ENT JC101: Facial Nerve Palsy And Salivary Gland Diseases

Question 1

Revision: CN7 anatomy

Answer 1

• Complex course
• Intimate relationship to middle ear + parotid gland
• Travel in a bony canal for a long distance

3 parts (Temporal bone as landmark):
1. Pre-temporal part
- just before Internal acoustic meatus / Geniculate ganglion
- 1st branch: ***Greater petrosal nerve

2. Intra-temporal part
   - Geniculate ganglion —> Stylomastoid foramen
   - 2nd branch: ***Chorda tympani
3. Post-temporal part
   - Exit Stylomastoid foramen —> pierce Parotid gland
   - 5 terminal branches (Pes anserinus: 鴨腳) (or Upper / Lower trunk):
   —> Temporal (Frontalis)
   —> Zygomatic (Orbicularis oculi)

—> Buccal (upper / lower trunk) (Buccinator)

—> Marginal mandibular (Levator anguli oris)
—> Cervical (Platysma)

Question 2

Causes of CN7 palsy

Answer 2

Intracerebral / Pre-temporal:
1. Supranuclear
- UMN lesion
- Frontalis muscle spared (∵ bilateral innervation)
- Cause: CVA (commonest)

2. Lesion in Facial nucleus (rare)
   - Lesion in ***Pons
   - LMN (can be UMN depend on how much nucleus is involved)
   - Cause: CVA, tumour, demyelinating disease

Intra-temporal / Temporal bone:
1. Tumour in Internal acoustic meatus / Cerebellopontine angle
- Acoustic neuroma
- Meningioma
—> usually slow growing, not cause palsy until tumour very big
—> usually cerebellar signs first

2. Temporal bone fracture (common in head injury)

Middle ear (Facial nerve canal: normally a bony canal, 10% population do not have bone —> Facial nerve dehiscence —> CN7 only covered by mucosa in middle ear):
1. Acute otitis media
2. Chronic otitis media (Cholesteatoma: pressure effect / inflammation)
3. Bell’s palsy (CN7 neuritis, nerve swollen in rigid canal —> neuropraxia)
4. Herpes zoster oticus (Ramsay Hunt syndrome) vs Herpes zoster ophthalmicus (involve trigeminal ganglion: Hutchinson’s sign)
5. Tumour in middle ear (Glomus, carcinoma)

Post-temporal (beyond Stylomastoid foramen):
1. Facial trauma (blunt / penetrating) (may only affect a single branch)
2. Tumour in parotid gland (Malignant, benign will NOT cause palsy ∵ slow-growing)
3. Metastatic intraparotid LN (rare, very common in Australia ∵ skin cancer)

Other causes:
1. Facial nerve schwannoma / neurofibroma (tumour in CN7 itself)
2. Surgical injury (common)
3. CNS demyelinating disease (rare, usually accompanied by other CN palsy / neurological signs)

Question 3

Location of lesion

Answer 3

1. UMN lesion
   - ***Frontalis spared
2. Proximal to Geniculate ganglion
   - ***↓ in Lacrimation + Ipsilateral taste
3. Between Geniculate ganglion and Stylomastoid foramen
   - Lacrimation + Taste normal
   - ***Hyperacusis present (∵ Stapedial reflex affected)
4. Beyond Stylomastoid foramen
   - Lacrimation + Taste normal
   - Stapedial reflex normal
   - ***Only facial movements affected

Question 4

P/E of CN7

Answer 4

• Usually test motor function only
• Test all 5 branches systemically
• Examine other CN (∵ mostly polyneuropathies)
• Examine external + ***middle ear (exclude Otitis media, Zoster, Cholesteatoma etc.)
• Palpate ***parotids + neck (for any lesions)

House and Brackmann facial paralysis grading system:
- Grade degree of CN7 palsy
- Grade 1-6 (6 most severe)

Question 5

Investigations for CN7 palsy

Answer 5

Depends on clinical findings
- Bell’s palsy (commonest) —> Diagnosis of exclusion
- mostly clinical diagnosis + recover on its own

1. MRI brain
   - for suspected intracranial lesion / parotid lesion
2. MRI / CT temporal bone
   - if middle ear pathology suspected
3. CT temporal bone
   - if suspect temporal bone trauma (e.g. temporal bone fracture, Cholesteatoma)
   —> can look at bony canal whether damaged
4. MRI / CT parotid + USG FNAC
   - if parotid lesion suspected
5. Electrophysiological testing
   - to differentiate neuropraxia (just stretched, will recover) vs more severe nerve injury (e.g. axonotmesis, neurotmesis)
   - to assess need for operative decompression / anastomosis
   - to assess prognosis
6. Electromyography (EMG)
   - determines activity of muscle itself
   - NOT require comparison with normal side
   - not very useful, only used to predict recovery
7. **Electroneurography (ENoG)
   - most accurate of electrodiagnostic tests
   - maximum stimulus to CN7 at Stylomastoid foramen (↑ stimulation until response cannot go bigger)
   —> **summation potential recorded in nasal alar
   —> **peak to peak amplitude is proportional to no. of intact axons
   —> 2 sides are compared as % of response
   - **90% degeneration (i.e. damage is more than neuropraxia) —> Surgical decompression should be done
   - ***<90% degeneration within 3 weeks —> predict 80-100% spontaneous recovery
   - disadvantage: discomfort, cost, test-retest variability

Question 6

Treatment of CN7 palsy

Answer 6

1. Identify cause
   - cancer: remove cancer
   - Bell’s palsy: steroid
2. Removal of causative agent
   - e.g. mastoid surgery to remove Cholesteatoma
3. Consider nerve exploration + surgical decompression in ***traumatic cause with immediate complete palsy
   - if delayed palsy after injury —> more likely due to swelling of nerve rather than transection —> observe
4. Other surgical options
   - **Facial nerve grafting
   - **Surgery for facial animation
   —> Tarsorrhaphy
   —> Gold weight implant to eyelid
   —> Facial sling
   —> Muscle sling

Question 7

Bell’s palsy

Answer 7

• Idiopathic CN7 palsy
• Commonest cause of CN7 palsy
• Now identified as ***Herpes reactivation neuritis (Herpes virus reactivating at Geniculate ganglion —> neuritis)
• Nerve swollen in rigid facial canal —> Neuropraxia
• > 90% good recovery

Management:
- Diagnosis by **exclusion
- P/E to rule out other causes e.g. CVA, Parotid tumour, Middle ear infection etc.
- May progress in first 3 weeks —> warn patient (∵ degeneration comes first in 1-2 weeks before recovery)
- Consider imaging if no improvement / deterioration after **6 weeks
—> if imaging on 1st day
—> will show up very swollen CN7, contrast enhancing
—> can be mistaken as tumour

Treatment:
1. ***Steroid (Prednisolone)
- to reduce swelling
- 1 mg/kg/day in divided dose for 7-14 days if no CI

2. Antiviral (Aciclovir / Famciclovir for 5 days)
   - vesicles in herpes (Ramsay Hunt syndrome) may not show up in first 2 days of palsy
   - only useful when given early
3. Eye protection / Eye drops
   - prevent exposure keratitis
4. CN7 physiotherapy
   - maintain muscle tone + hasten recovery
   - prevent disuse atrophy
5. Consider other causes if no improvement after 6 weeks

Question 8

Surgical decompression of nerve

Answer 8

Indications:
1. Traumatic cause
2. Middle ear infection
3. Iatrogenic injury (middle ear / parotid surgery)

• Earlier the better (within 2 weeks)
• Electrical testing as indication for decompression: ***ENoG of affected side <10% of normal side
• Imaging for site of decompression
• Bell’s palsy: No proven benefit

Question 9

Facial nerve grafting

Answer 9

1. Primary anastomosis (將斷開兩邊駁埋)
   - only if tension free
2. **Sural nerve / **Great auricular nerve grafting
   - after primary resection of CN7 in parotid cancer
   - damage of a segment of nerve in traumatic cases
3. ***Facial-Hypoglossal anastomosis
   - if grafting not feasible
   - train patient to move tongue in order to move face
4. ***Cross (Contralateral) facial nerve grafting
   - anastomosis of normal contralateral buccal branch to the defective side
   - also avoid disuse atrophy
5. Neurovascular free-muscle transfer
   - free ***gracilis muscle flap together with neurovascular bundle
   - put it on face
   - reanatomose artery + vein
   - reanatomose nerve to contralateral buccal nerve
   - only for chronic facial palsy where nerve is not salvageable

Question 10

Surgery for facial animation

Answer 10

1. Tarsorrhaphy
   - partial closure of eyelid
   - for corneal protection
   - but poor cosmetic outcome
2. Gold weight implant to eyelid
   - gold: inert + heavy
3. Facial sling
   - static sling to correct drooping of angle of mouth
   - aesthetic correct
4. Muscle sling
   - suture **temporalis muscle to angle of mouth, can have voluntary movement
   - free **gracilis muscle graft with neurovascular bundle

Question 11

Revision: Salivary gland anatomy

Answer 11

Major salivary glands:
- Parotid x2
- Submandibular x2
- Sublingual x2

Minor salivary glands:
- Hundreds
- Oral cavity, Tongue base, Larynx, Trachea, NP

i.e. Cancer can occur anywhere along upper aerodigestive tract

Question 12

Revision: Parotid gland anatomy

Answer 12

Boundary:
- Superior boundary: Zygomatic arch
- Posterior boundary: EAC
- can extend anterior / inferiorly (esp. in elderly) but never posteriorly / superiorly
- Tail of Parotid: Posteriorly can attach on SCM (can extend posteriorly to cover nearly whole SCM)

Location:
- 80% overlies Masseter + Mandible
- 20% Retromandibular
- Posterior attaches on SCM + EAC

Parts:
- Superficial + Deep lobe
—> divided by CN7 (NO true capsule as landmark)
—> only an imaginary line
—> CT: drawn from Mandible to Mastoid
—> MRI: deep lobe: medial to Retromandibular vein

**Stensen’s duct (Parotid duct):
- arise from anterior border
- **1.5cm inferior to zygomatic arch, parallel
- opening: pierces Buccinator at ***2nd upper molar
- length: 4-6 cm
- diameter: 5 mm

Question 13

Revision: Submandibular gland anatomy

Answer 13

• “Submaxilla”
• Submandibular triangle
• Has a true capsule: from superficial layer of Deep cervical fascia
• Gland wraps around ***Mylohyoid (FOM) —> a real physical boundary
• 3 nerves close in proximity
  —> **Marginal mandibular nerve (CN7)
  —> between superficial + deep lobe: **Lingual nerve + ***Hypoglossal nerve (inferior + deep to Hyoglossus muscle)

**Wharton’s duct:
- exits medial surface (just lateral to frenulum) at FOM
- **between Mylohyoid + Hyoglossus
- length: 5 cm
- wraps around Lingual nerve

Question 14

Revision: Sublingual gland

Answer 14

• Between Mandible + Genioglossus
• Lateral to submandibular duct
• No capsule —> Sialogram not possible
• No true duct (multiple ducts)

Question 15

Revision: Minor salivary glands

Answer 15

• 600-1000
• Simple ducts
• Buccal, Labial, Palatal, Lingual
• NP, Larynx, Hypopharynx
• Tumour sites: Palate, Upper lip, Cheek

Question 16

History taking of Salivary gland diseases

Answer 16

2 common scenarios (Inflammation / Neoplastic):
1. Pain (acute / intermittent)
2. Painless swelling

Differentiate between inflammation / neoplastic:
1. Pain (after a meal?)
2. Swelling (persistent / progressive / intermittent?)
3. Presence of symptoms of ***acute infection (fever, tenderness, pus)

Rarer presentations:
- CN7 palsy
- Metastatic LNs

Question 17

***P/E of Salivary gland diseases

Answer 17

1. Confirm genuine Parotid swelling —> P/E + USG
   - Masseter hypertrophy
   - Neck LN
   - Lipoma, Vascular malformations
2. Confirm genuine Submandibular gland swelling —> P/E + USG
   - Enlarged submandibular LN (**very hard to differentiate)
   - Oral cavity mass (e.g. tongue cancer) with direct extension to submandibular space: **Intraoral examination
   - Stones: Bimanual palpation (sometimes can feel stone within submandibular duct)

Inspection:
1. Both sides
2. Scar
3. CN7 (esp. sometimes subtle palsy in parotid cancer)
4. **Symmetrical swellings (e.g. can be **Sjögren’s syndrome)
5. Intraoral
- **Duct openings: Parotid duct, Submandibular duct, Pus
- **FOM swelling
- Tumour in FOM / Oral cavity —> Deviation of tonsils

Palpation:
1. Confirm lesion not arising from skin (e.g. sebaceous cyst)
2. Difficult to differentiate submandibular LN / gland —> USG
3. Difficult to ascertain mass is a parotid tumour —> USG
4. Palpate ducts
- Stones
- Express pus

Other examinations:
1. Complete HN ENT examination
2. **CN7 examination
3. Palpation of neck **LN
4. Endoscopy of upper ***aerodigestive tract

Question 18

Investigations of Salivary gland diseases

Answer 18

1. **USG (1st line)
   - confirm **origin of mass
   - detect enlarged neck LN / stones / dilated ducts
2. Plain X-ray (obsolete)
   - ***90% parotid stones radiolucent
   - 90% submandibular stones radio-opaque
   - still can miss small stones
3. **Sialogram
   - injection of dye into duct
   - useful for **chronic sialolithiasis
   - superseded by USG / ***Sialoendoscopy
   - cannulation of duct may be difficult
   - may be therapeutic: may flush out stones / debris
4. CT scan / CT sialogram (obsolete)
   - poor soft tissue differentiation
   - delineate deep lobe vs superficial lobe tumour
   - differentiate salivary gland swelling vs other pathologies
   - also can show enlarged LN
5. ***MRI
   - best soft tissue differentiation —> e.g. lesion extension to other space
   - multiple planes of imaging
   - still cannot see CN7 / Lingual nerve
6. ***FNA
   - may not be totally accurate in differentiating benign + malignant lesions (80%)
   - difficult in differentiating different pathologies (i.e. exact histology of tumour)
7. **Biopsy
   - Trucut: may not have enough tissue
   - Incisional: **not recommended, **tumour spillage, for minor salivary glands only
   - **Excisional: Parotidectomy, Submandibulectomy

Conclusion: FNAC first —> then Excisional biopsy (other biopsy not recommended)

Question 19

Infection of Salivary glands

Answer 19

1. Acute parotitis
   - bacterial infection of gland: **Staphylococcus aureus
   - **dehydrated infirmed elderly —> reduced salivary flow —> blocked duct + poor oral hygiene —> infection
   - tender + swelling + pus from duct opening
   - treatment: rehydration (reestablish salivary flow) + IV antibiotics
2. Viral infection
   - Mumps (commonest) (affect all **exocrine glands: pancreas, submandibular, parotid, testes)
   - Coxsackie virus
   - CMV
   - Influenza
   - high fever + **symmetrical swelling on both sides
   - diagnosis by **clinical + **serology
3. Chronic sialoadenitis
   - chronic inflammation of gland
   - caused by **stones (commonest) / **recurrent infection
   - can be caused by **autoimmune diseases (e.g. Sjögren’s syndrome)
   - **destruction of gland tissue —> blockage of saliva —> stasis + repeated infection
   - mild pain, worsen after meal
   - recurrent swelling (parotid / submandibular) after meal
   - investigations:
   —> Clinical
   —> Blood test to rule out Sjögren’s syndrome
   —> Sialogram to rule out stones
   —> USG for status of gland (destroyed or not)

Question 20

Treatment of Sialoadenitis

Answer 20

Conservative:
1. Hydration
2. Sialogogues, Massage, Heat
3. Antibiotics during acute attacks

Definitive:
4. Remove stones
- exploration of submandibular duct
- Sialoendoscopy (superceded Sialogram)

5. Excision of gland

Question 21

Sialolithiasis

Answer 21

• 80% ***submandibular, 20% parotid
• only 1 stone in 75% cases
• 90% parotid stones radiolucent, 90% submandibular stones radio-opaque (∵ more mucous, higher Ca content)

Presentation:
- **Recurrent swelling
- **Pain worse with eating

Complications:
1. Sialoadenitis
2. Ductal ectasia
3. Stricture

Treatment:
1. **Conservative: small stones pass by themselves (hydration, pro-secretory food e.g. sour food)
2. Transoral removal / excision
3. **Sialoendoscopy + removal
4. ***Excision of gland
- Proximal stone (inaccessible by scope / transoral excision)
- Recurrent stones
- Multiple stones

Question 22

Sjögren’s syndrome

Answer 22

• Autoimmune disease attacking exocrine gland
• ***Lymphocyte mediated destruction of salivary + lacrimal gland
• Parotid gland: largest HN exocrine gland (usually swollen)

Presentation:
- F>M
- usually in 3rd/4th decade
- **Keratoconjunctivitis sicca (dry eyes)
- **Xerostomia (dry mouth)
- Diffuse, tender enlargement of parotid + submandibular glands (with fluctuations)
- Injected cornea, conjunctivitis
- Features of other associated autoimmune diseases e.g. Fatigue, Low grade fever

Types:
1. Primary Sjögren’s syndrome
- not associated with other autoimmune diseases

2. Secondary Sjögren’s syndrome
   - associated with other autoimmune diseases e.g. RA, SLE

Serology (~ pattern to **SLE):
1. ANA (50-80%)
2. RF (75%)
3. **Anti-Ro/SSA Ab (up to 90%)
4. ***Anti-La/SSB Ab (up to 90%)

Diagnosis:
1. ↑ ESR, CRP (during acute phase)
2. Anti-Ro/SSA Ab + Anti-La/SSB Ab
3. Biopsy of sub-labial minor salivary glands (diagnostic)
- gland destruction with lymphocyte infiltration

Treatment:
- Rheumatologist: Steroid, Treat underlying causes
- Artificial saliva, adequate hydration
- Eye drops (for dry eyes)
- Monitor for **Lymphoma (44x ↑ risk) in parotid / submandibular gland (∵ chronic lymphocytic inflammation)
—> **non-symmetrical parotid / submandibular swelling warrants FNAC / biopsy!!!

Question 23

Other non-neoplastic diseases

Answer 23

1. Sarcoidosis (Heerfordt syndrome)
2. Benign lymphoepithelial lesions
   - associated with immunosuppression e.g. HIV, transplant patients
3. Cysts
   - congenital / acquired

Question 24

***Causes of Bilateral parotid enlargement

Answer 24

1. ***Pseudoparotidmegaly
   - e.g. bruxism (磨牙), masseter hypertrophy
2. Bulimia nervosa (binge eating then purging)
   - repeated vomiting
3. ***Alcoholic cirrhosis
4. DM
5. Drugs e.g. phenytoin
6. ***Sjögren’s syndrome
7. ***Warthin’s tumour

Question 25

Salivary gland neoplasms

Answer 25

• Diverse histopathology
• Relatively uncommon (2% of HN neoplasms)

Distribution:
- Parotid: 80% overall, 80% benign, 80% pleomorphic adenoma (記: 80 80 80)
- Submandibular: 15% overall, 50% benign
- Sublingual / Minor: 5% overall, 40% benign
(***記: smaller size of gland —> higher chance of malignancy)

Question 26

Pleomorphic adenoma

Answer 26

Most common of all salivary gland neoplasms
- 80% parotid tumours
- 50% submandibular tumours
- 45% minor salivary gland tumours
- 6% sublingual tumours

Epidemiology:
- 4-6th decade
- F:M = 3-4:1

Presentation:
- **Slow-growing, painless mass
- Parotid: 90% superficial lobe, mostly in **tail of gland
- Minor salivary gland: lateral palatal / submucosal mass
- ***malignant transformation 10-15% risk in 10 years

Treatment:
1. Complete surgical excision
- Parotidectomy with CN7 preservation
- Submandibular gland excision
- Wide local excision of minor salivary gland
- Avoid enucleation + tumour spillage
—> high risk of seeding —> take it out ***without rupture capsule!!!

2. RT
   - consider for recurrent tumour / prevention of recurrence in case of spillage

Question 27

Warthin’s tumour

Answer 27

Aka Papillary cystadenoma lymphomatosum
- tumour arise from ***intraparotid LN
- 6-10% parotid neoplasms
- older males 60-70
- smokers

Presentation:
- Slow-growing, painless mass
- **Soft cystic mass
- Multifocal, 10% bilateral, usually in **tail of parotid
- Not cause CN7 palsy / malignant transformation

Question 28

Other benign tumours of Salivary glands

Answer 28

1. Oncocytoma
2. Monomorphic adenoma
3. Basal cell adenoma
4. Myoepithelioma

Question 29

***Mucoepidermoid carcinoma

Answer 29

• most common salivary gland malignancy
• ***mucoepidermoid: mucus secreting component + squamous component
• 5-9% salivary neoplasms
• parotid 45-70% cases
• palate 18%
• peak in 5th decade (30-80)
• F>M

Presentation:
- Low-grade: Slow-growing, painless mass (~Pleomorphic adenoma)
- High-grade: Rapidly enlarging +/- Pain
- ***Minor salivary glands: may be mistaken for benign / inflammatory process (ulcerates in later stages)

Treatment:
- depend on Site, Stage, Grade
1. Localised to gland —> Excision
2. Neck node metastasis —> Neck dissection
3. RT for high grade tumour, close margin, extraglandular spread

Question 30

Adenoid cystic carcinoma

Answer 30

2nd most common malignancy
- Most common in ***submandibular, sublingual, minor salivary glands
- M=F
- 5th decade

Presentation:
- Asymptomatic enlarging mass
- ***Propensity to invade nerve: Pain (great auricular nerve), Paresthesia, Facial weakness / paralysis, Tongue paralysis / numbness

Treatment:
1. Complete local excision
2. CN7 sacrifice? (∵ tendency for perineural invasion)
3. Post-op RT (for perineural invasion esp. to skull base)

Prognosis:
- ***Local recurrence: 42% (high ∵ spread far away along nerve)
- Distant metastasis common: Lung
- Indolent course: 75% 5-year survival, 13% 20-year survival (∵ slow-growing)

Question 31

Acinic cell carcinoma

Answer 31

• 2nd most common parotid + ***paediatric malignancy
• rather low-grade tumour
• 5th decade
• F>M
• Bilateral parotid disease in 3%

Presentation:
- Solitary, slow-growing, often painless mass
- usually NO nerve palsy

Treatment:
1. Complete local excision
2. +/- Post-op RT

Prognosis (Good):
- 5-year survival: 82%
- 10-year survival: 68%
- 20-year survival: 50%

Question 32

Carcinoma ex-pleomorphic adenoma

Answer 32

• Malignant transformation of Pleomorphic adenoma (1.5% first 5 years, 10% after 15 years)
• Rare cancer
• 6-8th decade

Presentation:
- **Longstanding painless mass (Pleomorphic adenoma) that undergoes **sudden enlargement (Carcinoma ex-pleomorphic adenoma)
- Benign tumour suddenly becomes very aggressive

Gross pathology:
- Poorly circumscribed
- Infiltrative, Very aggressive
- Haemorrhage + necrosis

Treatment:
1. Radical excision
2. Neck dissection (usually needed, 25% with LN involvement at presentation)
3. Post-op RT

Prognosis (not good):
- Dependent upon stage + histology
- ∵ complete excision usually not possible at presentation

Question 33

Squamous cell carcinoma

Answer 33

• Rare (1.6% of all salivary gland neoplasms)
• 7-8th decade
• M:F = 2:1

Must rule out:
1. High-grade mucoepidermoid carcinoma (squamous differentiation, need to look for mucoid differentiation as well)
2. ***Metastatic SCC of skin cancer to intraglandular LN, usually from scalp SCC
3. Direct extension of skin SCC

Question 34

Undifferentiated carcinoma / Lymphoepithelial carcinoma (LELC)

Answer 34

• Histopathology ***exactly like NPC
• ***EBV related (tumour cells EBER +ve)

Presentation:
- Metastatic LN, unknown primary

Treatment:
- Surgery + Post-op RT (to primary site + neck)

Prognosis:
- better than SCC, adenocarcinoma

Question 35

Investigations of Parotid mass

Answer 35

1. History
   - tumour vs inflammation
2. P/E
   - parotid / submandibular mass vs other structures
3. **USG
   - **tumour vs inflammation
   - **stones
   - location of tumour
   - **lymphadenopathy
   - malignant vs benign (not always accurate)
4. Sialogram
   - only for stones / sialoadenitis, most replaced by USG
   - may be therapeutic
5. CT scan
   - good for inflammatory disease
6. MRI
   - better for tumour, accurate delineation of extent of invasion
   - still cannot see nerve invasion
   - differentiate other pathologies e.g. CN7 schwannoma
7. FNAC
   - not totally accurate
   - guideline only, not for sole decision making
   - prepare patient better (e.g. if positive FNAC —> neck dissection)

Question 36

Parotidectomy

Answer 36

• Excision of CN7
• Excision of tumour with a cuff of normal parotid tissue
• Excisional biopsy of parotid tumour

Modified Blair’s incision (aka Lazy S incision)

Complications:
Early:
1. Bleeding / haematoma
2. **CN7 palsy
- transient ~5%, permanent ~1%
3. Wound infection
4. **Salivary fistula

Late:
1. Recurrence
2. Frey’s syndrome (Gustatory sweating) —> sweating of parotid area during eating (∵ parasympathetic nerve of parotid area cannot innervate parotid since gone —> grow into skin —> innervate sweat gland)
3. Hypertrophic scar / Keloid
4. Sunken parotid area, cosmetic problem

Question 37

Submandibulectomy

Answer 37

Complications:
Early:
1. Bleeding / haematoma
2. Nerve injury
- **Marginal mandibular nerve
- **Lingual nerve
- ***Hypoglossal nerve
3. Salivary fistula (rare)
4. Wound infection / abscess
- accidental breach of FOM mucosa

Late:
1. Permanent nerve damage
2. Hypertrophic scar / keloid
3. Frey’s syndrome (very rare as whole gland is excised + nerve ligated)
4. Recurrence

Question 38

***Summary of Salivary gland diseases

Answer 38

Infection:
1. Acute parotitis
2. Viral infection (e.g. Mumps, Coxsackie virus, CMV, Influenza)
3. Chronic sialoadenitis
4. Sialoadenitis

Stones:
1. Sialolithiasis

Autoimmune:
1. Sjögren’s syndrome (Primary / Secondary)

Other diseases:
1. Sarcoidosis (Heerfordt syndrome)
2. Benign lymphoepithelial lesions
3. Cysts (congenital / acquired)

***Neoplasms:
Benign:
1. Pleomorphic adenoma
2. Warthin’s tumour
3. Oncocytoma
4. Monomorphic adenoma
5. Basal cell adenoma
6. Myoepithelioma

Malignant:
1. Mucoepidermoid carcinoma
2. Adenoid cystic carcinoma
3. Acinic cell carcinoma
4. Carcinoma ex-pleomorphic adenoma
5. Squamous cell carcinoma
6. Undifferentiated carcinoma / Lymphoepithelial carcinoma (LELC)