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Summary Table

Category	Details
Risk Factors	Asthma, aspirin sensitivity, cystic fibrosis, allergic fungal rhinosinusitis, eosinophilic granulomatosis with polyangiitis (Churg-Strauss), chronic rhinosinusitis
Etiology	Chronic eosinophilic inflammation of the sinonasal mucosa; exact trigger remains incompletely understood but strongly linked to type 2 (Th2) immune dysregulation
Patient Presentation	Progressive bilateral nasal obstruction, anosmia or hyposmia, anterior rhinorrhea, facial pressure, postnasal drip
Classic Physical Exam	Pale, glistening, grape-like, pedunculated masses in the nasal cavity that are insensitive to palpation and do not bleed on contact; bilateral involvement is the rule
Key Diagnostic Results	Anterior rhinoscopy or nasal endoscopy showing bilateral translucent polyps; CT sinuses showing opacification and polypoidal mucosal thickening; biopsy shows eosinophilic infiltration with edematous stroma
Management	Intranasal corticosteroids (first-line); short-course oral corticosteroids for severe disease; endoscopic sinus surgery for refractory cases; biologics (dupilumab) for recalcitrant disease
Keywords	"Bilateral nasal masses," "painless," "grape-like," "nontender," "anosmia," "aspirin-exacerbated respiratory disease," "Samter triad"

1. Pathophysiology

Nasal polyps arise from chronic type 2 inflammation of the sinonasal mucosa. The dominant immune pathway involves Th2 lymphocytes releasing IL-4, IL-5, and IL-13. IL-5 is the principal driver of eosinophil recruitment and survival within the tissue. These eosinophils degranulate and release toxic mediators (major basic protein, eosinophil cationic protein), which perpetuate mucosal damage, edema, and remodeling. Over time, the edematous mucosa herniates outward from the ostiomeatal complex, forming the characteristic pedunculated polyps.

This is why the patient develops progressive nasal obstruction: the polyps physically block airflow. Anosmia occurs because the polyps obstruct the olfactory cleft, preventing odorant molecules from reaching the olfactory epithelium in the cribriform plate region. The rhinorrhea and postnasal drip result from excessive mucus production driven by goblet cell hyperplasia, another consequence of IL-13 stimulation.

A critical association to understand is Samter triad (also called aspirin-exacerbated respiratory disease, or AERD). This triad consists of nasal polyps + asthma + aspirin/NSAID sensitivity. The mechanism involves a shift in arachidonic acid metabolism: cyclooxygenase (COX) is constitutively underexpressed, leading to decreased prostaglandin E2 (a bronchoprotective mediator), while the 5-lipoxygenase pathway is upregulated, producing excessive cysteinyl leukotrienes (LTC4, LTD4, LTE4). When aspirin or NSAIDs further inhibit COX, the already-dominant leukotriene pathway floods the tissue, triggering bronchoconstriction and polyp exacerbation.

In cystic fibrosis, nasal polyps develop through a different mechanism. Defective CFTR channels lead to thick, dehydrated mucus that obstructs sinus drainage, promoting chronic infection and inflammation. A vignette presenting a child or adolescent with bilateral nasal polyps should immediately raise suspicion for cystic fibrosis, as isolated nasal polyposis is uncommon in pediatric populations.

2. Classification and Clinical Manifestation

Classification	Characteristics	Clinical Significance
Antrochoanal polyp	Unilateral, originates from maxillary sinus, extends posteriorly into nasopharynx through the choana	More common in children and young adults; unilateral obstruction with possible oropharyngeal mass on exam; treatment is surgical excision
Ethmoidal polyp (most common type)	Bilateral, arises from ethmoidal sinus mucosa via the middle meatus	The classic adult presentation; strongly associated with asthma and AERD; responds to corticosteroids
Polyps associated with fungal sinusitis	Unilateral or bilateral; thick "peanut butter" mucin with fungal hyphae; bony erosion possible	Look for allergic mucin on CT (hyperdense material within sinuses); eosinophilic mucin with fungal elements on histology
Polyps in systemic disease	Bilateral; may have granulomatous features on biopsy	Consider eosinophilic granulomatosis with polyangiitis (EGPA) if polyps coexist with asthma, peripheral eosinophilia, neuropathy, and p-ANCA positivity

Clinical staging is often described by the degree of obstruction:

Grade	Description
Grade 0	No visible polyps
Grade 1	Small polyps confined to the middle meatus, not reaching below the inferior turbinate
Grade 2	Polyps extending between the superior and inferior borders of the inferior turbinate
Grade 3	Polyps extending below the inferior border of the inferior turbinate or polyps medial to the middle turbinate visible in the nasal cavity
Grade 4	Polyps causing complete nasal obstruction

3. Diagnostic Workup

Test	Role	Key Findings
Anterior rhinoscopy / Nasal endoscopy	Best initial test	Pale, translucent, bilateral, nontender, mobile, grape-like masses arising from the middle meatus
CT of the paranasal sinuses	Best imaging study; preoperative planning	Opacification of ethmoid and other sinuses, polypoidal mucosal thickening, widening of the ostiomeatal complex; rules out bony erosion or features suggesting malignancy
Biopsy	Confirmatory when diagnosis is uncertain or malignancy is a concern	Edematous stroma with dense eosinophilic infiltration, basement membrane thickening, goblet cell hyperplasia
Sweat chloride test	Screening for cystic fibrosis	Order in any child with bilateral nasal polyps or any adult with polyps plus recurrent pulmonary infections
CBC with differential	Supportive	Peripheral eosinophilia supports the diagnosis and may prompt evaluation for EGPA if markedly elevated
Serum total IgE, skin prick testing	Evaluate for allergic component	Helps guide allergen avoidance strategies and immunotherapy considerations

The workup begins with direct visualization. Anterior rhinoscopy can identify polyps in many cases, but nasal endoscopy is the preferred method because it allows full examination of the middle meatus, sphenoethmoidal recess, and nasopharynx. The polyps appear as pale, glistening, pedunculated masses. A critical distinguishing point: they are insensitive to touch and do not bleed when probed, unlike the vascular mucosa of turbinates (which are often mistaken for polyps by beginners).

CT of the sinuses without contrast is ordered when surgery is being considered, when the diagnosis is uncertain, or when complications are suspected. It provides anatomic detail of the sinuses and ostiomeatal complex. Look for diffuse mucosal thickening and opacification. Unilateral disease, bony destruction, or heterogeneous soft tissue should raise concern for inverted papilloma or sinonasal malignancy, prompting biopsy.

Tissue biopsy is not routinely needed for bilateral, typical-appearing polyps. However, it becomes essential when the polyp is unilateral, friable, or associated with bony erosion. The histologic hallmark of benign inflammatory polyps is eosinophil-predominant infiltration with stromal edema.

Do not forget to order a sweat chloride test for pediatric patients. This is a high-yield test-writer favorite: a child presenting with nasal polyps should trigger cystic fibrosis evaluation.

4. Management and Treatment

Setting	Treatment	Details
First-line (all patients)	Intranasal corticosteroids	Mometasone furoate 200 mcg per nostril daily or fluticasone propionate 200 mcg per nostril daily; continuous long-term use
Moderate to severe disease	Short-course oral corticosteroids	Prednisone 0.5 mg/kg/day for 5 to 14 days; used as a "medical polypectomy" to shrink polyps before reassessment
Adjunctive	Saline nasal irrigation	High-volume (240 mL) isotonic or hypertonic saline irrigation twice daily; improves mucociliary clearance
Refractory to medical therapy	Endoscopic sinus surgery (ESS)	Functional endoscopic sinus surgery to remove polyps and open obstructed sinuses; followed by continued intranasal corticosteroids postoperatively to prevent recurrence
Recalcitrant / post-surgical recurrence	Biologic therapy	Dupilumab (anti-IL-4R alpha, blocks IL-4 and IL-13): 300 mg subcutaneously every 2 weeks; FDA-approved for chronic rhinosinusitis with nasal polyps. Omalizumab (anti-IgE) and mepolizumab (anti-IL-5) are alternatives
AERD (Samter triad)	Aspirin desensitization	Performed after ESS; daily maintenance aspirin (325 to 650 mg) reduces polyp recurrence; must be done under supervised protocol
Allergic component	Allergen avoidance, consider immunotherapy	Reduces the inflammatory burden contributing to polyp growth

The first-line treatment for all patients with nasal polyps is intranasal corticosteroids. These are used continuously and indefinitely. They reduce polyp size, improve nasal obstruction, and restore olfaction in many patients. The mechanism is suppression of local eosinophilic inflammation and reduction of mucosal edema.

If the patient has moderate to severe symptoms, add a short course of oral prednisone. This acts as a medical debulking, rapidly shrinking the polyps. The duration should be limited to 5 to 14 days to minimize systemic steroid side effects. After the course, reassess symptom control and polyp burden.

Patients who fail medical therapy after adequate trials (typically 8 to 12 weeks of topical steroids with at least one course of oral steroids) are candidates for endoscopic sinus surgery. The goal of surgery is not curative but rather to remove the polyp burden and restore sinus ventilation so that topical medications can access the sinus mucosa more effectively. Postoperative intranasal steroids are mandatory because recurrence rates are high, particularly in patients with AERD or EGPA.

Dupilumab represents a paradigm shift for patients with recurrent or refractory disease. By blocking IL-4 and IL-13 signaling, it targets the upstream drivers of type 2 inflammation. It reduces polyp size, improves olfaction, and decreases the need for revision surgery and systemic steroids.

For patients with AERD, aspirin desensitization followed by daily aspirin maintenance is recommended after surgery. This modifies the leukotriene-driven pathology and significantly reduces polyp recurrence.

Contraindications and cautions: Long-term oral corticosteroids should be avoided due to cumulative toxicity (osteoporosis, adrenal suppression, hyperglycemia). Leukotriene receptor antagonists (montelukast) may be used as adjunctive therapy in AERD but are not a substitute for intranasal steroids.

5. Differential Diagnosis and Distractors

Differential Diagnosis	Why It Is Similar	Key Discriminator
Turbinate hypertrophy	Bilateral nasal obstruction, visible intranasal mass	Turbinates are erythematous (not pale), sensitive to touch, and shrink with topical decongestant application; polyps do not respond to decongestants and are pale/insensitive
Inverted papilloma	Unilateral nasal mass, obstruction, may appear polypoid	Unilateral presentation, arises from lateral nasal wall, tendency for local bony destruction, carries risk of squamous cell carcinoma transformation; requires surgical excision, not steroids
Juvenile nasopharyngeal angiofibroma	Nasal obstruction in a young patient, visible mass	Occurs in adolescent males; the mass is highly vascular and bleeds profusely on biopsy; CT/MRI shows enhancing mass in the pterygopalatine fossa with Holman-Miller sign (anterior bowing of the posterior maxillary wall); never biopsy before imaging
Sinonasal malignancy (SCC, adenocarcinoma, esthesioneuroblastoma)	Unilateral obstruction, mass on endoscopy	Unilateral, friable, bleeds easily, associated with bony erosion, cranial nerve involvement, or cervical lymphadenopathy; exposure history (woodworking for adenocarcinoma)
Encephalocele / meningocele	Nasal mass, may appear translucent	Typically presents at birth or in early childhood; pulsatile, positive Furstenberg test (expands with crying or straining); CT/MRI shows intracranial communication; never biopsy before imaging
Churg-Strauss (EGPA)	Nasal polyps with asthma	Distinguished by peripheral neuropathy (mononeuritis multiplex), markedly elevated eosinophils (often >1500/microL), p-ANCA positivity, and multisystem vasculitis findings
Allergic fungal rhinosinusitis	Bilateral polyps, nasal obstruction, often in atopic patients	CT shows hyperdense material within sinuses (allergic mucin); histology reveals Charcot-Leyden crystals and fungal hyphae within eosinophilic mucin

6. Traps and High-Yield Pearls

The most common way students lose points on nasal polyp questions is by failing to recognize the critical associations that change management. A vignette describing a child with bilateral nasal polyps is not simply asking you to treat polyps; it is testing whether you will order a sweat chloride test to evaluate for cystic fibrosis. Similarly, a patient with nasal polyps, asthma, and a history of a severe reaction after taking ibuprofen is testing your knowledge of Samter triad and whether you understand that the mechanism is leukotriene overproduction, not an IgE-mediated allergy.

Another common trap involves unilateral polyps. Test-writers use this detail deliberately. Bilateral, pale, nontender polyps point toward benign inflammatory disease. A unilateral mass, especially one that bleeds, should make you consider inverted papilloma, angiofibroma (in an adolescent male), or malignancy. The "next best step" in these cases is imaging before biopsy, particularly for angiofibroma, where blind biopsy can cause catastrophic hemorrhage.

Students also confuse turbinate hypertrophy with polyps. Remember: turbinates are red and shrink with decongestants; polyps are pale and do not respond to decongestants. If the vignette mentions that the intranasal mass "did not change with application of oxymetazoline," the answer is polyps.

Finally, be aware that questions may test the step after failed medical therapy. If a patient has been on intranasal steroids and oral steroid courses without improvement, the next best step is endoscopic sinus surgery, not indefinite systemic steroids. For the most refractory cases (recurrence after surgery), the answer increasingly involves biologic therapy with dupilumab.

The core competency being tested across nasal polyp questions is pattern recognition of key associations (cystic fibrosis in children, AERD in adults, EGPA in systemic disease) and the ability to distinguish benign bilateral polyposis from sinister unilateral pathology.

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