Rhinitis

Epidemiology and Etiology

Epidemiology

• 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

Etiology

Pathophysiology

Infectious rhinitis

• 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.

Allergic rhinitis

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)

Non-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).
• Subtypes:
  • 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

Clinical Presentation

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.
• Sneezing
• 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:
  • Sinusitis
  • Otitis media
  • Croup
  • Pharyngitis
  • 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

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
  • Chronicity
  • 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
    • Polyps
    • 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.

Management

Infectious rhinitis

• 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).

Allergic rhinitis

• 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

Non-allergic rhinitis

• 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

Differential Diagnosis

• 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.