Rhinitis, Nasal Obstruction & Nasal Trauma
From the boggy allergic nose to the black turbinate that means surgery tonight
Allergic rhinitis
Mechanism and presentation. Allergen cross-links IgE on mast cells, and released histamine and leukotrienes cause paroxysmal sneezing, nasal and eye itch, and clear rhinorrhea; a late eosinophilic phase sustains congestion. Disease is seasonal (pollens) or perennial (dust mites, pets, mold, cockroach). Look for pale-blue boggy turbinates, allergic shiners, a transverse nasal crease from the allergic salute, and Dennie-Morgan lines; asthma and eczema often coexist. Diagnosis is clinical, and skin-prick or specific-IgE testing is used when the trigger is unclear or before immunotherapy.
| Option | Role | Caveats |
|---|---|---|
| Intranasal glucocorticoid (fluticasone, mometasone, budesonide) | Most effective single agent, including for congestion | Full effect after days; epistaxis, rarely septal perforation, so aim away from the septum |
| Second-generation oral antihistamine (cetirizine, loratadine, fexofenadine) | Itch, sneezing, rhinorrhea | Weak against congestion |
| Intranasal azelastine | Fast relief; also works in vasomotor rhinitis | Bitter taste |
| Montelukast | Adjunct only | FDA boxed warning: agitation, depression, suicidality |
| Allergen immunotherapy (subcutaneous or sublingual) | Only disease-modifying option | For poor control or patient preference |
Nonallergic rhinitis
| Type | Clues | Treatment |
|---|---|---|
| Vasomotor | Temperature change, odors, perfume, smoke, alcohol, spicy food; little itch; negative allergy tests | Intranasal azelastine or glucocorticoid; ipratropium for watery rhinorrhea |
| Rhinitis medicamentosa | Topical decongestant for >3–5 days; beefy red, swollen turbinates | Stop the spray; intranasal glucocorticoid |
| Drug-induced | α-blockers (prazosin, tamsulosin), PDE5 inhibitors (sildenafil), other antihypertensives | Change the drug if possible |
| Pregnancy rhinitis | Congestion ≥6 weeks without allergy or infection; clears within ~2 weeks of delivery | Saline irrigation, nasal strips, head elevation |
Rhinitis medicamentosa. Oxymetazoline and phenylephrine are α-agonists that shrink the mucosa, but beyond 3–5 days tachyphylaxis and rebound vasodilation set in, so the patient sprays more and blocks worse. The spray is stopped, one nostril at a time if needed, while an intranasal glucocorticoid bridges the rebound. Intranasal cocaine produces the same rebound plus septal ischemia and perforation.
Other clues. Watery drip triggered by eating (gustatory rhinitis) responds to intranasal ipratropium, which dries rhinorrhea but does not relieve congestion. In pregnancy, oral decongestants are avoided in the first trimester.
Nasal polyps and unilateral nasal disease
Bilateral polyps. Chronic rhinosinusitis with nasal polyps produces pale-gray, glistening, insensate grape-like masses from the middle meatus, with obstruction and anosmia. Treatment is intranasal glucocorticoids, short oral steroid bursts, endoscopic sinus surgery, and biologics such as dupilumab for refractory disease. Asthma, polyps, and reactions to aspirin or NSAIDs form aspirin-exacerbated respiratory disease (AERD): COX-1 inhibition shunts arachidonic acid toward leukotrienes. COX-2–selective NSAIDs are usually tolerated, and aspirin desensitization after sinus surgery slows polyp regrowth.
Polyps in a child → sweat chloride test for cystic fibrosis. A unilateral polyp or mass → CT (± MRI) and biopsy for inverted papilloma (can harbor SCC), SCC, adenocarcinoma, esthesioneuroblastoma, or lymphoma. A midline nasal mass in an infant is imaged before any biopsy because an encephalocele may connect to the CSF.
Nasal foreign body. Unilateral foul-smelling purulent discharge, sometimes with bleeding, in a 2–5-year-old is a foreign body until proven otherwise. Positive-pressure removal (a parent blows into the child's mouth while occluding the open nostril), forceps, suction, or a balloon catheter usually works. Button batteries and paired magnets are removed urgently because they necrose and perforate the septum.
| Feature | Juvenile angiofibroma | Nasopharyngeal carcinoma |
|---|---|---|
| Patient | Adolescent male | Adult; southern China, Southeast Asia |
| Presentation | Unilateral obstruction, recurrent heavy epistaxis | Painless upper neck mass (most common), new unilateral serous otitis, epistaxis, CN V or VI palsy |
| Nature | Benign, locally aggressive, vascular; near the sphenopalatine foramen; internal maxillary artery supply | Malignant, EBV-associated undifferentiated carcinoma |
| Diagnosis | Contrast CT and MRI ± angiography; never biopsy in clinic | Nasopharyngoscopy with biopsy |
| Treatment | Preoperative embolization, then endoscopic resection | Radiation ± cisplatin |
Nasal trauma
- Control bleeding, protect the airwaypressure, packing if needed
- Inspect the septum in every patienta septal hematoma is drained now
- Look for associated injuryCSF leak, orbital or other facial fractures (CT if suspected); plain films add little for an isolated nasal fracture
- Re-examine in 3–5 daysonce swelling subsides, judge deformity and obstruction
- Closed reduction within ~1–2 weekssooner in children, whose bones knit faster
Septal hematoma. Blood collects between the septal cartilage and its perichondrium, the cartilage's only nutrient supply, forming a boggy, bluish-purple, fluctuant bulge with obstruction. Without urgent incision and drainage, packing to prevent reaccumulation, and antistaphylococcal antibiotics, the cartilage necroses, becomes a septal abscess, perforates, and collapses into a saddle-nose deformity. Nasal fracture is the most common facial fracture and remains a clinical diagnosis.
CSF rhinorrhea. Cribriform plate or skull-base fractures, or sinus surgery, can cause a clear, watery, often unilateral drip that worsens when leaning forward and may taste salty. β2-transferrin in the fluid confirms CSF; the halo sign and glucose testing are unreliable. Thin-cut CT localizes the defect. Most traumatic leaks close with head elevation and avoidance of nose blowing and straining; persistent leaks are repaired endoscopically because meningitis is the danger.
Invasive fungal rhinosinusitis
Mucormycosis. Rhizopus and Mucor thrive in diabetic ketoacidosis (acidosis and freed iron), neutropenia, high-dose corticosteroids, and deferoxamine therapy. Inhaled spores invade blood vessels, causing thrombosis and infarction: a black necrotic eschar on the turbinate or palate, facial pain and swelling, then proptosis, ophthalmoplegia, cranial nerve palsies, and cavernous sinus or brain spread. Biopsy shows broad, ribbon-like, nonseptate hyphae branching at right angles.
Treat within hours: emergent surgical debridement, high-dose liposomal amphotericin B, and correction of acidosis or immunosuppression. Voriconazole has no activity against Mucorales; posaconazole or isavuconazole are step-down or salvage options.