EN4.{21-26,28-29} | Nose Airway and Rhinitis Disorders — Practice Quiz

Correct. Ethmoidal polyps are the commonest type of nasal polyps. They are bilateral, multiple, arise from the ethmoidal labyrinth, and are strongly associated with allergic rhinitis and chronic rhinosinusitis. Their smooth, pale, grape-like appearance and insensitivity to probing distinguish them from inferior turbinate hypertrophy.

Ethmoidal polyps = bilateral, multiple, allergic origin, arising from ethmoid labyrinth, common in adults. Antrochoanal (Killian's) polyp = unilateral, single, from the maxillary antrum, common in children/young adults. Never swap laterality.

Antrochoanal polyps (Killian's polyp) are characteristically unilateral and single, arising from the maxillary antrum and extending through the choana to the nasopharynx — they are common in children and young adults. This patient's bilateral, allergic presentation is classic for ethmoidal polyps.

Correct. Little's area (Kiesselbach's plexus) is the richly vascular area on the antero-inferior nasal septum, approximately 1 cm from the columella. It is a watershed anastomosis between four arterial systems: the sphenopalatine artery (ICA-derived via maxillary), anterior ethmoidal artery (ICA-derived via ophthalmic), greater palatine artery, and superior labial artery. It is the commonest site of epistaxis — especially anterior bleeds in children.

Little's area = Kiesselbach's plexus = anterior nasal septum; supplied by sphenopalatine (posterior septal branches), anterior ethmoidal, greater palatine, and superior labial arteries. This is the commonest site for anterior epistaxis, especially in children. Woodruff's plexus (posterior lateral nasal wall, sphenopalatine area) is the source of posterior bleeds in elderly hypertensives.

Woodruff's plexus is located on the posterior lateral nasal wall (inferior meatus) and is supplied by the sphenopalatine and ascending pharyngeal arteries — it is the source of posterior epistaxis in elderly hypertensives, which presents as blood trickling down the throat and is harder to control. The anterior septal location and paediatric context here confirm Little's area.

Correct. Intranasal corticosteroids (e.g., mometasone furoate, fluticasone propionate) are the first-line pharmacotherapy for moderate-to-severe or persistent allergic rhinitis. They reduce all nasal symptoms — sneezing, rhinorrhoea, pruritus and congestion — and are superior to oral antihistamines for nasal obstruction. Once-daily dosing and excellent safety profile make them the recommended choice.

Allergic rhinitis first-line: intranasal corticosteroids (INCS) are the most effective single agent — superior to antihistamines for nasal congestion. Second-line: oral antihistamines (especially for sneezing/rhinorrhoea). Avoid topical decongestants >3–5 days (rhinitis medicamentosa). Allergen avoidance + INCS = standard management per ARIA guidelines.

Oral decongestants provide short-term relief but are not first-line and have systemic side effects (hypertension, insomnia). Systemic corticosteroids are reserved for severe refractory cases, not first-line outpatient management. Topical decongestants like oxymetazoline are appropriate for ≤3–5 days only — prolonged use causes rhinitis medicamentosa (rebound congestion).

Correct. Vasomotor rhinitis is a diagnosis of exclusion characterised by nasal congestion and watery rhinorrhoea triggered by non-allergic stimuli (temperature change, spicy food, alcohol, strong smells, emotions). It reflects autonomic hyperresponsiveness. Crucially, allergy tests (IgE, SPT) are negative and the nasal smear shows no eosinophilia — ruling out allergic rhinitis and NARES. Management includes avoidance of triggers, ipratropium nasal spray, and intranasal corticosteroids.

Vasomotor rhinitis (non-allergic rhinitis, autonomic rhinitis): nasal congestion and rhinorrhoea triggered by non-immunological stimuli (temperature, humidity, spicy food, alcohol, emotion); normal allergy tests (IgE, skin prick tests); nasal smear shows no eosinophilia. Distinguishable from NARES (eosinophilia on smear despite negative allergy tests) and allergic rhinitis (positive IgE/SPT).

Perennial allergic rhinitis would show positive SPT or elevated specific IgE. NARES features eosinophilia on nasal smear despite negative allergy tests. Drug-induced rhinitis from amlodipine (a calcium channel blocker) is possible but is a diagnosis of exclusion after the characteristic trigger pattern of vasomotor rhinitis is identified.

Correct. Septoplasty is the modern standard surgery for symptomatic DNS, replacing the older submucous resection (SMR). Septoplasty conserves the L-strut of cartilage, preserves perichondrium, and minimises the risk of saddle nose deformity and perforation. In this 16-year-old, the procedure should ideally wait until nasal growth is complete (age 17–18); if done earlier, the indication must be compelling.

Septoplasty is the current preferred surgery for DNS — it conserves cartilage and mucoperichondrium, preserves nasal support and function, and has largely replaced submucous resection (SMR). SMR removes excessive cartilage/bone and risks saddle nose deformity. Minimum age for septoplasty: 17–18 years (nasal growth complete). FESS is for sinus disease, not septal deviation.

Submucous resection (SMR) removes more cartilage and is associated with greater risk of saddle nose deformity and septal perforation — it has been largely superseded by septoplasty. FESS addresses paranasal sinus disease, not a pure septal deviation. Inferior turbinate reduction addresses the compensatory turbinate hypertrophy but not the primary septal deviation causing obstruction.

Correct. The primary indication for adenoidectomy in this child is significant nasal airway obstruction causing mouth breathing, snoring, sleep disturbance, and recurrent URTI attributable to the adenoid mass. Adenoid facies (long face, open mouth, recessed chin, crowded teeth) is a consequence of prolonged mouth breathing — adenoidectomy at this stage can prevent further dentofacial malformation.

Adenoidectomy indications: (1) significant nasal obstruction → mouth breathing, snoring, sleep-disordered breathing; (2) recurrent/chronic otitis media with effusion (glue ear) — adenoidectomy ± grommet insertion; (3) recurrent adenoiditis (>4 episodes/year); (4) obstructive sleep apnea. Adenoid facies is a consequence, not an indication by itself — the structural damage is already done.

Cosmetic correction is not a surgical indication — the facies results from chronic mouth breathing; treating the obstruction prevents progression. An adenoid shadow on X-ray alone is not an indication; adenoids are physiologically present and prominent in all children under 10. Nasal discharge without obstruction reflects mucosal rhinitis, not necessarily adenoid disease requiring surgery.

Correct. Polysomnography (PSG) is the gold standard investigation for OSA. It continuously records airflow, oxygen saturation, EEG, EMG, ECG, and respiratory effort, and calculates the Apnea-Hypopnea Index (AHI). This patient's high ESS score, witnessed apnoeas, and systemic consequences (road accidents, morning headaches) give a high pre-test probability. PSG confirms the diagnosis and grades severity, guiding therapy (CPAP, positional therapy, or surgery).

OSA diagnosis: polysomnography (PSG) is the gold standard — records AHI (apnea-hypopnea index): mild 5–14/h, moderate 15–29/h, severe ≥30/h. Epworth Sleepiness Scale screens for daytime somnolence. Portable home sleep testing (Level 3) is an alternative in uncomplicated suspected OSA. Müller's manoeuvre (nasendoscopy during sniff) maps the collapse site but does not diagnose or grade OSA.

Chest X-ray and lateral neck views can show soft-tissue features but do not diagnose OSA. Metabolic investigations (glucose, TFTs) screen for secondary causes of OSA (obesity, hypothyroidism) but do not confirm the diagnosis. Müller's manoeuvre localises the site of airway collapse for surgical planning but does not measure AHI or grade disease severity.

Correct. Hypertrophic rhinitis is characterised by irreversible fibrotic enlargement of the inferior turbinates. The key diagnostic finding is failure of turbinate shrinkage after topical vasoconstrictor (decongestant test negative). This distinguishes it from simple mucosal engorgement in vasomotor or allergic rhinitis where turbinates shrink. Management: chemical cautery, submucosal diathermy, turbinoplasty, or partial turbinectomy.

Hypertrophic rhinitis: turbinates are enlarged, firm (fibrosed), and DO NOT shrink after topical vasoconstrictor (decongestant test negative) — unlike simple mucosal congestion (vasomotor/allergic). Atrophic rhinitis (ozaena) presents with wide nasal cavities, foetor, dry greenish crusts, and paradoxical nasal obstruction despite a roomy nasal cavity. The turbinates are atrophied, not hypertrophied.

Atrophic rhinitis (ozaena) presents with paradoxical spacious nasal cavities, greenish-grey foul-smelling crusts, parosmia, and turbinate atrophy — the opposite of hypertrophy. Allergic rhinitis would show positive IgE/SPT and responsive turbinates. Rhinitis sicca (dry rhinitis) features dry, scaly anterior nasal mucosa without turbinate hypertrophy.

Correct. Posterior epistaxis in an elderly hypertensive patient arises from Woodruff's plexus (posterior lateral nasal wall, inferior meatus, sphenopalatine artery territory). The blood flows down the throat because the bleeding point is posterior to the posterior choana. Management is posterior nasal packing — typically a Foley catheter balloon inflated in the nasopharynx to tamponade the posterior nasal aperture, combined with anterior packing. This is a hospital procedure requiring monitoring.

Posterior epistaxis in elderly hypertensives = Woodruff's plexus (sphenopalatine area, posterior lateral nasal wall). Presents as blood trickling down the throat (posterior flow), profuse, not visible on anterior rhinoscopy. First-line: posterior nasal packing (Foley catheter balloon or Brighton balloon) + anterior pack or formal Brighton pack. Silver nitrate cautery is for anterior bleeds at Little's area. Never attempt blind silver nitrate of the posterior nose.

Little's area (anterior nasal septum) is the site of anterior epistaxis — visible on rhinoscopy, controllable with silver nitrate cautery, direct pressure, or anterior packing. Silver nitrate cautery cannot be safely applied to the inaccessible posterior nasal cavity. In an elderly hypertensive with blood flowing down the throat and no visible anterior source, posterior packing is the emergency standard.

Correct. Juvenile nasopharyngeal angiofibroma (JNA) is a benign but locally aggressive, highly vascular tumour arising in adolescent males from the sphenopalatine foramen area. The Holman-Miller sign (anterior bowing of the posterior wall of the maxillary sinus) on CT is pathognomonic. Biopsy is absolutely contraindicated due to the risk of catastrophic haemorrhage. Management involves preoperative angiographic embolisation (to reduce intraoperative blood loss) followed by surgical resection — endoscopic or open depending on stage.

Juvenile nasopharyngeal angiofibroma (JNA): adolescent males, recurrent epistaxis + progressive nasal obstruction, highly vascular benign tumour arising from the sphenopalatine foramen. DO NOT BIOPSY — catastrophic haemorrhage risk. Diagnosis: contrast CT (Holman-Miller sign = bowing of posterior maxillary wall) + MRI. Management: preoperative angiography + embolisation → endoscopic/open surgical excision. Biopsy contraindicated.

Biopsy of a suspected JNA under any anaesthesia — local or general — risks life-threatening haemorrhage. The diagnosis is established on clinical and imaging criteria (adolescent male + recurrent epistaxis + unilateral mass + Holman-Miller sign on CT) without tissue sampling. Intranasal corticosteroids are used for inflammatory nasal polyps — not vascular tumours.