Nonallergic rhinitis

Nonallergic rhinitis (NAR) is an acute or chronic rhinitis that is not immune mediated. Common clinical features of NAR are persistent nasal congestion, postnasal drip, rhinorrhea, and intermittent sneezing. There are several types of NAR, including atrophic rhinitis, vasomotor rhinitis, drug-induced rhinitis, and nonallergic rhinitis with eosinophilia syndrome. Diagnosis is usually clinical; allergen testing is not routinely recommended. Management includes avoidance of triggers and topical pharmacological treatment with intranasal antihistamines (INAH) and/or intranasal corticosteroids (INCS). Additional therapies (e.g., intranasal ipratropium, intranasal decongestants) are considered for certain types of NAR. Refractory or severe symptoms require specialist referral for advanced treatments (e.g., oral medications, surgery).

Infectious rhinitis is a type of NAR that often occurs in conjunction with sinusitis (rhinosinusitis); see “Sinusitis” for details. Allergic rhinitis is a distinct entity and is detailed separately.

See “Management of NAR” for diagnostic and treatment considerations for all types of NAR except atrophic rhinitis and infectious rhinosinusitis, which are detailed separately.

• Headache, sinus pressure
• Persistent nasal congestion, mouth breathing, snoring, and/or obstructive sleep apnea
• Rhinorrhea, postnasal drip, throat clearing, cough
• Intermittent sneezing
• Possible anosmia, eustachian tube dysfunction, or allergic shiners
• See “Types of NAR” for findings according to subtypes.

Nonallergic and allergic rhinitis often manifest with similar symptoms (e.g., rhinorrhea, sneezing, mouth breathing), but postnasal drip is more common in NAR, and pruritus of the mouth, nose, and ear are more common in allergic rhinitis. ^[1]

Vasomotor rhinitis (VMR) ^[1][3]

Vasomotor rhinitis, often referred to as idiopathic rhinitis; , is a type of NAR that is caused by an increase in blood flow to the nasal mucosa, usually in response to an irritant or stimulant. ^[1]

Etiology

• Irritant odors; (e.g., cigarette smoke, perfumes)
• Cold and/or dry air
• Changes in humidity, temperature, and air pressures
• Exercise
• Foods (e.g., hot temperature, spicy)
• Alcohol

Pathophysiology ^[1]

• ↑ Parasympathetic activity: Parasympathetic stimulation causes vasodilatation of blood vessels in the nasal mucosa and increases mucous secretion.
• ↓ Sympathetic activity: Sympathetic stimulation causes vasoconstriction of the nasal blood vessels.

Clinical features

• Nasal congestion
• Clear nasal discharge
• Cough
• Sneezing and itching are typically absent.
• See also “Common clinical features of NAR.”

Management

• Diagnosis is clinical; see “Diagnosis of NAR.”
• Initial treatment of VMR ^[1]
  • Avoid triggers, if feasible.
  • Start monotherapy with INAH or INCS.
  • Persistent symptoms: Add or switch to intranasal ipratropium to control anterior rhinorrhea.
• Severe or refractory symptoms: Endoscopic vidian neurectomy may be considered. ^[6]
• See “Treatment of NAR” for details; and dosages.

Vasomotor rhinitis is a diagnosis of exclusion. ^[1]

Atrophic rhinitis ^[1][7]

Atrophic rhinitis is a chronic condition in which nasal crusting and dry mucosa are associated with atrophy of the nasal mucosa.

Etiology

• Primary atrophic rhinitis
  • Idiopathic; often associated with bacterial colonization (K. pneumoniae subsp. ozaenae is most common)
  • More common in individuals residing in resource-limited settings with a dry climate
• Secondary atrophic rhinitis
  • Trauma (e.g., repeated surgery, radiotherapy) involving the nasal mucosa
  • Granulomatous diseases of the nasal cavity (e.g., syphilis, sarcoidosis, tuberculosis, leprosy)

Clinical features

• Foul-smelling nasal cavity with or without anosmia
• Nasal dryness and crusting
• Epistaxis
• Empty nose syndrome (in secondary atrophic rhinitis)

Diagnosis

• Diagnosis is clinical.
• In cases of diagnostic uncertainty, consider:
  • Bacterial culture of the nasal mucosa
  • Biopsy of the nasal mucosa
  • Evaluation for suspected underlying systemic conditions, e.g.:
    • Diagnostics for sarcoidosis
    • Diagnostics for syphilis
    • Diagnostics for leprosy
    • Diagnostics for tuberculosis
• See also “Diagnostics of NAR.”

Treatment

Atrophic rhinitis is managed differently from other types of NAR. Refer to an ENT specialist for management.

• Conservative management options to reduce nasal crusting include:
  • Nasal saline irrigation
  • Glycerin drops
  • Emollients
  • Antibiotics targeting specific pathogens
  • Nasal estradiol
• Surgical options to decrease the volume of the nasal cavity: e.g., modified Young procedure, prostheses ^[7]

• NAR is a clinical diagnosis.
• Perform a physical examination, including:
  • Focused head and neck examination (e.g., otoscopy, nasal inspection with anterior rhinoscopy)
  • Skin examination: to evaluate for signs of atopy and/or systemic disease
• In cases of diagnostic uncertainty, consider additional diagnostic studies and/or referral to a specialist (e.g., ENT) for: ^[3]
  • Diagnostics for allergic rhinitis
  • CT maxillofacial or MRI head for suspected sinusitis or tumor
  • Nasopharyngoscopy to evaluate for structural abnormalities and/or complications

For patients with mucosal edema of the nasal turbinate, consider using an intranasal decongestant before the examination to improve visibility. ^[1]

• There is no standard treatment algorithm for the management of NAR. ^[1]
• The following approach primarily applies to nonpregnant patients. Consult relevant specialists to determine the safety of pharmacological treatment during pregnancy. ^[1][3]
• Treatment of atrophic rhinitis and infectious rhinosinusitis are detailed separately.

First-line treatment

• Avoid triggers when possible; see “Types of NAR.”
• Start monotherapy with either of the following:
  • Intranasal antihistamines (INAH): azelastine (off-label except for VMR)
  • Intranasal corticosteroids (INCS): fluticasone or beclomethasone (off-label except for VMR)
• Consider adding the following:
  • Intranasal saline as needed for symptom control ^[1]
  • Intranasal decongestants for ≤ 5 days for severe symptoms or mucosal edema
    • Oxymetazoline (off-label)
    • Phenylephrine (off-label)

Further management

Reassess patients 5–7 days after starting monotherapy.

Symptom improvement

• Triggers are controlled or absent: Stop or taper off treatment.
• Triggers cannot be controlled: Continue treatment as needed (PRN).

Persistent symptoms

• Consider alternative monotherapy (preferred).
• Add or switch to a symptom-specific agent.
  • Predominant anterior rhinorrhea (e.g., VMR, gustatory rhinitis, rhinitis in older adults): intranasal ipratropium ^[1][4]
  • Predominant nasal congestion: intranasal decongestant for ≤ 5 days; see “First-line treatment” for dosages.

Severe symptoms or symptoms refractory to monotherapy ^[1]

• Consider combination intranasal therapy (i.e., INAH + INCS); see “First-line treatment” for dosages. ^[1]
• Refer to ENT for oral pharmacotherapy options and/or surgery (e.g., vidian neurectomy for VMR, turbinectomy).

Oral antihistamines and leukotriene-receptor antagonists are not recommended because of insufficient evidence on their efficacy. ^[1]

In patients with intermittent, clear, watery nasal discharge that worsens with dependent head positioning, evaluate for CSF rhinorrhea, especially if there is a history of recent skull trauma, neurosurgery, or suspected CNS tumor. ^[1]

The differential diagnoses listed here are not exhaustive.