The following CBME core competencies are covered in this chapter. AN37.3: Describe the anatomical basis of sinusitis. EN4.25: Elicit document and present a correct history, demonstrate and describe the clinical features, choose the correct investigations and describe the principles of management of nasal polyps. EN4.33: Elicit document and present a correct history, demonstrate and describe the clinical features, choose the correct investigations and describe the principles of management of acute and chronic sinusitis.

Rhinosinusitis

Definition of Rhinosinusitis

Rhinosinusitis refers to the inflammation of the nasal cavity and paranasal sinuses. Previously, clinicians used the term “sinusitis” to describe inflammation of the sinuses alone. However, we now understand that the nasal cavity and paranasal sinuses share a continuous lining of respiratory epithelium, so inflammation almost always involves both structures simultaneously. Hence, the term “rhinosinusitis” has replaced “sinusitis” in modern practice.

Diagnosis of Rhinosinusitis

Rhinosinusitis represents one of the most common conditions encountered in ENT practice, affecting millions of individuals worldwide. The European Position Paper on Rhinosinusitis and Nasal Polyps (EPOS 2020) provides the current gold-standard definition. The diagnosis requires two essential components:

1. Characteristic Symptoms: The patient must have at least 2 symptoms, one of which must be nasal blockage/obstruction/congestion or nasal discharge (anterior or posterior).
2. Objective Evidence: This inflammation must be confirmed by either nasal endoscopy or CT imaging.

Table: Diagnostic Criteria for Rhinosinusitis (EPOS 2020)

Component	Findings / Details
Symptoms	At least two symptoms, one of which must be either: • Nasal blockage/obstruction/congestion • Nasal discharge (anterior or posterior) Additional supportive symptoms (if only one primary symptom present): • Facial pain/pressure • Olfactory dysfunction (hyposmia/anosmia)
Duration	• Acute: >10 days but <12 weeks • Chronic: ≥12 weeks
Nasal Endoscopy (any of these)	• Nasal polyps • Mucopurulent discharge from the middle meatus • Oedema / mucosal obstruction in the middle meatus • Mucosal changes in the osteomeatal complex (OMC)
CT Scan (either seen independently or along with endoscopic findings)	• Mucosal thickening/opacification within OMC or sinuses • Fluid levels • Bony changes (in chronic cases)

Risk Factors & Aetiology of Rhinosinusitis

1. Host-related factors: Anatomical obstruction (deviated septum, concha bullosa, Haller cells, paradoxical middle turbinate), systemic diseases (allergic rhinitis, asthma, AERD, immunodeficiency, cystic fibrosis, ciliary dyskinesia, GPA/sarcoidosis), and genetic predisposition (CFTR mutation, TNF-α/IL-4 polymorphisms) increase susceptibility and promote chronic inflammation.
2. Environmental and microbial factors: Viral infections (rhinovirus, influenza), bacterial infections (ARS: S. pneumoniae, H. influenzae, M. catarrhalis; CRS: S. aureus, P. aeruginosa), fungal causes (allergic fungal rhinosinusitis), allergens, smoking, pollution, and occupational irritants trigger mucosal oedema, impair mucociliary clearance, and sustain inflammation. Biofilms contribute to antibiotic resistance and persistent CRS.
3. Other contributory causes: Odontogenic infections (periapical abscess, oroantral fistula) commonly cause unilateral maxillary sinusitis, while iatrogenic factors (nasal intubation, NG tube, dental procedures) and GERD-related microaspiration may worsen or perpetuate sinus inflammation.

Classification of Rhinosinusitis

There are three classifications based on duration, its phenotype and extent of disease.

Classification Basis	Type	Definition / Duration	Key Features	Inflammatory Pattern / Associations	Clinical Significance
1. Duration	Acute Rhinosinusitis (ARS)	Symptoms < 12 weeks (3 months); resolves completely with treatment.	• Most cases are viral in origin. • Bacterial superinfection occurs in <2% of cases. • Symptoms: nasal blockage, discharge, facial pain, hyposmia.	Viral (rhinovirus, influenza, etc.) → may progress to bacterial (S. pneumoniae, H. influenzae, M. catarrhalis) in a small subset.	Guides initial management: supportive care for viral; antibiotics reserved for confirmed bacterial (ABRS) with specific criteria (purulent discharge, double sickening, fever, etc.).
	Chronic Rhinosinusitis (CRS)	Symptoms persist > 12 weeks despite medical therapy.	• Subdivided into two distinct phenotypes: – CRS with nasal polyps (CRSwNPs) – CRS without nasal polyps (CRSsNPs) • Requires objective evidence (endoscopy/CT).	Varies by phenotype (see below).	Prognosis and treatment differ significantly between the two phenotypes; distinction is essential for selecting medical therapy (steroids, biologics, long-term antibiotics) and surgical planning.
	Recurrent Acute Rhinosinusitis	Four or more episodes of ARS per year, with complete symptom resolution between episodes.	• Pattern suggests underlying predisposing factors. • Episodes are discrete and fully resolve. • May be associated with anatomical variations, allergy, or immunodeficiency.	Typically not a chronic inflammatory state; episodes are acute bacterial/viral.	Workup includes nasal endoscopy, CT, allergy testing, and immunological evaluation to identify correctable causes (e.g., deviated septum, concha bullosa, allergic rhinitis).
2. Phenotype	CRS with Nasal Polyps (CRSwNPs)	Chronic inflammation with bilateral nasal polyps visible on endoscopy.	• Polyps are pale, glistening, grape-like masses. • Often bilateral and diffuse. • Strong association with asthma and aspirin sensitivity (Samter’s triad). • Higher recurrence risk after surgery.	Eosinophilic-driven, Type 2 inflammation • Cells: eosinophils, mast cells, basophils, Th2 lymphocytes. • Mediators: IL-4, IL-5, IL-13, IgE. • Associated with atopy, fungal sensitization, AERD.	• Responds well to topical/systemic corticosteroids and biologics (anti-IgE, anti-IL-5). • Surgery (FESS) improves drug delivery, but recurrence is common. • Requires management of comorbid asthma.
	CRS without Nasal Polyps (CRSsNPs)	Chronic inflammation without polyps; often more localized disease.	• May be associated with anatomical obstruction (deviated septum, concha bullosa, Haller cells, etc.). • Biofilm formation common in diffuse cases. • Odontogenic origin in ~10% of localized cases. • Discharge is often mucopurulent.	Neutrophilic or mixed inflammation; Type 1 or Type 3 • Cells: neutrophils, Th1/Th17 lymphocytes. • Mediators: IFN-γ, IL-17, TNF-α. • Biofilms (P. aeruginosa, S. aureus) contribute to antibiotic resistance.	• Medical therapy: long-term macrolides (anti-inflammatory effect), saline irrigations, treatment of underlying anatomical issues. • Surgery (FESS) aimed at restoring ventilation and drainage; outcome generally better than CRSwNPs if anatomical obstruction is corrected.
3. Extent of Disease	Localized Disease	Inflammation confined to a single sinus or a limited anatomical region.	• Examples: isolated maxillary sinusitis, frontal sinusitis, or sphenoiditis. • Antrochoanal polyp (unilateral, arising from maxillary sinus) is a localized form of CRSwNPs. • Often caused by anatomical variation or odontogenic source.	Pathophysiology depends on underlying cause (e.g., obstruction, dental infection).	Management can be targeted (e.g., endoscopic antrostomy for isolated maxillary, dental extraction, balloon sinuplasty). Usually has a good prognosis after correcting the local factor.
	Diffuse Disease	Involvement of multiple sinuses on one or both sides.	• Pansinusitis: all sinuses on one side affected. • Bilateral diffuse polyposis indicates a systemic inflammatory condition (e.g., AERD, eosinophilic CRS, cystic fibrosis, primary ciliary dyskinesia). • Often associated with biofilms and more severe symptoms.	Diffuse inflammation often driven by systemic factors (Type 2 immunity in CRSwNPs; biofilm-related in CRSsNPs).	Requires comprehensive management of underlying systemic condition. Surgery (complete FESS) is often necessary but recurrence is common. May require biologic agents or long-term anti-inflammatory therapy.

 

Acute Rhinosinusitis (ARS)

• Causative Organisms for ARS. Acute rhinosinusitis affects millions of people annually, ranking among the most common reasons for outpatient visits. Viral aetiology accounts for approximately 98% of all cases. The most common viral pathogens include rhinoviruses (50%), influenza viruses, parainfluenza viruses, adenoviruses, respiratory syncytial virus, and enteroviruses.
• Pathophysiology of ARS. The pathogenesis begins with viral infection of the nasal and sinus mucosa, causing ciliary dysfunction, mucosal oedema, and obstruction of sinus ostia. This obstruction leads to stagnation of secretions, creating an environment conducive to bacterial superinfection—less than 2% of patients with viral ARS progress to develop acute bacterial rhinosinusitis (ABRS). The “double sickening” phenomenon (worsening after initial improvement) is classic for this transition.

Acute Bacterial Rhinosinusitis (ABRS)

When bacterial superinfection occurs, the most common pathogens include Streptococcus pneumoniae (27%), Haemophilus influenzae (44%), and Moraxella catarrhalis (14%). Less commonly, Streptococcus pyogenes and Staphylococcus aureus may be implicated. Dental infections can introduce anaerobic organisms and mixed flora.

Diagnostic Criteria for ABRS:

The diagnosis of ABRS requires at least three of the following five features:

1. Purulent nasal discharge (thick, discoloured secretions)
2. Severe facial pain, typically unilateral and localised
3. Fever exceeding 38°C (100.4°F)
4. Elevated ESR or CRP on laboratory testing
5. “Double sickening” phenomenon (deterioration after initial improvement)

The gold standard for confirming ABRS remains positive bacterial culture from maxillary sinus aspirate. However, this invasive procedure carries patient morbidity and requires specialist expertise. Therefore, clinicians typically rely on clinical criteria for diagnosis.

Treatment of Acute Rhinosinusitis

1. Viral ARS Management: Treatment focuses on symptomatic relief and supportive care. Nasal saline irrigation (nasal douching) helps clear mucus, proinflammatory mediators, and crusts. Steam inhalation provides symptomatic relief by moisturising the nasal passages. Intranasal corticosteroids reduce mucosal oedema and inflammation, though their benefit in viral ARS remains modest. Oral decongestants (pseudoephedrine) and topical decongestants (oxymetazoline, xylometazoline) provide temporary relief of nasal congestion. However, we must caution patients against using topical decongestants for more than 5-7 days to prevent rhinitis medicamentosa (rebound congestion).
2. Acute Bacterial Rhinosinusitis Management: When ABRS is diagnosed, antibiotic therapy becomes necessary. Amoxicillin-clavulanate (co-amoxiclav) represents the first-line empiric therapy for adults, administered for 5-7 days. This combination covers beta-lactamase-producing strains of H. influenzae and M. catarrhalis. Second-line antibiotics include respiratory fluoroquinolones (levofloxacin, moxifloxacin) or the combination of clindamycin with a third-generation cephalosporin (cefixime or cefpodoxime). These options are reserved for patients with penicillin allergy or those who fail first-line therapy.
3. Adjunctive Therapies: Managing underlying allergic rhinitis reduces the risk of recurrent ARS episodes. Nasal decongestants provide symptomatic relief but do not shorten the overall duration of illness. Analgesics (paracetamol, ibuprofen) help control pain and fever.

Classification of Acute Sinusitis by Anatomical Site 

Features	Maxillary Sinusitis	Frontal Sinusitis	Ethmoid Sinusitis	Sphenoid Sinusitis
ETIOLOGY
Most Common Cause	Viral rhinitis; dental infections (periapical abscess, oroantral fistula); swimming/diving in contaminated water; penetrating trauma of the maxilla.	Viral URI; secondary to maxillary/ethmoid sinusitis; swimming/diving; external trauma.	Associated with infection of other sinuses; common in infants/children (ethmoids present at birth).	Usually part of pansinusitis; rarely isolated; often with posterior ethmoiditis.
Anatomical Predisposition	Most commonly involved sinus. Ostium lies high on the medial wall → dependent drainage → retention of secretions.	Frontonasal duct obstruction due to oedema.	Multiple thin-walled cells; early development in children.	Deep location near the skull base; close to the optic nerve, cavernous sinus.
CLINICAL FEATURES
Pain Location	Upper jaw, gums, teeth; may refer to the forehead.	Forehead (supraorbital).	Bridge of the nose, medial and deep to the eye.	Occiput, vertex; may radiate to the mastoid.
Headache Pattern	Dull, aggravated by stooping, coughing, and chewing.	Periodic (office headache): starts on waking, increases, peaks midday, subsides by evening.	Worsens with eye movement.	Constant, deep-seated; no periodicity.
Tenderness	Anterior maxillary wall (cheek) on palpation/percussion.	Floor of frontal sinus (just above the medial canthus) on upward pressure; tapping over the anterior wall.	Medial canthus (deep).	No external tenderness.
Nasal Discharge	Pus/mucopus in the middle meatus. Postural test: after decongestion, turning the head, discharge appears in the middle meatus.	Vertical streak of mucopus in the anterior part of the middle meatus. May be absent if the ostium is closed.	Middle meatus (anterior ethmoid) or superior meatus (posterior ethmoid).	Postnasal drip; pus on the roof and posterior wall of the nasopharynx or above the superior turbinate.
Other Signs	Redness/oedema of cheek (especially children); puffy lower eyelid; fever, malaise.	Upper eyelid oedema; conjunctival suffusion; photophobia; fever.	Bilateral eyelid oedema/puffiness; increased lacrimation; early orbital cellulitis.	Often no external signs.
DIAGNOSIS
Physical Exam	Anterior rhinoscopy/endoscopy: pus in the middle meatus. Postural test positive.	Nasal endoscopy: pus high in the anterior middle meatus.	Endoscopy: pus in the middle or superior meatus; swollen middle turbinate.	Posterior rhinoscopy/endoscopy: pus on the nasopharynx roof or above the middle turbinate.
Imaging	Transillumination: opacity. Water’s view X-ray: opacity or fluid level. CT: provides superior detail	Water’s & lateral X-ray: opacity/fluid level. CT: preferred.	CT: essential; early complications better visualised.	Lateral X-ray (supine/prone) for fluid level. CT: mandatory for diagnosis and surgical planning.
TREATMENT
Medical	Antibiotics (amoxicillin-clavulanate), nasal decongestant drops (1% ephedrine, 0.1% xylometazoline), steam inhalation, analgesics, and hot fomentation.	Same + placing vasoconstrictor-soaked pledget in the middle meatus once/twice daily to relieve ostial oedema.	Same medical principles as maxillary.	Same medical principles as other sinuses.
Surgical	– Antral puncture and irrigation: Allows removal of pus and exudates – Intranasal antrostomy: Creates a window in the inferior meatus for drainage – Caldwell-Luc operation: Sublabial approach to remove irreversible disease and create an inferior meatal window	– Intranasal drainage procedures: Correct anatomical obstruction, remove polyps – Trephination: External drainage when medical therapy fails – External frontoethmoidectomy (Howarth or Lynch operation): Creates a new frontonasal duct – Osteoplastic flap operation: Allows complete mucosal removal and sinus obliteration with fat	– Intranasal ethmoidectomy: Removes ethmoid air cells and diseased tissue – External ethmoidectomy: Medial orbital approach, often combined with frontal and sphenoid surgery	Endoscopic sphenoidotomy or through external ethmoidectomy if medical fails.
COMPLICATIONS
Local Spread	Progression to subacute/chronic sinusitis; frontal sinusitis (due to oedema); osteitis/osteomyelitis of maxilla, Orbital cellulitis or abscess	Orbital cellulitis; osteomyelitis of the frontal bone with fistula; chronic frontal sinusitis.	Orbital cellulitis/abscess; visual deterioration/blindness (optic nerve); cavernous sinus thrombosis; intracranial complications (extradural abscess, meningitis, brain abscess).	Cavernous sinus thrombosis; meningitis; optic nerve involvement.
Intracranial	Rare	Meningitis, extradural abscess, frontal lobe abscess (if infection breaks through the posterior wall).	Meningitis, brain abscess.	Meningitis, brain abscess.

Chronic Rhinosinusitis (CRS)

• Pathophysiology of CRS. Chronic rhinosinusitis represents a complex inflammatory condition lasting more than 12 weeks despite appropriate medical therapy. Unlike acute sinusitis, CRS involves persistent inflammation rather than infection, though bacterial colonisation and biofilms play important roles. The initial acute infection destroys normal ciliated epithelium, impairing drainage from the sinus. Pooling and stagnation of secretions invite persistent infection, causing further mucosal changes, including loss of cilia, oedema, and polyp formation. This vicious cycle continues indefinitely without appropriate intervention.
• Clinical Features. Clinical features often remain vague and subtle compared to acute sinusitis. Purulent nasal discharge represents the most common complaint. Foul-smelling discharge suggests anaerobic infection. Local pain and headache are typically mild except during acute exacerbations. Some patients complain primarily of nasal stuffiness and anosmia.

Types of Chronic Rhinosinusitis (CRS)

1. CRS with Nasal Polyps (CRSwNPs) – Localised/Antrochoanal Polyp (AC Polyp) and Diffuse Nasal Polyposis (Ethmoidal polyps)
2. CRS without Nasal Polyps (CRSsNPs) – Primary CRS and Secondary CRS

CRS with Nasal Polyps (CRSwNPs): Click on the link: https://www.entlecture.com/nasal-polyps/

CRS without Nasal Polyps (CRSsNPs)

CRSsNPs demonstrate fibrosis, basement membrane thickening, goblet cell hyperplasia, oedema, and mononuclear cell infiltration. Unlike CRSwNPs, this form lacks polyp formation and typically involves neutrophilic inflammation.

Primary CRS: Primary CRS arises from intrinsic mucosal inflammation, local bacterial infection, and mucociliary dysfunction. It divides into localised and diffuse types.

• Localised CRS: Anatomical variations predispose to inflammation limited to one sinus. These variations include Haller cells (infraorbital ethmoidal air cells), concha bullosa (pneumatized middle turbinate), deviated nasal septum, paradoxical middle turbinate, paradoxical uncinate process, and large bulla ethmoidalis. Approximately 10% of localised CRS cases have an odontogenic cause, particularly an unnoticed oroantral fistula following dental extraction.
• Diffuse CRS: Pansinus involvement associates with biofilm formation. Biofilms represent bacterial colonies that develop a polysaccharide matrix around themselves, conferring resistance to antibiotics. This resistance explains why some patients fail to respond to conventional antimicrobial therapy. Bacterial species involved in biofilm formation include Pseudomonas aeruginosa, Staphylococcus aureus, Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis.

Treatment of Chronic Rhinosinusitis

Medical Management of CRS. Medical therapy aims to reduce inflammation, decrease bacterial load, and optimise ciliary function by removing mucus.

1. First-line therapy (for all CRS patients): Start high-volume nasal saline irrigation (>150 mL per side daily) along with intranasal corticosteroids (INCS). Use high-potency sprays (mometasone furoate, fluticasone propionate) or steroid irrigations (budesonide respules 0.5 mg/2 mL added to saline) for CRSwNP, and standard-dose INCS for CRSsNP.
2. Second-line therapy (persistent or uncontrolled CRS): Add short-course oral steroids (Prednisolone 0.5-1 mg/kg/day for 5-14 days with a taper) for severe CRSwNP exacerbations, and consider macrolides (clarithromycin 250 mg daily for 3–12 weeks) in CRSsNP with normal IgE. Use doxycycline (100 mg daily for 3 weeks) in CRSwNP with raised IgE, and add montelukast 10 mg daily especially in asthma/AERD patients.
3. Third-line therapy (refractory CRSwNP despite medical therapy ± surgery): Use biologics targeting Type 2 inflammation, such as dupilumab (300 mg SC every 2 weeks), mepolizumab (100 mg SC every 4 weeks), or omalizumab (75–600 mg SC every 2–4 weeks), particularly in severe recurrent polyposis with asthma.

Surgical Management of CRS

1. Preoperative Evaluation: A CT scan of the nose and paranasal sinuses is mandatory before any surgical intervention. The scan should include axial, coronal, and sagittal cuts, with coronal cuts serving as the surgical “road map.” When using navigation systems during surgery, CT cuts of 1 mm thickness in DICOM format are required.
2. Functional Endoscopic Sinus Surgery (FESS). Click on the link to read more on FESS: https://www.entlecture.com/functional-endoscopic-sinus-surgery-fess/During FESS, injury to the anterior ethmoidal artery can cause orbital hematoma. The anterior ethmoidal artery, a branch of the ophthalmic artery, leaves the orbit through the anterior ethmoidal foramen between the superior oblique and medial rectus muscles. On coronal CT, it appears as a projection in the lamina called Kennedy’s nipple. The artery then courses through the nasal cavity to supply the septum.
3. Balloon Sinuplasty: This minimally invasive technique uses balloon dilation of sinus ostia. It is indicated for localised CRSsNP affecting the frontal, sphenoid, or maxillary sinuses. The procedure can be performed in an outpatient setting under local anaesthesia. When combined with FESS, it is called a hybrid procedure.

Secondary CRS (Systemic Conditions). Several systemic conditions cause or contribute to chronic rhinosinusitis:

1. Granulomatous Diseases: Wegener’s granulomatosis (granulomatosis with polyangiitis), sarcoidosis, and tuberculosis
2. Ciliary Dyskinesias: Primary ciliary dyskinesia and Kartagener’s syndrome (situs inversus, bronchiectasis, chronic sinusitis)
3. Immunodeficiency: HIV, chemotherapy-induced, immunosuppressive drugs, IgA and IgG deficiency
4. Cystic Fibrosis: Abnormal sweat test, CFTR gene mutation on chromosome 7
5. Churg-Strauss Syndrome: Eosinophilic granulomatosis with polyangiitis
6. Atrophic Rhinitis: Excessive crusting following radical nasal surgery
7. Metabolic Conditions: Malnutrition, low BMI

Complications of Rhinosinusitis

Complications are more common in acute bacterial infections, but can occur in CRS.

1. Orbital Complications (Chandler Classification). Ethmoid sinusitis is the most common source of orbital complications.

• Preseptal cellulitis – lid oedema, no proptosis
• Orbital cellulitis – Pain, fever, mild proptosis
• Subperiosteal abscess – Proptosis, restricted eye movement
• Orbital abscess – Severe proptosis, vision threat
• Cavernous sinus thrombosis – Bilateral signs, cranial nerve palsy

2. Intracranial Complications – Meningitis, Epidural abscess, Subdural empyema, Brain abscess (frontal lobe), Cavernous sinus thrombosis. The Warning Features are severe headache, vomiting, altered sensorium and seizures

3. Bony Complications – Osteomyelitis of the frontal bone and Pott’s puffy tumour (frontal swelling due to osteomyelitis)

Management of Complications

• Admit patient
• IV broad-spectrum antibiotics
• Contrast CT/MRI
• ENT + ophthalmology/neurosurgery referral
• Drain the abscess if required
• Emergency surgery for vision-threatening disease

—-End of the Chapter—-

High-Yield Points (NEET PG & University Exams)

• Definition: Rhinosinusitis = inflammation of the nasal cavity AND paranasal sinuses.
• Diagnosis: Requires symptoms (2 of: blockage/discharge +/- pain/anosmia) AND objective evidence (endoscopy or CT).
• Acute: <12 weeks. Viral (98%) vs. Bacterial (ABRS, <2%).
• Chronic: >12 weeks with objective evidence. Subdivided into CRSwNP and CRSsNP.
• Pathogenesis: ARS = viral infection → obstruction → bacterial superinfection. CRS = chronic inflammation driven by Type 2 (CRSwNP) or Type 1/3 (CRSsNP) immune dysregulation.
• Red Flags: Periorbital swelling, proptosis, visual changes, frontal swelling (Pott’s), severe headache, neurological signs.
• Key Anatomical Structure: Osteomeatal complex (OMC) – final common pathway for sinus drainage.
• First-Line Rx for CRS: High-volume saline irrigations + intranasal corticosteroids.
• ABRS First-Line Antibiotic: Amoxicillin-clavulanate for 5-7 days.
• CRSsNP Therapy: Long-term macrolides (clarithromycin) for their anti-inflammatory effect.
• CRSwNP Therapy: Topical/systemic steroids; biologics for refractory cases.
• Biologics: Dupilumab (anti-IL-4Rα), mepolizumab (anti-IL-5), omalizumab (anti-IgE). Indicated for severe, recalcitrant CRSwNP.
• Imaging: CT for pre-op planning; MRI for soft tissue differentiation (tumour vs. fungal vs. inflammation).
• Lund-Mackay Score: CT scoring system (0-24).
• Surgery (FESS): Indicated for failed medical therapy, complications, mucoceles, and polyps. Goal = restore ventilation and drainage.
• Major FESS Complications: CSF leak, orbital hematoma, blindness, and carotid injury.
• Orbital Complications (Chandler): Preseptal cellulitis → Orbital cellulitis → Subperiosteal abscess → Orbital abscess → Cavernous sinus thrombosis.
• Pott’s Puffy Tumour: Osteomyelitis of the frontal bone presents as forehead swelling.
• Differential: Allergic rhinitis, migraine, dental pain, GPA, tumour.
• Prognosis: CRSsNP is generally better than CRSwNP. Type 2 inflammation, asthma, AERD = worse prognosis.

Common Examiner Questions

• Why is it called rhinosinusitis and not sinusitis?
• What is osteomeatal complex and why is it important?
• What are EPOS criteria?
• How will you differentiate viral ARS from ABRS?
• What is the treatment of antrochoanal polyp?
• What is the CT sign of allergic fungal sinusitis?
• Which sinus causes orbital cellulitis most commonly?
• Indications of FESS?

NEET PG Style MCQs (10 Questions)

1. According to EPOS, diagnosis of chronic rhinosinusitis requires symptoms for at least: A. 4 weeks B. 8 weeks C. 12 weeks D. 24 weeks
2. The most common sinus involved in acute sinusitis is: A. Frontal B. Ethmoid C. Maxillary D. Sphenoid
3. “Office headache” with pain peaking at midday is typical of: A. Maxillary sinusitis B. Ethmoid sinusitis C. Frontal sinusitis D. Sphenoid sinusitis
4. The sinus most commonly responsible for orbital cellulitis in children is: A. Maxillary B. Ethmoid C. Frontal D. Sphenoid
5. A unilateral polyp arising from maxillary sinus extending into choana is: A. Ethmoidal polyp B. Antrochoanal polyp C. Inverted papilloma D. Juvenile angiofibroma
6. The best imaging modality to plan FESS is: A. X-ray Water’s view B. MRI brain C. CT PNS (coronal cuts) D. Ultrasonography
7. “Double density sign” on CT is typical of: A. Atrophic rhinitis B. Allergic fungal rhinosinusitis C. Nasopharyngeal carcinoma D. CSF rhinorrhea
8. Samter’s triad includes all except: A. Asthma B. Nasal polyposis C. Aspirin sensitivity D. Allergic rhinitis
9. Most common organism causing acute bacterial rhinosinusitis is: A. Pseudomonas aeruginosa B. Haemophilus influenzae C. Mycobacterium tuberculosis D. Candida albicans
10. Surgery of choice for chronic rhinosinusitis with polyps is: A. Caldwell-Luc operation B. Polypectomy alone C. Functional endoscopic sinus surgery D. Septoplasty only

Answers with Explanations

1. C 2. C 3. C 4. B 5. B 6. C 7. B 8. D 9. B 10. C

—-End—-

Reference Textbooks.

• Scott-Brown, Textbook of Otorhinolaryngology-Head and Neck Surgery.
• Cummings, Otolaryngology-Head and Neck Surgery.
• Stell and Maran’s Textbook of Head and Neck Surgery and Oncology.
• Ballenger’s, Otorhinolaryngology Head And Neck Surgery
• Susan Standring, Gray’s Anatomy.
• Frank H. Netter, Atlas of Human Anatomy.
• B.D. Chaurasiya, Human Anatomy.
• P L Dhingra, Textbook of Diseases of Ear, Nose and Throat.
• Hazarika P, Textbook of Ear Nose Throat And Head Neck Surgery Clinical Practical.
• Mohan Bansal, Textbook of Diseases of Ear, Nose and Throat Head and Neck Surgery.
• Hans Behrbohm, Textbook of Ear, Nose, and Throat Diseases With Head and Neck Surgery.
• Logan Turner, Textbook of Diseases of The Nose, Throat and Ear Head And Neck Surgery.
• Arnold, U. Ganzer, Textbook of  Otorhinolaryngology, Head and Neck Surgery.
• Ganong’s Review of Medical Physiology.
• Guyton & Hall Textbook of Medical Physiology.

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