Director, Division of Allergy and Inflammation, Clinical Director, Center for Eosinophilic Disorders, Beth Israel Deaconess Medical Center

Javed Sheikh, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Allergy, Asthma and Immunology

Disclosure: Received grant/research funds from Genentech for other.

Coauthor(s)

Umer Najib, MD Clinical Research Fellow, Department of Medicine, Division of Allergy and Inflammation, Beth Israel Deaconess Medical Center

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Stephen C Dreskin, MD, PhD Professor of Medicine, Departments of Internal Medicine, Director of Allergy, Asthma, and Immunology Practice, University of Colorado Health Sciences Center

Stephen C Dreskin, MD, PhD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Association for the Advancement of Science, American College of Allergy, Asthma and Immunology, Clinical Immunology Society, Joint Council of Allergy, Asthma and Immunology, American Association of Immunologists

Disclosure: Received consulting fee from Genentech for consulting; Received grant support from NIH for research; Received consulting fee from Clinical Immunization and Safety Assessment (CISA) Network (administered by Vanderbilt University) for consulting; Received consulting fee from o Member, Medical Expert Panel, Division of Vaccine Injury Compensation (DVIC), Department of Health and Human Services. for med legal reviews; Received consulting fee from o Member, Medical Expert Panel, Vaccine Review, Pfize.

Chief Editor

Michael A Kaliner, MD Clinical Professor of Medicine, George Washington University School of Medicine; Medical Director, Institute for Asthma and Allergy

Michael A Kaliner, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Association of Immunologists, American College of Allergy, Asthma and Immunology, American Society for Clinical Investigation, American Thoracic Society, Association of American Physicians

Disclosure: Nothing to disclose.

Additional Contributors

William F Schoenwetter, MD Consultant in Allergic Diseases, Brainerd Medical Center, Brainerd, Minnesota

William F Schoenwetter, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Allergy, Asthma and Immunology, American College of Physicians, American Medical Association, Joint Council of Allergy, Asthma and Immunology, Minnesota Medical Association

Disclosure: Nothing to disclose.

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