DNB Otorhinolaryngology ENT Paper 2 — Model Answers

Question 1 [10 Marks]

a) Clinical Features of Type 2 Disease in a Patient of Chronic Rhinosinusitis [3]

• CRS with nasal polyps (CRSwNP) in >80% of cases
• Severe anosmia/hyposmia — often the dominant symptom
• Bilateral, recurrent, large nasal polyps
• Asthma association in 30–50% (the "united airway" concept)
• Aspirin/NSAID hypersensitivity (Samter's triad: CRSwNP + asthma + aspirin sensitivity)
• High recurrence rate after FESS
• Elevated peripheral eosinophil count (>300 cells/µL)
• Elevated serum IgE and tissue eosinophils on biopsy
• Poor response to topical steroids alone
• Thick, eosinophilic mucin in sinuses
• Central olfactory cleft involvement on CT/MRI

b) Indications for Surgical Treatment in Type 2 Disease [3]

1. Failure of maximum medical therapy (topical + systemic steroids, saline irrigation, antibiotics) for ≥12 weeks
2. Extensive nasal polyps (grade 3–4) obstructing nasal airway
3. Symptomatic sinus obstruction with recurrent acute-on-chronic sinusitis
4. Orbital/intracranial complications
5. Suspected malignancy requiring biopsy
6. Mucocele formation
7. Before initiation of biologics — FESS reduces polyp bulk and improves drug penetration
8. Anosmia unresponsive to medical treatment
9. Patient preference and quality-of-life impairment (SNOT-22 score >20)

c) Various Biologicals and Indications in Chronic Rhinosinusitis [2+2]

• Bilateral polyps on endoscopy
• ≥3 of: tissue eosinophilia, elevated total IgE, comorbid asthma, NSAID sensitivity, loss of smell, polyp recurrence after 2 prior surgeries
• Failed FESS + maximal medical therapy
• Oral steroid-dependent disease
• Significantly impaired QoL (SNOT-22 >40)

Question 2 [10 Marks]

a) Surgical Steps of Endoscopic Sphenopalatine Artery Ligation [5]

• Decongestion with topical oxymetazoline or cocaine
• Endoscopy and nasal examination under GA
• Endotracheal intubation (to protect airway)
• Head-ring position, 0° or 30° Hopkins rod endoscope

1. Uncinectomy and middle meatal antrostomy to gain access to the posterior nasal space
2. Identification of the posterior fontanelle — the mucosal fold at the posterior end of the middle meatus
3. Mucosal incision — vertical incision at the posterior attachment of the middle turbinate to the lateral nasal wall, approximately 1 cm anterior to the posterior wall of the maxillary sinus
4. Elevation of the mucoperiosteal flap anteriorly and posteriorly to expose the SPF on the medial wall of the pterygopalatine fossa
5. Identification of the crista ethmoidalis — a bony ridge that is a reliable landmark pointing to the SPF
6. Exposure of the SPA — the artery exits through the SPF and divides into the posterior nasal (septal) artery and the nasopharyngeal branch. Multiple branches (1–3) may be present
7. Haemostasis:
   • Bipolar diathermy (preferred): The artery is desiccated with a 2mm bipolar forceps
   • Or: Haemoclips (surgical clips) applied to the main trunk
   • All visible branches must be clipped/cauterised to prevent recurrence
8. Check for haemostasis — the nasal cavity is inspected; the mucosal flap is repositioned
9. Post-operative care: Nasal packing for 24–48 hours; antibiotics; moisturising nasal sprays

b) Clinical Features, Diagnosis and Management of Juvenile Recurrent Parotitis [5]

• Age: Usually 3–6 years; can extend to puberty
• Episodic unilateral parotid swelling (left > right)
• Accompanying pain, fever, malaise
• Trismus may be present during acute episodes
• Milky/turbid saliva expressed from Stensen's duct
• Episodes last 2–7 days; frequency: 2–3 times/year
• Spontaneous resolution often at puberty
• No systemic disease in primary JRP
• Associated with: Sjogren's syndrome (secondary JRP), HIV infection, IgA deficiency

• Ultrasound: Multiple hypoechoic areas within the parotid parenchyma; dilated ducts; absence of calculi (differentiates from sialolithiasis)
• Sialography: Punctate/globular sialectasis ("snowstorm" appearance) — gold standard for diagnosis
• MR sialography: Non-invasive alternative; shows dilated ducts
• Serology: Rule out Sjogren's (anti-Ro/SSA, anti-La/SSB antibodies), HIV
• Salivary flow rate and IgA levels
• Biopsy (rarely needed): Lymphocytic infiltration, acinar atrophy

• Warm compresses, analgesics, hydration
• Sialagogues (lemon drops) to stimulate saliva flow
• Antibiotics: Amoxicillin-clavulanate for bacterial superinfection
• Massage of the gland from posterior to anterior

• Parotid duct irrigation (sialendoscopy): Saline/saline + corticosteroid irrigation via Stensen's duct — most effective intervention; dilates the duct, flushes debris, reduces inflammation. Success rate >90%
• Sialendoscopy: Diagnostic and therapeutic; permits direct visualisation, lavage, and balloon dilation of strictures
• Intraductal steroid injection (hydrocortisone, methyl prednisolone)

• Parotidectomy: Reserved for refractory cases with parenchymal destruction; rare given risk to facial nerve
• Duct ligation/parotid neurectomy: Rarely used

Question 3 [10 Marks]

a) Various Open Surgical Approaches for Frontal Sinus Disease [4]

• Small incision in the medial eyebrow or glabella
• A trephine/drill creates a hole in the anterior wall of the frontal sinus
• Used for: Acute frontal sinusitis with intracranial/orbital complications, access for irrigation and ventilation
• Minimally invasive; used as bridge procedure

• Incision: Lynch incision (midway between medial canthus and dorsum of nose)
• Removal of anterior ethmoid cells, lacrimal bone, and floor of the frontal sinus
• Creates fronto-nasal communication
• Drawback: High rate of re-stenosis (cicatricial closure) of the fronto-nasal tract

• Gold standard open procedure for chronic frontal sinusitis
• Approach: Coronal (bicoronal) incision or "gull-wing"/brow incision; the anterior wall of frontal sinus is osteotomised using a template derived from Caldwell X-ray (PA view at 6-foot distance)
• The mucosal lining is completely stripped
• Sinus cavity obliterated with abdominal fat graft (adipose tissue)
• Indications: Failed FESS, frontal sinus osteoma, frontal sinus trauma, neo-osteogenesis (NOS) obliterating the frontal recess, frontal sinus mucocele
• Complications: Fat resorption, mucocele formation, osteomyelitis, numbness of scalp, alopecia along incision

• Entire frontal sinus mucosa removed; posterior wall drilled away; sinus merges with anterior cranial fossa
• Used for frontal sinus fractures, osteomyelitis, or when sinus cannot be reconstructed

• Sublabial incision with anterior maxillary wall fenestration; occasionally combined for drainage

b) What is Hybrid FESS? [2]

• Endoscopic endonasal approach (FESS) — from below, working upward through the nose into the frontal recess (Draf I/IIa/IIb/III)
• External approach — from above, typically frontal sinus trephination or osteoplastic flap

• When the frontal sinus cannot be adequately accessed endoscopically alone (e.g., hyperpneumatized frontal sinus, complex anatomy, frontal sinus osteoma extending laterally)
• Allows simultaneous endoscopic visualisation from below with instrumentation from above (trephine)
• Facilitates retrograde or antegrade approach to the frontal recess

c) Indications of Frontal Balloon Sinuplasty [4]

1. Chronic frontal sinusitis (CRS with or without nasal polyps) unresponsive to medical treatment — mild to moderate disease
2. Acute recurrent frontal sinusitis — ≥4 episodes/year with documented sinus opacification
3. Frontal sinus barotrauma (inability to equalize pressure — aviators, divers)
4. Isolated frontal sinusitis without extensive ethmoid disease
5. Revision cases with scarring/adhesions around the frontal ostium where conventional FESS risks injury
6. Paediatric frontal sinusitis — reduces risk of injury to developing structures
7. Office-based procedure in medically fit patients where GA is undesirable
8. As adjunct to FESS for frontal recess opening (hybrid balloon + conventional FESS)

• Frontal sinus osteoma
• Grade 4 nasal polyps obliterating frontal recess
• Neo-osteogenesis (Draf III may be preferred)
• Frontal sinus mucocele (needs wide drainage)
• Sinonasal malignancy

Question 4 [10 Marks]

a) Indications of Dacryocystorhinostomy (DCR) [2]

1. Primary acquired nasolacrimal duct obstruction (PANDO) — most common indication; idiopathic fibrotic obstruction of the NLD
2. Dacryocystitis — acute/chronic; recurrent lacrimal sac infection with mucocele formation
3. Failed nasolacrimal duct probing/syringing in adults
4. Post-traumatic NLD obstruction (nasal bone fracture, midfacial trauma)
5. Iatrogenic NLD obstruction — post-rhinoplasty, post-endoscopic sinus surgery, post-radiotherapy
6. Lacrimal sac mucocele/pyocele
7. Functional epiphora — patent NLD on syringing but symptomatic tearing (pump failure)
8. Prior to DCR-assisted lacrimal bypass tube (Jones tube) insertion

b) Advantages of Endoscopic DCR over External DCR [3]

• No disruption of medial canthal tendon
• Better illumination and magnification
• Simultaneous correction of sinonasal disease causing secondary NLD obstruction
• Suitable for trauma cases with medial canthal disruption (avoids further scarring)

c) Complications of Endoscopic DCR [3]

• Haemorrhage: From angular/dorsal nasal vessels, anterior ethmoidal artery
• Orbital fat herniation: If periorbita is breached (medial orbital wall is very thin — lamina papyracea)
• CSF leak: If ethmoid roof is inadvertently opened
• Damage to medial rectus muscle or optic nerve (rare)

• Haemorrhage/epistaxis: Most common early complication
• Infection: Dacryocystitis, cellulitis
• Tube displacement/extrusion of silicone stent

• Rhinostomy closure/stenosis: Most common cause of failure; due to granulation tissue or scarring at the anastomosis
• Granuloma formation at rhinostomy
• Canalicular injury during cannulation
• Cheese-wiring of canaliculus by silicone stent
• Persistent epiphora — functional failure
• Synechia formation — between rhinostomy and middle turbinate
• Mucocele formation if rhinostomy is too small

d) What is Lacrimal Sump Syndrome and How is it Avoided? [2]

• It is a complication of external DCR where the rhinostomy is created too high (superiorly) on the lacrimal sac
• This leaves a dependent, blind-ended inferior pouch (the "sump") of the lacrimal sac below the level of the rhinostomy
• Tears and debris collect in this sump but cannot drain
• Results in: Persistent epiphora, mucopurulent discharge, and recurrent dacryocystitis despite a patent rhinostomy

1. Make the rhinostomy at the correct level — the anastomosis should be at the level of the medial canthal tendon/equator of the lacrimal sac, ensuring all of the sac drains
2. Create a large rhinostomy — at least 10–15 mm in diameter; large anastomosis prevents sump formation
3. Endoscopic DCR advantage: Endoscopic approach allows better visualisation of the inferior sac, reducing the risk of high rhinostomy placement
4. Management of established sump syndrome: Revision DCR — excision of the inferior sac remnant or conversion to endoscopic DCR with a more inferiorly placed ostium

Question 5 [10 Marks]

Aetiology of BIH (Idiopathic Intracranial Hypertension — IIH)

• Obese women of childbearing age (classic patient — BMI >30)
• Tetracycline, doxycycline, isotretinoin, vitamin A toxicity
• Steroid withdrawal
• Oral contraceptives
• Hypothyroidism, Addison's disease
• Anaemia, SLE, venous sinus thrombosis

Radiological Features Seen in BIH/IIH [2]

• Empty sella turcica (partial/complete flattening of pituitary gland)
• Small ventricles (slit-like ventricles)
• No mass lesion, hydrocephalus, or cerebral oedema

1. Empty sella — herniation of subarachnoid space into sella, flattening the pituitary gland
2. Perioptic subarachnoid space distension — widening of CSF space around the optic nerve sheath
3. Posterior globe flattening — flattening of the posterior sclerae (pathognomonic sign)
4. Transverse venous sinus stenosis — narrowing of the transverse and sigmoid sinuses on MRV
5. Optic nerve tortuosity on orbital MRI
6. Skull base thinning — especially in the lateral recess of the sphenoid sinus and cribriform plate — this leads to CSF rhinorrhoea
7. High-riding jugular bulb

• Gold standard for localising the CSF leak site
• Demonstrates contrast or CSF tracking through the skull base defect into the nasal cavity

• Thinning or dehiscence of the cribriform plate, fovea ethmoidalis, or lateral sphenoid recess
• Site-specific defect identification

Clinical Features, Diagnosis and Management [2+6]

• Obese female, typically 20–50 years
• Chronic, unilateral, watery nasal discharge (especially on bending forward or Valsalva)
• Headache — positional, worse on lying down, pulsatile
• Pulsatile tinnitus ("heartbeat in the ear")
• Visual symptoms — transient visual obscurations, diplopia (VI nerve palsy — false localising sign)
• Papilloedema on fundoscopy (may be absent in long-standing cases)
• "Halo sign" — CSF mixed with blood produces a central blood spot with clear halo on filter paper
• Sweet/salty taste of nasal secretions
• Meningitis: Ascending bacterial meningitis is a major complication

1. β-2 transferrin test — gold standard for confirming CSF. This protein is present only in CSF, perilymph, and aqueous humour; not in blood or nasal secretions
2. β-trace protein (prostaglandin D-synthase) — alternative CSF marker
3. Glucose testing of nasal secretion — unreliable; also present in mucus
4. Lumbar puncture: Opening pressure >25 cmH₂O (>20 cmH₂O is suspicious); normal CSF composition
5. MRI brain with cisternography — identifies skull base defect and confirms BIH features
6. CT skull base (HR-CT) — localises defect (cribriform, fovea ethmoidalis, sphenoid)
7. Intrathecal fluorescein — 0.1 mL of 10% fluorescein injected intrathecally 30–60 minutes before endoscopy; green fluorescence seen at the leak site under endoscopy (with blue-light filter)
8. Radionuclide cisternography — useful for slow leaks

• Weight reduction (most important long-term measure in IIH) — target BMI <30
• Acetazolamide (carbonic anhydrase inhibitor) — reduces CSF production, first-line drug; dose 500 mg–2 g/day
• Topiramate — alternative to acetazolamide; also aids weight loss
• Furosemide — adjunct to acetazolamide
• Bed rest, avoidance of Valsalva
• Antibiotics if meningitis develops

• Endoscopic skull base repair (preferred approach):
  • Under GA with intrathecal fluorescein guidance
  • Identify the defect endoscopically
  • Multilayer repair: underlay with fascia lata/fat + overlay with mucoperiosteal flap
  • Fibrin glue and Gelfoam
  • Post-op: Lumbar drain for 48–72 hours to reduce ICP
• Lumbar drain — temporary; reduces CSF pressure to aid healing; used perioperatively
• CSF diversion — if medical treatment fails and repair is not possible:
  • Ventriculoperitoneal (VP) shunt
  • Lumboperitoneal (LP) shunt
• Optic nerve sheath fenestration — for progressive visual loss despite medical therapy
• Venous sinus stenting — emerging treatment for transverse sinus stenosis causing IIH

Question 6 [10 Marks]

a) Classify Various Types of Neck Dissection as per Levels of the Neck Nodes [3]

1. Radical Neck Dissection (RND): Removes levels I–V + SCM + internal jugular vein (IJV) + accessory nerve (CN XI). Gold standard; most morbid.
2. Modified Radical Neck Dissection (MRND):
   • Removes levels I–V but preserves one or more: SCM, IJV, or CN XI
   • Type I MRND: CN XI preserved
   • Type II MRND: CN XI + IJV preserved
   • Type III MRND (Functional/Bocca): CN XI + IJV + SCM preserved
3. Selective Neck Dissection (SND): Removes specific levels based on primary tumour site:
   • Supraomohyoid ND (I–III): Oral cavity tumours
   • Lateral ND (II–IV): Oropharynx, hypopharynx, larynx
   • Posterolateral ND (II–V): Skin/thyroid
   • Central compartment ND (VI): Thyroid/larynx
4. Extended Neck Dissection: Any of the above + removal of additional structures (carotid artery, skin, parapharyngeal nodes, retropharyngeal nodes)

b) Management of N₀ Neck in Oral Cavity Cancer [3]

1. Elective Neck Dissection (END) — Preferred:
   • Supraomohyoid ND (levels I–III) is standard for most oral cavity tumours
   • Indicated when: Depth of invasion (DOI) >4 mm on imaging/pathology (AJCC 8th edition — DOI now incorporated into T staging); T2–T4 lesions; floor of mouth/tongue primaries
   • Advantages: Pathological staging; therapeutic if occult nodes found; avoids missed nodes; sentinel node biopsy may guide extent
   • If pN+: Post-operative radiotherapy to the dissected field
2. Sentinel Lymph Node Biopsy (SLNB):
   • Emerging technique; technetium-99m nanocolloid injected around tumour; gamma probe guides excision of sentinel node(s)
   • If SLN negative: Neck observation
   • If SLN positive: Formal neck dissection
   • Validated for T1–T2 N0 oral cancer
3. "Wait and Watch" with close surveillance:
   • Acceptable only if: Low DOI (<4 mm), T1 lesion, reliable follow-up assured
   • Risk: Late presentation of nodal metastasis may result in worse prognosis
4. Elective neck irradiation: Acceptable when neck is in the radiotherapy field (e.g., post-surgery RT for primary) but inferior to surgery for occult metastases

c) Diagnosis and Management of Chyle Leak Post-operatively [4]

• Classically appears on post-operative day 2–3 (after refeeding)
• High-volume, milky/creamy fluid in drain
• Volume: >500 mL/day suggests significant leak
• Drain output increases after a high-fat meal
• Can lead to hypoproteinaemia, electrolyte disturbances, lymphopenia, immunocompromise

• Clinical: Milky fluid in drain; increases with fat intake
• Triglyceride level >110 mg/dL in drain fluid — confirmatory
• Sudan III staining: Fat globules visible on microscopy
• Lymphocyte count >90% in fluid
• CT neck with oral fat challenge — may localise the defect

1. Dietary modification:
   • Nil by mouth initially or low-fat diet
   • Medium-chain triglyceride (MCT) diet — MCTs absorbed directly into portal blood, bypassing lymphatics; reduces chyle flow
2. Total parenteral nutrition (TPN) — if oral feeding causes high output
3. Octreotide/somatostatin analogue — reduces chyle production; 100 µg TID subcutaneous
4. Pressure dressing over the neck
5. Serial aspirations if not on drain

1. Surgical re-exploration and ligation of the thoracic duct — via cervical or combined thoracoscopic approach
2. Direct suture ligation of the chyle fistula — fibrin glue/haemoclips applied
3. Sclerotherapy — injection of doxycycline, OK-432 into the fistula
4. Thoracic duct embolisation — percutaneous, image-guided; high success rate

Question 7 [10 Marks]

Clinical Features [3]

• Slow-growing, painless, lateral neck mass at the level of the carotid bifurcation (anterior triangle)
• Typically pulsatile; transmitted pulsation
• Fontaine's sign: Horizontal mobility but vertically fixed (due to tethering to carotid vessels)
• Lyre sign on angiography: Widening/splaying of the carotid bifurcation
• Mostly benign; malignancy rate 6–12%
• Bilateral in 5–10% of sporadic cases; 30–50% in familial cases (SDH gene mutations)
• Familial association: SDH-B, SDH-C, SDH-D mutations (succinate dehydrogenase)
• Altitude association: Higher incidence at high altitudes (chronic hypoxia stimulates carotid body)
• Cranial nerve involvement (large tumours):
  • Horner's syndrome (sympathetic chain)
  • Dysphagia (CN IX/X)
  • Hoarseness (CN X)
  • Shoulder weakness (CN XI)
  • Tongue deviation (CN XII)
• Catecholamine secretion in <5% (vasoactive amines — flushing, hypertension, palpitations)

• Type I: Tumour <5 cm, easily dissected from carotid vessels; minimal vessel involvement
• Type II: Tumour intimately adherent to, but not encasing, the carotid arteries
• Type III: Tumour completely encases the common and/or internal carotid artery; requires carotid resection and reconstruction

• Large tumour (typically >5 cm)
• Completely envelopes the internal/external/common carotid artery
• High risk of carotid artery sacrifice
• Significant surgical morbidity (stroke risk, cranial nerve injury)
• May extend to skull base (jugular foramen)

Diagnosis [3]

1. Clinical examination: Pulsatile neck mass with horizontal mobility at carotid bifurcation; bruit may be audible
2. Ultrasound + Doppler: Hyperechoic, hypervascular mass at carotid bifurcation; widened carotid fork; increased vascularity on colour Doppler — confirms feeding vessels
3. CT with contrast (CT angiography): "Salt and pepper" appearance on MRI; highly vascular mass splaying the carotid bifurcation; extent of encasement evaluated — essential for Shamblin staging
4. MRI/MRA: T1: Low signal; T2: Characteristic "flow voids" within tumour (salt and pepper pattern); delineates relationship to skull base, cranial nerves; MRA shows vascular anatomy
5. Digital Subtraction Angiography (DSA):
   • Gold standard for surgical planning
   • Shows "lyre sign" — widening of carotid bifurcation
   • Identifies feeding vessels (ECA branches)
   • Pre-operative embolisation performed at same sitting (reduces intraoperative bleeding)
   • Balloon occlusion test: For Shamblin III, tests adequacy of collateral cerebral circulation if ICA sacrifice anticipated
6. MIBG scan (¹²³I-MIBG): Identifies catecholamine-secreting paragangliomas; rules out multicentre/metastatic disease
7. Urine/plasma catecholamines and metanephrines: Rule out functional tumour (mandatory pre-op)
8. Genetic testing: SDH gene panel (SDHB/C/D) especially if young, bilateral, or familial
9. PET-CT (68Ga-DOTATATE): Superior sensitivity for paragangliomas; detects multicentre or metastatic disease

Management [4]

• Multidisciplinary planning (ENT/vascular surgery/neurosurgery/interventional radiology)
• Pre-operative embolisation (24–48 hours before surgery) to reduce vascularity — reduces intraoperative blood loss by 40–60%
• Balloon occlusion test of the internal carotid artery — neurological monitoring; if passed, ICA sacrifice is safer
• Pre-operative shunting/autologous blood donation — vascular bypass planning
• Catecholamine screen; if elevated — alpha-blockade (phenoxybenzamine) before surgery

1. Surgical excision — mainstay of treatment
   • Position: Supine, head extended and rotated
   • Incision: Longitudinal along anterior border of SCM or "hockey-stick"
   • Proximal and distal control of carotid arteries obtained first (before tumour manipulation)
   • Shamblin III specific: Sub-adventitial dissection in the plane between tumour and adventitia is the key; however, for Type III with complete encasement, this plane is lost
   • Carotid artery resection and reconstruction is required in Type III:
     • Segmental resection of the involved ICA segment
     • Reconstruction with reversed saphenous vein graft or prosthetic graft (PTFE/Dacron)
     • Intraoperative shunting to maintain cerebral perfusion
   • CN X, XII, XI at risk — careful identification and preservation
   • Carotid body "peeling": Blunt dissection between the tumour pseudocapsule and carotid wall
2. Radiotherapy:
   • Not first-line; used for: Unresectable tumours, skull base extension, elderly/poor surgical candidates, residual disease
   • Stereotactic body radiotherapy (SBRT) or conventional fractionated RT
   • Controls growth rather than curing
3. Observation:
   • Elderly patients with small Type I/II tumours; tumours grow slowly (~0.8 cm/year)

• Stroke — most feared; ICA injury or thromboembolism; incidence 5–10% for Type III
• Cranial nerve injury — CN X (hoarseness, dysphagia), CN XII (tongue deviation), CN IX, Horner's syndrome
• Haemorrhage — intraoperative from tumour vascularity
• Wound infection, haematoma
• Carotid occlusion/thrombosis — post-reconstructive

Question 8 [10 Marks]

a) Submandibular Duct Sialolithiasis [5]

• Long, narrow duct (Wharton's duct, 5 cm)
• Saliva flows against gravity (upward direction)
• Thicker, mucous, alkaline saliva
• Higher calcium and phosphate content in submandibular secretions
• Stagnation due to narrow orifice at floor of mouth

• Recurrent, painful swelling of the submandibular gland at mealtimes ("mealtime syndrome")
• Pain and swelling appear with eating and subside within 30–60 minutes
• Tender, palpable lump in the floor of the mouth or neck
• Bimanual palpation: Stone may be palpable in the duct along the floor of the mouth
• Wharton's duct orifice may be oedematous/erythematous
• Purulent discharge from orifice in infected cases
• Chronic cases: Gland becomes fibrotic, indurated, non-tender

• Plain X-ray (occlusal/oblique mandible view): 80% of submandibular stones are radiopaque (calcium phosphate/carbonate); first-line investigation
• Ultrasound: Hyperechoic focus with posterior acoustic shadowing; evaluates gland parenchyma; detects stones >2 mm
• CT (non-contrast): Most sensitive; detects small radiolucent stones; evaluates gland
• Sialography: Filling defect; useful if stone is radiolucent; maps duct anatomy
• MR sialography: Non-invasive; shows strictures and dilatation
• Sialendoscopy: Diagnostic + therapeutic gold standard

• Hydration, sialagogues (sour sweets, lemon), warm compresses, massage
• Antibiotics for acute sialadenitis (amoxicillin-clavulanate)
• NSAIDs for pain

1. Intraoral incision and stone removal (ductotomy):
   • For palpable stones in anterior 2/3 of Wharton's duct (anterior to mylohyoid)
   • Incision over the stone in the floor of the mouth
   • Stone extracted directly; duct marsupialised
   • Safe and effective if stone is distal to mylohyoid
2. Sialendoscopy:
   • For stones <4 mm: Directly visualised and extracted with mini-forceps, basket retrieval, or laser lithotripsy through the endoscope
   • For stones 4–8 mm: Extracorporeal shock wave lithotripsy (ESWL) ± sialendoscopy
   • Combined approach (sialendoscopy + intraoral incision) for large anterior stones
3. Extracorporeal Shock Wave Lithotripsy (ESWL):
   • For stones <7 mm; fragments cleared by natural salivary flow
   • Multiple sessions may be required
4. Laser lithotripsy (holmium:YAG or Tm:YAG through sialendoscope):
   • Fragmenting large intraglandular stones

• For: Posterior stones within the gland hilum inaccessible via ductotomy; chronic sclerotic gland with multiple stones; recurrent sialadenitis with irreversible parenchymal damage; failed endoscopic treatment
• Approach: External cervical incision 2 cm below mandible (Patey's approach)
• Risk: Marginal mandibular branch of facial nerve, lingual nerve, hypoglossal nerve

b) Pleomorphic Adenoma of Deep Lobe of Parotid [5]

• The deep lobe lies medial to the facial nerve (stylomandibular tunnel)
• Bounded by: Medially — parapharyngeal space; laterally — facial nerve; posteriorly — styloid process
• Deep lobe tumours may extend into the parapharyngeal space ("dumbbell tumour" — hourglass shape through the stylomandibular tunnel)

• Slow-growing, painless parotid swelling — may present only as a neck mass
• Classically no facial nerve palsy (malignancy in PA is rare — carcinoma ex-pleomorphic adenoma)
• Oropharyngeal bulge: Deep lobe PA extending into the parapharyngeal space pushes the soft palate and lateral pharyngeal wall medially — visible as a peritonsillar/parapharyngeal bulge
• May be missed on examination if purely deep lobe
• Intraoral examination essential — medialisation of soft palate/tonsil
• No trismus (differentiates from malignant tumours with pterygoid involvement)

• Ultrasound: Limited for deep lobe due to bone shadow
• MRI (investigation of choice): T1 — intermediate signal; T2 — characteristically bright (high water content of chondromyxoid stroma); MRI delineates the relationship to the facial nerve, parapharyngeal extension ("dumbbell" configuration), and tumour capsule
• CT scan: Good for bony involvement; may show parapharyngeal extension
• FNAC (fine needle aspiration cytology): Guided — confirms benign nature; "characteristic" findings: Epithelial cells + myxochondroid stroma; sensitivity ~85%
• Warthin's tumour (bilateral) excluded by Tc-99m pertechnetate scan
• Core biopsy: Rarely needed; risk of seeding if PA

1. Total/Subtotal parotidectomy with facial nerve preservation:
   • The standard approach — superficial parotidectomy + deep lobe dissection
   • The facial nerve is identified at its exit from the stylomastoid foramen and dissected along all its branches
   • The deep lobe is then delivered from medial to the facial nerve (the nerve is elevated and the lobe passed beneath it)
2. Transparotid approach (conventional): Identification of facial nerve trunk → dissection of superficial lobe → elevation of facial nerve → delivery of deep lobe
3. Combined Transparotid-Transcervical approach: For large dumbbell tumours extending into the parapharyngeal space
4. Transcervical approach (mandibulotomy if required): For large parapharyngeal tumours extending inferiorly; stylomandibular ligament divided; rarely requires mandibulotomy
5. Transoral approach: Reserved for small purely parapharyngeal tumours (access through tonsillar fossa)

• Avoid tumour spillage (capsule rupture) — leads to multifocal recurrence (pleomorphic adenoma has a tendency for seeding)
• Cuff of normal parotid tissue should surround the tumour
• Facial nerve monitoring intraoperatively (electromyographic stimulator)

• Facial nerve palsy (temporary > permanent): Most feared; identification at stylomastoid foramen and careful dissection is key
• Frey's syndrome (auriculotemporal syndrome): Gustatory sweating from aberrant reinnervation of parasympathetic fibres to sweat glands; occurs in 30–60% after parotidectomy
• Haematoma, seroma
• Wound infection
• Great auricular nerve damage (numbness of auricle)
• Salivary fistula
• Recurrence: 1–5% after total parotidectomy; much higher (up to 45%) after enucleation — hence total parotidectomy is preferred

Question 9 [10 Marks]

a) Sternberg's Canal [5]

• During development, the sphenoid sinus pneumatises laterally through the greater wing of the sphenoid
• The Sternberg's canal represents the junction between the orbitosphenoidal and alisphenoidal components of the greater wing of the sphenoid — a persistent embryonic synchondrosis or dehiscence
• Described by Sternberg in 1888; this lateral wall defect may be congenitally dehiscent or thin
• Located in the lateral recess of the sphenoid sinus adjacent to the vidian (pterygoid) canal region, close to the carotid canal

• A well-recognised site of spontaneous/non-traumatic CSF rhinorrhoea, particularly in:
  • Obese women with BIH/IIH (high CSF pressure gradually erodes the thin bone)
  • Arachnoid granulations that herniate through the defect (meningocele/meningoencephalocele)
• May contain meninges, brain tissue, or CSF pulsation cyst
• The canal can allow encephalocele (lateral sphenoid encephalocele) to present as a smooth, pulsatile, blue-tinged mass in the nasopharynx
• Diagnosis: High-resolution CT skull base (bone windows) — shows lateral sphenoid defect; MRI — arachnoid/meningeal tissue herniation; CT cisternography confirms CSF leak

• Repair via endoscopic transsphenoidal approach:
  • Wide sphenoidotomy with identification of the lateral recess
  • May require navigation guidance (due to proximity of ICA and optic nerve)
  • Multilayer repair: Adipose tissue plug + fascial overlay + mucosal flap + fibrin glue
  • High-riding or medialised ICA increases surgical risk
  • Some surgeons use a transpterygoid or transorbital approach for better lateral access
• Post-operative ICP management (lumbar drain, acetazolamide) is mandatory to prevent recurrence

b) Internal Nasal Valve [5]

• Medially: Nasal septum (anterior septal angle)
• Laterally: Caudal edge of the upper lateral cartilage (ULC)
• Inferiorly: Head of the inferior turbinate
• Superiorly: Nasal bones

• Normal cross-sectional area: ~40–100 mm²
• Normal valve angle (between septum and ULC): 10–15 degrees in Caucasians (narrower in Asians); less than 10° = stenotic
• Site of maximum nasal airway resistance — accounts for 50% of total respiratory resistance

• The INV acts as a Venturi-like constriction — during inspiration, negative pressure tends to collapse the lateral wall (dynamic collapse), resisted by the stiffness of the ULC
• Cottle's test: Lateral traction on the cheek opens the INV; if nasal breathing improves = positive Cottle test = INV compromise
• Modified Cottle test: Cotton pledget placed in INV to mechanically prop it open

1. Structural: Deviated nasal septum causing angulation at the valve
2. Collapsed/weak upper lateral cartilages (post-rhinoplasty, ageing)
3. Paradoxical middle turbinate
4. Inferior turbinate hypertrophy (head)
5. Synechiae/adhesions at the valve angle
6. Post-traumatic collapse of the nasal dorsum
7. Iatrogenic: Over-resection of ULC during rhinoplasty (inverted-V deformity)

• Nasal obstruction — typically worse on inspiration
• Nasal obstruction worse on the side of septal deviation
• Positive Cottle test
• Flaring of nostrils during inspiration (attempting to widen INV)
• Snoring, sleep disordered breathing

• Clinical examination + anterior rhinoscopy: Narrow valve angle visible
• Nasal endoscopy: Narrow cross-sectional area at INV level
• Acoustic rhinometry: Measures cross-sectional area; identifies minimum cross-sectional area (MCA) at the valve
• Rhinomanometry: Measures nasal airway resistance; confirms functional obstruction
• CT scan: For structural assessment (bony/septal abnormalities)

1. Spreader grafts (gold standard): Cartilage grafts (septal/rib/ear) placed between the septum and ULC bilaterally to widen the INV angle
2. Spreader flaps (autospreader/turn-in flap): ULC is turned in on itself as a flap to widen the valve — avoids need for cartilage harvesting
3. Flaring sutures: Sutures placed through the ULC to the dorsal septum to lateralise the ULC
4. Butterfly graft: Conchal cartilage graft shaped like a butterfly; placed across the dorsum to widen both INV and external nasal valve
5. Alar batten grafts: For dynamic collapse at the lateral nasal wall
6. Inferior turbinoplasty/submucosal diathermy of inferior turbinate head: Addresses the inferior limb of the valve
7. Latera implant (Vibrex): A bioabsorbable implant inserted under the ULC (LATERA procedure) — minimally invasive; supports lateral nasal wall

Question 10 [10 Marks]

Differential Diagnosis [2]

1. Rhinocerebral mucormycosis (Rhino-orbito-cerebral mucormycosis — ROCM): Angioinvasive fungal infection by Mucorales (Rhizopus, Mucor, Rhizomucor species). The black eschar/necrosis is due to vascular invasion and tissue infarction.

Investigations [3]

1. Blood glucose (urgent): Check capillary glucose; HbA1c for chronicity
2. Serum electrolytes, urea, creatinine: DKA screening (pH, bicarbonate, ketones in urine)
3. Arterial blood gas: Metabolic acidosis in DKA
4. CBC: Leukocytosis; neutrophilia or neutropenia (granulocytopenia increases risk)
5. LFT, KFT: Baseline for antifungal therapy (Amphotericin B nephrotoxicity)

• Histopathology: H&E and PAS staining — aseptate hyphae invading blood vessel walls with thrombosis and tissue necrosis
• Culture: Mucorales (Rhizopus, Mucor) — but culture sensitivity is low; histopathology is more reliable

1. Serum galactomannan / beta-D-glucan: Often negative in mucormycosis (useful to exclude aspergillosis); mucormycosis does NOT produce galactomannan

• Soft tissue thickening in sinuses (maxillary, ethmoid initially)
• Bony erosion — most important sign; erosion of medial orbital wall (lamina papyracea), ethmoid, sphenoid walls
• Orbital apex involvement
• Thrombosis of ophthalmic vessels

1. MRI brain + orbits (most sensitive):
   • T1 with gadolinium: Perineural spread, orbital apex involvement, cavernous sinus thrombosis, cerebral infarction
   • T1 without contrast: Loss of flow void in cavernous sinus = thrombosis
   • T2: Sinus opacification; orbital fat stranding
   • DWI: Cerebral infarcts (angioinvasion)
   • Most critical for surgical planning and prognosis
2. Visual acuity, IOP, pupillary reactions, fundoscopy (ophthalmological assessment): Central retinal artery occlusion, optic nerve infarction
3. Optic nerve function tests — VEP, ERG for prognosis of vision

Management [5]

1. Control of diabetes/DKA: Aggressive IV insulin therapy, fluid resuscitation, electrolyte correction — the single most important step; hyperglycaemia and acidosis impair neutrophil function and facilitate fungal growth
2. Discontinue immunosuppressants if applicable
3. IV fluids, nutritional support

1. Liposomal Amphotericin B (L-AmB) — first-line:
   • Dose: 5–10 mg/kg/day IV (some protocols up to 10 mg/kg/day in CNS involvement)
   • Standard formulation (deoxycholate AmB) also used if L-AmB unavailable but more nephrotoxic
   • Monitor: Serum creatinine, K⁺, Mg²⁺ daily (nephrotoxicity, hypokalaemia)
   • Minimum duration: Until clinical and radiological resolution + immunosuppression corrected
2. Posaconazole or Isavuconazole — step-down oral therapy or for L-AmB intolerant:
   • Isavuconazole: 200 mg TID × 2 days (loading) then 200 mg OD (approved for mucormycosis)
   • Posaconazole: Extended-release tablet 300 mg OD (after loading)
   • Used as combination with L-AmB in severe disease or step-down oral therapy
3. Combination therapy: L-AmB + posaconazole/isavuconazole for refractory or severe ROCM (not universally proven but used in practice)
4. Echinocandins (caspofungin): May have adjunctive role (inhibit Mucorales cell wall) — evidence limited

1. Endoscopic debridement (functional endoscopic surgery):
   • Aggressive endoscopic removal of all necrotic tissue from the nasal cavity, sinuses
   • Involved middle turbinate excision, ethmoidectomy, maxillary antrostomy
   • Extend to: Sphenoid sinus clearance if involved
2. External approaches if required:
   • Medial maxillectomy (via degloving or Caldwell-Luc) for extensive maxillary involvement
   • Orbital exenteration: If orbit is extensively involved and vision is already lost — removes the nidus of infection; preserves life over eye
3. Repeat debridements (every 48–72 hours): Daily wound inspection under endoscopy; repeat debridement until clear surgical margins

• If vision is preserved and orbital apex is involved: Urgent decompression of orbital apex (endoscopic orbital apex decompression)
• If vision is already lost and orbit is invaded: Orbital exenteration — improves survival
• Ophthalmology team management of corneal exposure, IOP

• Hyperbaric oxygen (HBO): Adjunct; increases tissue oxygen tension, inhibits fungal growth, promotes wound healing; high-pressure O₂ is directly fungicidal
• Deferasirox (iron chelation): Iron chelation was proposed (Mucorales require iron for growth) but clinical trials showed no benefit; not currently recommended

• Repeat MRI every 2 weeks to monitor response
• Treatment continued for minimum 3–6 months
• Long-term diabetes management and glycaemic control

Note to candidate: All 10 answers are structured for the allocated mark distribution. For exam writing: Use headings, keep points concise, and draw tables/diagrams (e.g., Shamblin classification, neck levels, valve anatomy) wherever possible — they save time and earn marks. Each answer above corresponds to the stated page ranges in the question paper.