What Physical Exam Findings Would You Look For In A Patient With Allergies

Allergic rhinitis is a common disorder that is strongly linked to asthma and conjunctivitis. It is usually a long-standing condition that often goes undetected in the primary-care setting. The classic symptoms of the disorder are nasal congestion, nasal itch, rhinorrhea and sneezing. A thorough history, physical examination and allergen skin testing are important for establishing the diagnosis of allergic rhinitis. Second-generation oral antihistamines and intranasal corticosteroids are the mainstay of treatment. Allergen immunotherapy is an effective immune-modulating treatment that should be recommended if pharmacologic therapy for allergic rhinitis is not effective or is not tolerated, or if chosen by the patient. This article provides an overview of the pathophysiology, diagnosis, and appropriate management of this disorder.

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Rhinitis is broadly defined as inflammation of the nasal mucosa. It is a common disorder that affects up to 40% of the population <1>. Allergic rhinitis is the most common type of chronic rhinitis, affecting 10–20% of the population, and evidence suggests that the prevalence of the disorder is increasing <2>. Severe allergic rhinitis has been associated with significant impairments in quality of life, sleep and work performance <2>.

In the past, allergic rhinitis was considered to be a disorder localized to the nose and nasal passages, but current evidence indicates that it may represent a component of a systemic airway disease involving the entire respiratory tract. There are a number of physiological, functional and immunological relationships between the upper (nose, nasal cavity, paranasal sinuses, Eustachian tube, pharynx and larynx) and lower (trachea, bronchial tubes, bronchioles and lungs) respiratory tracts. For example, both tracts contain a ciliated epithelium consisting of goblet cells that secrete mucous, which serves to filter the incoming air and protect structures within the airways. Furthermore, the submucosa of both the upper and lower airways includes a collection of blood vessels, mucous glands, supporting cells, nerves and inflammatory cells. Evidence has shown that allergen provocation of the upper airways not only leads to a local inflammatory response, but may also lead to inflammatory processes in the lower airways, and this is supported by the fact that rhinitis and asthma frequently coexist. Therefore, allergic rhinitis and asthma appear to represent a combined airway inflammatory disease, and this needs to be considered to ensure the optimal assessment and management of patients with allergic rhinitis <1, 3>.

Comprehensive and widely-accepted Canadian guidelines for the diagnosis and treatment of allergic rhinitis were published in 2007 <1>. This article provides an overview and update of the recommendations provided in these guidelines as well as a review of current literature related to the pathophysiology, diagnosis, and appropriate management of allergic rhinitis.

In allergic rhinitis, numerous inflammatory cells, including mast cells, CD4-positive T cells, B cells, macrophages, and eosinophils, infiltrate the nasal lining upon exposure to an inciting allergen (most commonly airborne dust mite fecal particles, cockroach residues, animal dander, moulds, and pollens). In allergic individuals, the T cells infiltrating the nasal mucosa are predominantly T helper 2 (Th2) in nature and release cytokines (e.g., interleukin -3, IL-4, IL-5, and IL-13) that promote immunoglobulin E (IgE) production by plasma cells. Crosslinking of IgE bound to mast cells by allergens, in turn, triggers the release of mediators, such as histamine and leukotrienes, that are responsible for arteriolar dilation, increased vascular permeability, itching, rhinorrhea, mucous secretion, and smooth muscle contraction in the lung <1, 2>. The mediators and cytokines released during the early phase of an immune response to an inciting allergen trigger a further cellular inflammatory response over the next 4–8 h (late-phase inflammatory response) which results in recurrent symptoms (usually nasal congestion) that often persist <1, 4>.

Rhinitis is classified into one of the following categories according to etiology: IgE-mediated (allergic), autonomic, infectious and idiopathic (unknown). Although the focus of this article is allergic rhinitis, a brief description of the other forms of rhinitis is provided in Table 1.

Traditionally, allergic rhinitis has been categorized as seasonal (occurs during a specific season) or perennial (occurs throughout the year). However, not all patients fit into this classification scheme. For example, some allergic triggers, such as pollen, may be seasonal in cooler climates, but perennial in warmer climates, and patients with multiple “seasonal” allergies may have symptoms throughout most of the year <4>. Therefore, allergic rhinitis is now classified according to symptom duration (intermittent or persistent) and severity (mild, moderate or severe) (see Fig. 1) <1, 5>. The Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines have classified “intermittent” allergic rhinitis as symptoms that are present less than 4 days per week or for less than 4 consecutive weeks, and “persistent” allergic rhinitis as symptoms that are present more than 4 days/week and for more than 4 consecutive weeks <5>. Symptoms are classified as mild when patients have no impairment in sleep and are able to perform normal activities (including work or school). Symptoms are categorized as moderate/severe if they significantly affect sleep or activities of daily living, and/or if they are considered bothersome. It is important to classify the severity and duration of symptoms as this will guide the management approach for individual patients <1>.


Adapted from Small et al. <1>, Bousquet et al. <5>

In recent years, two additional types of rhinitis have been classified that deserve some mention here—occupational rhinitis and local allergic rhinitis.

Occupational rhinitis

Occupational rhinitis is defined as an inflammatory disease of the nose characterized by intermittent or persistent symptoms that include airflow limitation, hypersecretion, sneezing and pruritus that are attributable to a particular work environment and not to stimuli encountered outside the workplace <6>. Although the overall prevalence of occupational rhinitis is unknown, high-risk professions include laboratory or food-processing workers, veterinarians, farmers and workers in various manufacturing industries <6,7,8>. Occupational rhinitis usually develops within the first 2 years of employment. The condition may be IgE-mediated due to allergen sensitization, or due to exposure to respiratory irritants. Symptoms may develop immediately or several hours after exposure to the inciting stimuli. Often there are associated ocular and pulmonary symptoms. An evaluation of the patient suspected of having occupational rhinitis should include the usual history and physical examination (discussed later), as well as a site visit and skin testing or in vitro testing to inhalants. Treatment primarily involves avoiding exposure to the causative agent and pharmacotherapy as needed. There is little evidence to suggest that occupational rhinitis will progress to occupational asthma with ongoing exposure <6, 8>, although this is possible. Therefore, patients are generally not advised to leave their jobs if exposure cannot be eliminated but symptoms are adequately controlled.

Local allergic rhinitis

Local allergic rhinitis (LAR) is a clinical entity characterized by a localized allergic response in the nasal mucosa in the absence of evidence of systemic atopy <9,10,11>. By definition, patients with LAR have negative skin tests and/or in vitro tests for IgE, but have evidence of local IgE production in the nasal mucosa; these patients also react to nasal challenges with specific allergens <12>.

The symptoms of LAR are similar to those provoked in patients with allergic rhinitis, and the assumption is that LAR is an IgE-mediated disease based on both clinical findings and the detection of specific IgE in the nasal mucosa. To date, there is no evidence to suggest that LAR is a precursor to allergic rhinitis since follow-up does not show the evolution to typical allergic rhinitis in these patients <13>; however, patient follow-up may not have been long enough to detect this disease evolution. The implications for treatment of LAR are not well understood at this time, although some evidence suggests that allergen immunotherapy may be effective in this type of rhinitis <9, 11>.

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Allergic rhinitis is usually a long-standing condition that often goes undetected in the primary-care setting. Patients suffering from the disorder often fail to recognize the impact of the disorder on quality of life and functioning and, therefore, do not frequently seek medical attention. In addition, physicians fail to regularly question patients about the disorder during routine visits <1, 14>. Therefore, screening for rhinitis is recommended, particularly in asthmatic patients since studies have shown that rhinitis is present in up to 95% of patients with asthma <15,16,17,18>.

A thorough history and physical examination are the cornerstones of establishing the diagnosis of allergic rhinitis (see Table 2). Allergy testing is also important for confirming that underlying allergies cause the rhinitis <1>. Referral to an allergist should be considered if the diagnosis of allergic rhinitis is in question.


During the history, patients will often describe the following classic symptoms of allergic rhinitis: nasal congestion, nasal itch, rhinorrhea and sneezing. Allergic conjunctivitis (inflammation of the membrane covering the white part of the eye) is also frequently associated with allergic rhinitis and symptoms generally include redness, tearing and itching of the eyes <1>.

An evaluation of the patient’s home and work/school environments is recommended to determine potential triggers of allergic rhinitis. The environmental history should focus on common and potentially relevant allergens including pollens, furred animals, textile flooring/upholstery, tobacco smoke, humidity levels at home, as well as other potential noxious substances that the patient may be exposed to at work or at home. The use of certain medications (e.g., beta-blockers, acetylsalicylic acid , non-steroidal anti-inflammatory drugs , angiotensin-converting enzyme inhibitors, and hormone therapy) as well as the recreational use of cocaine can lead to symptoms of rhinitis and, therefore, patients should be asked about current or recent medication and drug use <1>.

The history should also include patient questioning regarding a family history of atopic disease, the impact of symptoms on quality of life and the presence of comorbidities such as asthma, mouth breathing, snoring, sleep apnea, sinus involvement, otitis media (inflammation of the middle ear), or nasal polyps. Patients may attribute persistent nasal symptoms to a “constant cold” and, therefore, it is also important to document the frequency and duration of “colds” <1>.

Before seeking medical attention, patients often attempt using over-the-counter or other medications to manage their symptoms. Assessing patient response to such treatments may provide information that can aid in the diagnosis and subsequent management of allergic rhinitis. For example, symptom improvement with newer, second-generation antihistamines (e.g., desloratadine , fexofenadine , loratadine , cetirizine ) is strongly suggestive of an allergic etiology. However, it is important to note that response to first-generation antihistamines (e.g., brompheniramine maleate , chlorpheniramine maleate , clemastine ) does not imply an allergic etiology since the anticholinergic and sedative properties of these agents reduce rhinorrhea and may improve sleep quality regardless of whether the inflammation is allergic. Previous response to intranasal corticosteroids may also be suggestive of an allergic etiology, and likely indicates that such treatment will continue to be beneficial in the future <1>.

Important elements of the history for patients with suspected allergic rhinitis are summarized in Table 2.

Physical examination

The physical examination of patients with suspected allergic rhinitis should include an assessment of outward signs, the nose, ears, sinuses, posterior oropharynx (area of the throat that is at the back of the mouth), chest and skin (see Table 2). Outward signs that may be suggestive of allergic rhinitis include: persistent mouth breathing, rubbing at the nose or an obvious transverse nasal crease, frequent sniffling or throat clearing, and allergic shiners (dark circles under the eyes that are due to nasal congestion). Examination of the nose typically reveals swelling of the nasal mucosa and pale, thin secretions. An internal endoscopic examination of the nose should also be considered to assess for structural abnormalities including septal deviation, nasal ulcerations, and nasal polyps <1>.

The ears generally appear normal in patients with allergic rhinitis; however, assessment for Eustachian tube dysfunction using a pneumatic otoscope should be considered. Valsalva’s maneuver (increasing the pressure in the nasal cavity by attempting to blow out the nose while holding it shut) can also be used to assess for fluid behind the ear drum <1>.

The sinus examination should include palpation of the sinuses for evidence of tenderness or tapping of the maxillary teeth with a tongue depressor for evidence of sensitivity. The posterior oropharynx should also be examined for signs of post nasal drip (mucous accumulation in the back of the nose and throat), and the chest and skin should be examined carefully for signs of concurrent asthma (e.g., wheezing) or dermatitis <1>.

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Diagnostic tests

Although a thorough history and physical examination are required to establish the clinical diagnosis of rhinitis, further diagnostic testing is necessary to confirm that underlying allergies cause the rhinitis. Skin-prick testing is considered the primary method for identifying specific allergic triggers of rhinitis. Skin prick testing involves placing a drop of a commercial extract of a specific allergen on the skin of the forearms or back, then pricking the skin through the drop to introduce the extract into the epidermis. Within 15–20 min, a wheal-and-flare response (an irregular blanched wheal surrounded by an area of redness) will occur if the test is positive. Testing is typically performed using the allergens relevant to the patient’s environment (e.g., pollen, animal dander, moulds and house dust mites). A reasonable alternative to skin prick testing is the use of allergen-specific IgE tests (e.g., performed by immunosorbent assay—previously performed by radioallergosorbent tests ) that provide an in vitro measure of a patient’s specific IgE levels against particular allergens. These in vitro tests can be performed when eczema is extensive, or if the patient cannot stop antihistamine therapy to allow for testing. However, skin prick tests are generally considered to be more sensitive and cost effective than allergen-specific serum IgE tests, and have the further advantage of providing physicians and patients with immediate results <1, 14>.


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