Rhinitis refers to inflammation of the nasal mucosa. The condition is classified into allergic, nonallergic, and infectious rhinitis. Allergic rhinitis is due to a type I hypersensitivity reaction. Non-allergic rhinitis is due to increased blood flow to the nasal mucosa. Infectious rhinitis is caused by an upper respiratory tract infection. All 3 types present with nasal congestion, rhinorrhea, and sneezing. Diagnosis is mainly clinical. Management includes antihistamines, decongestants, and immunotherapy.

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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 infectionType I hypersensitivity reactionAn increase in blood flow to the nasal mucosa due to irritants, but not allergens
  • Viral: rhinovirus (most common), coronavirus, influenza virus, adenovirus, parainfluenza virus
  • Bacterial: Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Staphylococcus aureus, Escherichia coli, Klebsiella
  • Fungal: Aspergillus, Rhizopus oryzae
  • Associated with immunodeficiency disorders
  • Seasonal (e.g., pollens, molds)
  • Perennial (e.g., house dust, mites)
  • Occupational (e.g., animal antigens; can be included in non-allergic if caused by irritants rather than allergens)
  • Rhinitis medicamentosa (e.g., overuse of decongestant nasal sprays)
  • Drug-induced rhinitis (e.g., antihypertensives, nonsteroidal anti-inflammatory drugs [NSAIDs])
  • Pregnancy rhinitis
  • Honeymoon rhinitis
  • Gustatory rhinitis (e.g., response to hot or spicy foods)
  • Non-airflow rhinitis (e.g., structural abnormalities)
  • Atrophic rhinitis


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
Pathological changes in non-allergic rhinitis

Pathological changes in non-allergic rhinitis. When the nasal mucosa is exposed to irritants, goblet cells overcrowd normal epithelia, causing mucin hypersecretion and decreased mucociliary activity, leading to congestion and other symptoms of rhinitis.

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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 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.


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.

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