Epidemiology and Etiology
- Infectious rhinitis (“common cold” or upper respiratory infection [URI]):
- Most common form
- Common in children. Estimated incidence: 6 episodes per patient per year
- Approximately 8% of URIs are complicated by rhinosinusitis in children aged 6–35 months
- Genetic disorders, such as Kartagener syndrome (with immobile cilia) impair mucosal ciliary movement and predispose individuals to recurrent rhinosinusitis episodes
- Allergic rhinitis:
- Most common type of rhinitis
- Occurs in approximately 10%–30% of adults and up to 40% of children annually in the United States
- Increased risk in individuals with atopy, including eczema or asthma
- Non-allergic rhinitis:
- Affects up to approximately 7% of the population in the United States
- Occurs later in life than allergic rhinitis
- 70% of patients present > 20 years of age; more common in females
|Usually caused by a viral or bacterial infection||Type I hypersensitivity reaction||An increase in blood flow to the nasal mucosa due to irritants, but not allergens|
- Viruses typically use intercellular adhesion molecule-1 host receptor to enter into nasal epithelial cells.
- Signaling within cells occurs via NF-kB leading to the elaboration of pro-inflammatory cytokines, which leads to:
- Plasma exudation from submucosal capillaries
- Recruitment of polymorphonuclear cells to nasal epithelium via interleukin-8
- Local production of cytokines and kinins results in the classic symptoms of infectious rhinitis/the common cold.
Type I hypersensitivity reaction triggers inflammation in the nose, which is immunoglobulin E (IgE)-mediated.
- After initial exposure to an allergen in atopic individuals, IgE antibodies bind to IgE receptors on mast cells throughout the respiratory mucosa and to basophils in the peripheral blood.
- B cells then differentiate into plasma cells and produce IgE antibodies specific to the antigen.
- When the same allergen is inhaled, IgE antibodies are bridged by the allergen’s antigen.
- Mast cells and basophils are activated → release of histamine, leukotrienes, and kinins + inflammatory infiltrates with eosinophils → sneezing, rhinorrhea, and congestion (symptoms of allergic rhinitis)
- No single unifying pathogenesis theory
- Hormonal or autonomic stimuli produce a decrease in sympathetic activity and/or an increase in parasympathetic activity.
- Sympathetic stimulation causes vasoconstriction of the nasal blood vessels (so decreased activity causes reduced vasoconstriction when needed).
- Parasympathetic stimulation causes vasodilatation of the nasal blood vessels and increased mucous secretions (so increased activity causes an over-response).
- Other abnormal responses to neurogenic stimuli include increased concentrations of vasoactive intestinal peptide (potent vasodilator) and substance P (pain reception).
- Rhinitis medicamentosa: rebound phenomenon after excessive use of decongestant nasal drops, usually seen after 3 consecutive days of use
- Drug-induced rhinitis: caused by antihypertensives and NSAIDs
- Pregnancy rhinitis: persistent edema of the nasal mucosa and even airway obstruction may be caused by hormonal changes during pregnancy.
- Honeymoon rhinitis: occurs following intense sexual excitement
- Gustatory rhinitis: associated with spicy food and/or alcohol, which stimulates the palatine sensory receptors and produces a cholinergic response
- Non-air flow rhinitis: associated with choanal atresia and tracheostomy
General symptoms of rhinitis include:
- Nasal congestion: Can increase sinus pressure, which leads to headaches
- Rhinorrhoea: The color of the nasal secretion may vary (clear, yellow, or green) in infectious rhinitis.
- Post-nasal drip
- Itching (usually of the nose, eyes, and/or throat)
- Conjunctival symptoms:
- Bilateral watery eyes
- Conjunctival injection
- Itching or burning
- Sensation of a foreign object
- Snorting, sniffing, coughing, clearing throat, palatal click
- Other constitutional symptoms may be seen, such as fever, malaise, chills, irritability, etc.
- Physical findings (see descriptions in Diagnosis):
- Allergic shiners
- Allergic facies
- Allergic salute
- Dennie-Morgan lines
Specific symptoms for the individual categories of rhinitis include the following:
- Infectious rhinitis is more likely to lead to complications:
- Otitis media
- Secondary bacterial pneumonia
- Allergic rhinitis presents in recurrent episodes easily linked to a specific allergen. Associated conditions include:
- Allergic conjunctivitis
- Atopic dermatitis
- Bronchial asthma
- Non-allergic rhinitis is characterized by the chronic presence of nasal congestion, rhinorrhea, and postnasal drainage. It is distinguished via:
- Its late onset
- Absence of sneezing and facial itching
- Congestion and drainage (prominent symptoms)
- Perennial symptomatology
Diagnosis is clinical, based on characteristic symptoms, suggestive clinical history, and supportive physical exam findings.
- Characteristic symptoms: sneezing, rhinorrhea, nasal itching and congestion, postnasal drip, cough, fatigue, etc.
- Suggestive clinical history (depending on the form of rhinitis):
- Pattern of episodes
- Seasonal variation of symptoms
- History of medication
- Presence of co-existing conditions
- Occupational exposures
- Environmental history
- Identification of precipitating factors
- Physical exam findings:
- Allergic shiners: infraorbital edema and darkening
- Dennie-Morgan lines: lines or folds below the lower lids
- Allergic salute: transverse nasal crease caused by rubbing of the nose
- Allergic facies: open mouth due to mouth breathing with highly arched palate and dental malocclusion
- Pale nasal mucosa that is sensitive to touch
- Edematous nasal turbinates
- Clear rhinorrhea
- Retracted tympanic membranes with serous fluid build-up
- Potential surgically correctable conditions:
- Deviated nasal septum
- Enlarged turbinates
- Allergen skin test, in-vitro testing, or radioallergosorbent test (RAST) is useful in detecting allergic rhinitis but not necessary for making a diagnosis. RAST measures serum concentrations of IgE antibodies against a specific allergen.
- Routine laboratory findings are typically normal and not indicated in diagnosis.
- The mainstay of treatment is symptomatic and supportive, as most cases of infectious rhinitis are of viral etiology, which is self-limiting and resolves spontaneously and steadily within a few days.
- Some patients may require antibiotics for laboratory-documented bacterial pharyngitis.
- Treat rhinitis due to group A beta-hemolytic streptococci with PO penicillin or amoxicillin for 10 days (cephalexin if penicillin is known to cause rash; clindamycin or macrolide if penicillin is known to cause anaphylaxis).
- Timely treatment is crucial for the prevention of acute rheumatic fever.
- Other underlying causes of rhinitis need to be identified and treated (e.g., retroviral therapy for HIV, penicillin for group A streptococcus, nystatin for candida).
- Avoidance of causative allergens (e.g., pollen, dust, animal fur)
- First-line options that may be used orally or as intranasal sprays:
- Antihistamines (e.g., fexofenadine, diphenhydramine, desloratadine, cetirizine, loratadine, azelastine)
- Decongestants or sympathomimetics (e.g., pseudoephedrine, phenylephrine)
- Corticosteroids (e.g., budesonide, fluticasone)
- Anticholinergics (e.g., ipratropium bromide)
- Mast cell stabilizers (e.g., cromolyn sodium nasal spray)
- Second-line options:
- Leukotriene receptor antagonists (e.g., montelukast)
- Immunotherapy (e.g., controlled exposure to gradually increasing doses of the allergen to downregulate the IgE response)
- Resection of hypertrophic nasal turbinates or polyps
- Nasal saline irrigation
- Correct the underlying cause (e.g., discontinue medication, correct choanal atresia, avoid consumption of spicy food and other triggers).
- First-line medical options:
- Topical antihistamines (e.g., azelastine)
- Topical intranasal glucocorticoids (e.g., fluticasone)
- Second-line medical options:
- Combination of topical antihistamines and topical intranasal glucocorticoids
- Decongestants or sympathomimetics (e.g., pseudoephedrine)
- Nasal lavage with hypertonic NaCl solution
- Resection of hypertrophic nasal turbinates or polyps
- Nasal polyps: benign lesions of the nasal mucosa or paranasal sinuses due to chronic mucosal inflammation that present with postnasal drip, bilateral nasal obstruction, and impaired olfactory function
- Foreign nasal body: common in children < 5 years old. Often involves food items or small toys. Presents with unilateral rhinorrhea that can become foul-smelling or purulent, signs of nasal obstruction, or epistaxis.
- Deviated nasal septum: a deviation of the nasal septum from the midline that can lead to unilateral dyspnea, nasal congestion, and snoring
- Adenoid hypertrophy: enlargement of the pharyngeal tonsils. Common among children. Presents with mouth breathing, mucopurulent nasal discharge, snoring, and/or impaired hearing.