Sinusitis and Rhinitis

Infectious causes

• Viral (most common): rhinovirus, influenza, parainfluenza, RSV, adenovirus, coronaviruses; direct epithelial and ciliary injury causes the ostial edema that precedes bacterial disease. Only a small minority of acute rhinosinusitis episodes are bacterial (IDSA 2012; AAO-HNS 2015).
• Bacterial superinfection: Streptococcus pneumoniae, nontypeable Haemophilus influenzae, Moraxella catarrhalis; Staphylococcus aureus and anaerobes are more typical of chronic and odontogenic disease. Unilateral foul-smelling maxillary disease after dental work suggests an odontogenic source.
• Fungal: allergic fungal rhinosinusitis (Aspergillus, dematiaceous molds) in atopic patients; invasive mucormycosis/aspergillosis in diabetic ketoacidosis, neutropenia, or transplant recipients.

Allergic and non-allergic inflammatory

• Atopy: IgE sensitization to pollens, dust mite, animal dander, mold — the dominant driver of allergic rhinitis and a major CRS risk factor.
• Aspirin-exacerbated respiratory disease: COX-1 inhibition shunts arachidonate toward cysteinyl leukotrienes — polyps, asthma, aspirin sensitivity (Samter triad).
• Drug- and hormone-induced: rhinitis medicamentosa from topical decongestants >3 days; ACE inhibitors, alpha-blockers, beta blockers, phosphodiesterase-5 inhibitors, oral contraceptives, intranasal cocaine; pregnancy and hypothyroidism.

Obstructive and clearance defects

• Anatomic: septal deviation, concha bullosa, adenoid hypertrophy (children), nasal foreign body, prolonged nasogastric tubes or nasal packing (nosocomial sinusitis in ICU patients), tumor.
• Mucociliary/immune: cystic fibrosis and primary ciliary dyskinesia (Kartagener syndrome: situs inversus, bronchiectasis, sinusitis), CVID/IgA deficiency, HIV, poorly controlled diabetes.

Rhinitis Mechanisms

• Allergic rhinitis: Type I hypersensitivity reaction where IgE-mediated mast cell degranulation releases histamine, leukotrienes, and prostaglandins, causing mucosal edema and mucus hypersecretion
• Viral rhinitis: Direct epithelial damage by rhinoviruses and other viruses triggers innate immunity, ciliary dysfunction, and increased mucus production
• Non-allergic rhinitis: Includes vasomotor (heightened vascular reactivity to irritants), occupational, hormonal, and medication-induced forms; involves autonomic nervous system dysregulation

Sinusitis Mechanisms

• Ostiomeatal complex obstruction: The key anatomical convergence zone where the maxillary, anterior ethmoid, and frontal sinuses drain; obstruction here prevents sinus ventilation and mucociliary clearance
• Impaired mucociliary clearance: Loss of ciliary function (from inflammation, smoking, or viral infection) and thickened secretions prevent normal drainage, creating favorable conditions for bacterial overgrowth
• Bacterial colonization and biofilm formation: Streptococcus pneumoniae, Haemophilus influenzae (nontypeable), and Moraxella catarrhalis invade stagnant secretions; bacteria form protective biofilms resistant to antibiotics and immune clearance
• Mucosal edema and inflammation: Cytokine and chemokine release sustains swelling of sinus mucosa, perpetuating obstruction in acute sinusitis; chronic sinusitis involves T-cell infiltration, IL-5 elevation, and possible eosinophilic involvement
• Eustachian tube dysfunction: Can occur secondary to sinusitis, affecting middle ear pressure regulation

Acute Rhinitis

• Nasal congestion, rhinorrhea (clear to mucoid discharge), and sneezing often preceded by sore throat and fatigue
• Symptoms peak at days 3–5 and typically resolve within 7–10 days; persistence beyond 10 days raises concern for secondary sinusitis
• Viral prodrome (malaise, low-grade fever) distinguishes from allergic rhinitis

Allergic Rhinitis

• Bilateral nasal congestion, rhinorrhea (clear and watery), nasal pruritus, and sneezing; often accompanied by ocular itching and lacrimation
• Seasonal pattern (tree/grass pollens) or perennial presentation (dust mites, pet dander, mold)
• Physical exam reveals pale, boggy nasal mucosa with clear secretions; dark circles under eyes ("allergic shiners") and a horizontal crease on the nose ("allergic salute") from repeated rubbing are classic signs
• Associated with allergic asthma, eczema, and food allergies (atopic march)

Acute Sinusitis

• Facial pain or pressure in the distribution of affected sinus(es): maxillary sinus pain over cheeks and upper teeth, frontal sinus pain over the forehead, ethmoid pain between the eyes, sphenoid pain deep behind the nose
• Nasal congestion with thick, purulent nasal discharge (often unilateral or asymmetric)
• Post-nasal drip, cough (worse at night from drainage), and hyposmia or anosmia
• Symptoms lasting 7–10 days after a viral URI, or worsening after initial improvement ("double sickening")
• Low-grade fever may be present; high fever or severe systemic toxicity suggests complications

Chronic Rhinosinusitis (CRS)

• Symptoms for ≥12 weeks including nasal congestion, post-nasal drip, facial pressure/pain, and cough; symptoms may be subtle and patients often report persistent "head congestion"
• Anosmia/hyposmia is more prominent than in acute disease
• Fatigue and sleep disturbance from nasal obstruction significantly impact quality of life
• CRS with nasal polyps (CRSwNP): Usually eosinophilic, associated with asthma and aspirin sensitivity (Samter's triad); polyps appear as pale, grape-like masses on nasal endoscopy
• CRS without nasal polyps (CRSsNP): More common, often involves neutrophilic inflammation

Important Pearls

• Pain upon palpation over the sinuses is not required for sinusitis diagnosis and is not highly specific
• Transillumination (darkening of opaque sinuses suggesting fluid) has poor sensitivity and specificity; endoscopy is more reliable
• Fever in acute sinusitis is typically low-grade; high fever suggests complications or sepsis

Acute Rhinitis

• Clinical diagnosis based on typical presentation; viral culture is unnecessary and not recommended
• No imaging required; diagnosis is straightforward when preceded by URI symptoms

Acute Sinusitis

• Clinical criteria (major diagnosis): Presence of symptoms for 7–10 days (or worsening after 5–7 days) plus either purulent nasal discharge or signs on nasal endoscopy (purulent secretions, edema)
• Imaging:
• CT of paranasal sinuses is the gold standard for diagnosis and complications; shows opacification, fluid levels, or air-fluid interfaces
• Plain radiographs (limited value, rarely used) may show opacification or air-fluid levels
• MRI reserved for suspected complications (cavernous sinus thrombosis, intracranial extension)
• Nasal endoscopy: Direct visualization allows assessment of mucosal edema, pus drainage, polyps, and structural abnormalities; increasingly preferred in clinic for acute sinusitis diagnosis without imaging
• Bacterial culture: Not routinely recommended for acute sinusitis; reserved for immunocompromised patients, treatment failures, or severe disease
• Blood tests: Not indicated for uncomplicated acute sinusitis; elevated WBC may suggest bacterial infection but lacks specificity

Chronic Rhinosinusitis

• Diagnostic criteria: ≥12 weeks of symptoms (nasal congestion, rhinorrhea, facial pain/pressure, or anosmia) plus either endoscopic signs (polyps, edema, discharge, mucosal changes) or CT imaging findings (mucosal thickening, opacification, bone changes)
• Nasal endoscopy: Superior to imaging for detecting polyps, inspecting ostiomeatal complex, and guiding biopsy if needed
• CT paranasal sinuses: Determines extent of disease, guides surgical planning, and helps rule out complications; may show chronic changes (bone sclerosis, osteitic remodeling) distinct from acute disease
• Allergy testing: Consider skin prick or serum-specific IgE testing if allergic component suspected
• Immunological workup: Consider if recurrent, severe, or atypical CRS (check immunoglobulin levels, complement function)

Allergic Rhinitis

• Clinical diagnosis based on characteristic symptoms and temporal pattern
• Allergy skin prick testing or serum-specific IgE confirm sensitization to particular allergens
• Nasal eosinophilia (Wright stain or cytology) supports allergic diagnosis but is not routinely obtained
• Absence of fever and purulent discharge help differentiate from infectious rhinitis/sinusitis

Acute Viral Rhinitis

• Supportive care (fluids, rest) and symptom management
• Nasal saline rinses (hypertonic or isotonic) facilitate mucus clearance and provide comfort
• Decongestants (pseudoephedrine 30–60 mg PO Q4–6H, phenylephrine nasal spray) for short-term congestion relief (limit nasal decongestants to ≤3 days to avoid rebound

• Red flags: proptosis, pain or restriction with extraocular movement, diplopia, chemosis, decreased visual acuity, afferent pupillary defect. Any of these mandates urgent contrast CT of orbits/sinuses, IV antibiotics, and ENT/ophthalmology consultation.
• Cavernous sinus thrombosis: headache, fever, and cranial neuropathies — CN VI is affected earliest because it runs free within the sinus; bilateral eye findings are the giveaway. MRI/MRV is the confirmatory study.

Treatment-related complications

• Topical decongestants: rebound congestion (rhinitis medicamentosa) beyond about 3 days; oral pseudoephedrine raises blood pressure and precipitates urinary retention.
• First-generation antihistamines: sedation and anticholinergic effects; avoid in older adults.
• Intranasal corticosteroids: epistaxis and rarely septal perforation — aim the spray away from the septum.
• Amoxicillin-clavulanate: diarrhea and C. difficile colitis; fluoroquinolones carry tendinopathy, QT, and aortic risks, so reserve them.
• Endoscopic sinus surgery: CSF rhinorrhea from cribriform plate injury, orbital hematoma, hemorrhage.

• Antibiotics require the right clock: IDSA and AAO-HNS both treat bacterial rhinosinusitis only when symptoms persist ≥10 days without improvement, are severe (high fever with purulent discharge for 3–4 days), or show double sickening — worsening after initial improvement. Antibiotics for a 5-day URI is the single most common distractor.
• Amoxicillin-clavulanate is the first-line agent in adults per IDSA, chosen over plain amoxicillin for beta-lactamase–producing H. influenzae and M. catarrhalis. In true penicillin allergy, use doxycycline or a respiratory fluoroquinolone; note that cephalosporin cross-reactivity is only about 1–3% and reflects shared R1 side chains, not the beta-lactam ring. Macrolides and TMP-SMX are not recommended because of pneumococcal resistance.
• Intranasal corticosteroids are the most effective single therapy for allergic rhinitis — more effective than oral antihistamines for congestion; the exam answer for moderate-to-severe or persistent symptoms.
• Nasal polyps in a child = cystic fibrosis until proven otherwise — order sweat chloride testing. In an adult, polyps plus asthma plus aspirin sensitivity is Samter triad (AERD), and aspirin desensitization is the association tested.
• Unilateral foul-smelling purulent discharge in a toddler is a nasal foreign body, not sinusitis.
• Clear watery unilateral rhinorrhea after head trauma or sinus surgery is a CSF leak: confirm with beta-2 transferrin, not glucose testing.
• Best next step for suspected orbital or intracranial complication is contrast-enhanced CT of the orbits and sinuses with IV antibiotics — never plain films, and never outpatient oral therapy. Pain with eye movement distinguishes orbital from preseptal cellulitis.
• Black eschar on the turbinate in DKA = mucormycosis; the answer is amphotericin B plus surgical debridement, not broader antibiotics.