JC101 (ENT) - Facial nerve palsy and salivary gland diseases Flashcards

(70 cards)

1
Q

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Three anatomical divisions and branches of the facial nerve

A
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2
Q

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Effectors innervated by the facial nerve

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From intra-temporal facial nerve:
- Lacrimal gland, nasal and palatine mucosal gland
- Stapedius muscle (together with V3)
- Anterior 2/3 of tongue:
o Sensation: lingual nerve (V3)
o Taste, secretomotor: chorda tympani
- Submandibular ganglion: submandibular gland, sublingual gland

From post-temporal facial nerve: after stylomastoid foramen and through posteromedial parotid gland:

1) Temporal/ frontal - Frontalis
2) Zygomatic - orbicularis oculi muscle
3) Buccal - Buccinators
4) Marginal mandibular - depressor anguli oris, the depressor labii inferioris, the inferior fibers of the orbicularis oris and the mentalis muscles (2-4)
5) Cervical - Platysma

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3
Q

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5 possible locations of facial nerve palsy

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Intracerebral:

  • Supranuclear/ UMN lesion
  • Facial nucleus, pons/ LMN lesion

Temporal bone:

  • Temporal bone fracture
  • Internal acoustic meatus/ cerebellopontine angle

Middle ear lesions - beyond geniculate ganglion

Post-temporal bone/ beyond stylomastoid foramen:

  • Facial trauma
  • Malignant parotid gland tumor
  • Metastatic intracarotid LN

Lesion on nerve itself

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4
Q

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Intracerebral lesions that cause facial nerve palsy

Sequelae

A
  1. Supranuclear (lesion proximal to facial nucleus):
    - UMN lesion
    - Commonest cause = CVA
    - Frontalis muscle spared (bilateral innervation)
  2. Lesion in the facial nucleus, pons (rare):
    - LMN lesion (sometimes UMN depending on how much of the facial nucleus is involved)
    - E.g. CVA, tumour, demyelinating disease
    - All effectors affected: Lacrimation, ipsilateral taste, facial movement
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5
Q

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Temporal bone lesions that cause facial nerve palsy

Sequelae

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  1. Tumour in internal acoustic meatus/ cerebellopontine angle: Acoustic neuroma, Meningioma
    - Facial nerve accommodates slow growing tumors, rarely palsy
  2. Temporal bone fracture

Sequelae: Between geniculate ganglion and stylomastoid foramen:
 Taste and lacrimation abnormal
 Stapedial reflex affected = hyperacusis present
 Facial movement affected

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6
Q

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Middle ear lesions that cause facial nerve palsy

Sequelae

A
  1. Acute otitis media
  2. Chronic suppurative otitis media – cholesteatoma
  3. Bell’s palsy: nerve swollen in the bony facial canal and neuropraxia
  4. Herpes zoster oticus: Ramsay Hunt Syndrome
  5. Tumour in middle ear (rare) – glomus, carcinoma

Sequelae: Between geniculate ganglion and stylomastoid foramen:
 Taste and lacrimation abnormal
 Stapedial reflex affected = hyperacusis present
 Facial movement affected

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7
Q

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Lesions distal to stylomastoid foramen that cause facial nerve palsy

Sequelae

A
  1. Facial trauma to lateral side of face
    - Neuropraxia or whole nerve cut
    - Single or multiple branches affected
  2. Malignant parotid tumor
    - Slow growing tumors allow nerve accommodation with no palsy
  3. Metastatic intraparotid LN (rare, e.g. skin cancer met.)

Sequelae:

  • Only affects facial movement
  • Normal stapedial reflex
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8
Q

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Lesions originating from facial nerve itself which cause palsy

Sequelae

A
  1. Surgical injury (common), e.g. traction during operation
  2. Facial nerve schwannoma/ neurofibroma (mimics malignant
    cancer in middle ear)
  3. CNS demyelinating disease (rare): affects whole facial nerve, usually accompanied by other cranial nerve palsy or other neurological signs

Sequelae:
Either segmental or all effectors affected

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9
Q

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Grading system for facial nerve palsy

A

House and Brackmann facial paralysis grading system

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10
Q

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Clinical P/E assessment of facial nerve palsy

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Usually test motor function only

  1. Test** all 5 branches** in a systematic manner, rate severity with House and Brackmann facial paralysis grading system
  2. Examine other cranial nerves
  3. Examine the external ear and middle ear (vesicles, AOM, cholesteatoma)
  4. Palpate the** parotids and the neck**
  5. Test for cerebellar signs (e.g. large cerebellopontine angle tumor compressing on cerebellum)
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11
Q

First-line investigations for facial nerve palsy

A

Intracranial lesion (e.g. cerebellopontine angle tumor) = MRI brain

Middle ear pathology (e.g. cholesteatoma in mastoid) = MRI/CT temporal bone

Temporal bone trauma (fracture) = CT temporal bone

Suspect parotid lesion (e.g. mass palpated) = MRI/CT parotid + USG FNA (histology to confirm malignancy)

Electrophysiological testing: Electromyography and Electroneurography

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12
Q

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Electrophysiological testing for facial nerve

  • Indication
  • Functions
  • Types
A

Indication:
To assess the need for operative decompression + anastomosis, e.g.:
 Bell’s: don’t do
Trauma: do
 Cancer case: don’t do as nerve will be sacrificed anyway

Functions:
To** differentiate neuropraxia (stretched and recover by itself) from more severe nerve injury **
To assess prognosis

Types:

  • Electromyography (EMG)
  • Electroneurography (ENoG)
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13
Q

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Electromyography (EMG) and Electroneurography (ENoG) for facial nerve palsy

Compare their application, procedure (simplified), Interpretation of results

A

EMG:

  • Check recovery
  • Insert electrode into muscle and record resting/ voluntary contraction
  • Assess muscle activity, no comparison with normal side

ENoG:

  • Diagnostic of damage
  • Stimulate nerve at stylomastoid foramen, record summation potential in nasal alar/ nasolabial fold/ orbicularis oculi
  • Compare 2 sides as a percentage of response:

If 90% degeneration (e.g. good side 10, bad side 1) = surgical decompression
If <90% degeneration = give steroids, spontaneous recovery

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14
Q

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Disadvantages of ENoG over EMG for facial nerve Electrophysiological testing

A

 Discomfort
 Cost
 Test-retest variability (where you put the electrode affects the
reading)

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15
Q

**

Bell’s palsy

  • Pathogenesis
  • Management, treatment options
A

commonest cause of facial nerve palsy

Pathogenesis:

  • idiopathic facial nerve palsy caused by** herpes reactivation at geniculate nucleus causing neuritis**
  • Nerve is swollen in the facial nerve canal (no space to expand), causing neuropraxia

Management:

- Diagnosis by exclusion after r/o causes
- Steroids, antivirals, eye protection, physiotherapy

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16
Q

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Detail treatment options for Bell’s palsy

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Steroid: Prednisolone 1mg/kg/day in divided dose for 7-14 days
- Reduce nerve swelling

Antiviral: **Acyclovir or famciclovir **for 5 days
- Give early, before vesicles

Eye protection, eye drops, no contact lenses
- Prevent exposure keratitis

Facial nerve physiotherapy
- Maintain muscle tone, prevent disuse atrophy

No improvement after 6 weeks: Imaging brain and parotid for ddx

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17
Q

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General treatment options for facial nerve palsy

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  1. Find underlying cause and treat
  2. **Surgical decompression **
  3. Nerve suture
  4. Surgery for facial reanimation: for corneal protection or mouth drooping
    5.** Treat as Bell’s palsy after Dx of exclusion**
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18
Q

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Surgical decompression of facial nerve

Indications

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Traumatic cause with immediate complete palsy

Middle ear infection or mass: surgical reduction e.g.mastoidectomy for cholesteatoma

Iatrogenic injury to middle ear/ parotids

Electrophysiology testing with ENoG <10% compared to normal

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19
Q

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Nerve suture for facial nerve

Indications
Types of suturing

A

Indications:

  • Parotid cancer needing primary resection
  • Traumatic damage to nerve segment

Types:

  1. Primary anastomosis (tension free)
  2. Facial hypoglossal anastomosis(tongue moves with face afterwards) with graft 3. Cross facial nerve graft (anastomosis of normal contralateral buccal branch to defective side)
  3. Free gracilis muscle flap transfer with neurovascular pedicle (long-term palsy)
    a) Adductor artery and vein anastomosed to facial artery and vein
    b) Anterior obturator nerve anastomosed to buccal nerve

Graft material: sural nerve (skin of sole, lateral border of foot)/ great auricular nerve

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20
Q

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Facial reanimation surgery for facial nerve palsy

2 functions
Types of surgeries

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Corneal protection against exposure keratosis

a) Tarsorrhaphy (surgical procedure to partially close the eyelid): poor cosmesis
b) Gold weight implant to eyelid

Correct mouth angle drooping

a) Fascial sling: fascia lata suture with zygoma (Static, does not move with contralateral side)
b) Muscle sling: Temporalis muscle, Free gracilis muscle grafts

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21
Q

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List all salivary glands*

A

6 major salivary glands
2 parotid glands
2 submandiubular glands
2 sublingual glands

minor salivary glands
o Labial, buccal, lingual (tongue base), palatal
o Nasopharynx, larynx, hypopharynx
o Trachea

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22
Q

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Define the boundaries of the parotid, submandibular and sublingual glands

A

Parotid:
o Superior: zygomatic arch
o Posterior: attaches on external auditory canal and sternocleidomastoid muscle

Submandibular glands:
At the ‘submaxilla’, in the submandibular triangle
Gland wraps around mylohyoid

Sublingual:
 Between mandible & genioglossus
 Lies below and lateral to the termination of submandibular duct

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23
Q

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Parotid gland

3 methods to divide into superficial and deep lobe

A

Divided by facial nerve into superficial & deep lobe

Nerve not shown on imaging, need imaginary line:
o Line drawn from mandible to mastoid

Retromandibular vein = deep to facial nerve

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24
Q

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Submandibular gland

Anatomical structures that cross the gland

A

Gland wraps around mylohyoid, which divides the gland into superficial and deep lobes

Relationship with 3 nerves and facial artery:
o Crossed by marginal mandibular branch of facial nerve

o Lingual nerve and hypoglossal nerve are in between superficial and deep lobe

o Facial artery grooves the gland before turning around inferior border of mandible

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25
# / Parotid gland duct - Name - Size - Course - Opening
Stensen’s duct:  Arises from anterior border  Parallel to zygomatic arch, 1.5cm inferior  Pierces buccinator at 2nd molar (opening)  4-6 cm in length
26
# / Submandibular gland duct - Name - Size - Course - Opening
Wharton’s duct:  5 cm in length  Exits medial surface  Between mylohyoid & hyoglossus 1. Lingual nerve (begins lateral to submandibular duct, courses anteromedially by looping beneath the duct; on hyoglossus) 2. Hypoglossal nerve (lies deep to submandibular gland; runs superficial to hyoglossus, deep to digastric)
27
# / Submandibular gland ducts - Opening
~15 ducts (no true duct):  Half open into submandibular duct  Half open directly on sublingual fold and papilla
28
# * Compare the presentation of inflammatory vs neoplastic salivary gland disease - swelling - pain - facial nerve palsy - LN - Signs of infection
Intermittent painless swelling or acute/ intermittent pain after meal + signs of acute infection (fever, tenderness, pus) = Inflammatory Persistently growing, painless mass + Facial nerve palsy + LN = Neoplastic
29
# * Outline P/E for salivary gland lesions
I. **Inspection for both sides:** - **Symmetrical swellings** (Sjogren)  Scar (parotidectomy)  Look from the front: facial nerve palsy (cancer may affect certain branch) - **Intraoral inspection:**  Parotid duct opening, submandibular duct opening: pus?  Floor of mouth swelling  Tumour  Displacement of tonsil (e.g. by deep lobe parotid tumor) II. **Palpation**: low sensitivity  Confirm lesion not arising from the skin (e.g. sebaceous cyst)  **Palpate the ducts: For stones and Express pus** III. Other examinations:  Complete H&N ENT examination  **Facial nerve examination**  Palpate **neck lymph nodes**  Endoscopy of the upper aerodigestive tract
30
# / Conditions that mimic parotid gland swelling How to rule out
 Masseter hypertrophy  Neck lymph nodes  Lipoma  Vascular malformations R/o with ultrasound
31
# / Conditions that mimic submandibular gland swelling How to rule out?
 Enlarged submandibular lymph node  Oral cavity mass with direct extension to submandibular space Rule out:  Intraoral examination (tongue cancer extending to floor of mouth)  Bimanual palpation of submandibular gland (may find stone)
32
# * First-line investigations for salivary gland diseases
1. **Ultrasound** 2. **Plane X-ray - submandibular stones** ONLY (radio-opaque) 3. **Sialogram**- sialolithiasis only, therapeutics 4. **MRI** - tumor, extent of invasion 5. **FNA** - benign vs malignant lesions 6. **Biopsy: Trucut, incisional and excisional**
33
# / Ultrasound for salivary gland diseases - Functions
 Confirm origin of mass, location of tumor  Enlarged neck lymph nodes  Stones  Tumor vs. inflammation  Malignant vs. benign (not always accurate)  Dilated ducts
34
# / Sialogram for salivary gland diseases - Functions - Limitations
Cannulate the duct, inject contrast into the duct for filling defect  Only for stones/ chronic sialolithiasis  Therapeutic (may flush out stones or debris) Limitations: Cannulation of the duct may be difficult superseded by USG/ sialoendoscopy
35
# / MRI for salivary gland disease - Function - Limitation
Best soft tissue differentiation, e.g.:  Submandibular vs. parapharyngeal space  Deep vs. superficial lobe Assess tumor, accurate delineation of extent of invasion Differentiate other pathologies, e.g. facial nerve schwannoma Limitation:** Cannot image the facial nerve*/ lingual nerve (e.g. cannot tell nerve invasion)
36
# / CT/ CT sialogram for salivary gland disease Functions Limitations
 Delineate deep lobe vs. superficial lobe tumor  Differentiate salivary gland swelling vs. other pathologies (good for inflammatory disease)  Can show enlarged lymph nodes Not done anymore (parotid prefer MRI)
37
# / FNA for salivary gland diseases Functions Limitations
 80% accurate in differentiating benign vs. malignant lesions  Better prepares the patient (e.g. malignant > prepare for neck dissection) Limitations: - 20% inaccurate in differentiating benign vs. malignant lesions, used as a guideline only - Cannot differentiate different pathologies (type of parotid cancer, cell of origin)
38
# * Biopsies for salivary gland diseases - Types of biopsy - Limitations
**Trucut** **Incisional** - minor salivary glands only (risk of tumor spillage for parotid) **Excisional - parotidectomy, submandibulectomy**
39
# * Ddx inflammatory causes of parotid gland enlargement
Most common: -**Acute parotitis** -**Viral infections** -**Chronic sialadenitis: stones, Sjogren's syndrome** - **Alcoholism, Bulimia, Starvation** Others:  Sarcoidosis (Heerfordt syndrome)  Benign lymphoepithelial lesions (associated with immunosuppression)  Cysts (congenital vs. acquired)  Diabetes mellitus  Drugs, e.g. phenytoin
40
# / Causes of bilateral parotid enlargement
 Pseudo-parotidemegaly, e.g. bruxism (grind/gnash/clench teeth), masseter hypertrophy  Bulimia nervosa (binge eating followed by purging)  Alcoholic cirrhosis  Diabetes mellitus  Drugs, e.g. phenytoin  Viral infection (e.g. mumps)  Sjogren’s Syndrome  Warthin tumor
41
# * Patient presents with acute onset of tender parotid swelling and spits out pus intermittently. Pt has mobility issues and seldomly drinks water. Most likely Dx
Acute parotitis
42
# * Pt presents with high fever, bilateral parotid swelling and pain, testicular discomfort Most likely Dx
Viral infection of parotid e.g. Mumps
43
# * Pt presents with mild parotid pain that's worse after meal, and intermittent swelling over the parotid glands Most likely Dx
Chronic sialadenitis e.g. stone obstruction, stasis and infection
44
# * Pt presents with dry eyes, large, tender enlargement of the parotid glands and submandibular glands Gland enlargement fluctuates and is diffuse Constitutional symptoms: fatigue, low-grade fever Most likely Dx
Sjogren's syndrome
45
# * Acute parotitis Pathogenesis Clinical features Tx
Cause: **Staphylococcus aureus infection ** - **Dehydrated, infirmed elderly** (no proper intake, stroke) decrease salivar flow, blocked duct -**poor oral hygiene ** Clinical features: **Tender** parotid swelling **Pus** from duct opening Tx:  **Rehydration** (drip to establish salivary flow)  **IV antibiotics (vancomycin)**
46
# * Viral infection of parotid and submandibular glands - Causative pathogens - Clinical presentation - Diagnosis
Pathogen:  **Mumps (commonest)**, but now vaccinated  Coxsackie virus  CMV  Influenza S/S:  **High fever**  Usually**bilateral parotid and submandibular enlargement**  Mumps also affects other exocrine glands: **pancreas, testes** Diagnosis:  Clinica picture (high fever + symmetrical swelling)  Serology
47
# * Chronic sialadenitis - 2 main causes - General clinical features - Diagnosis - General Tx
Main causes: **Stones, Sjogren's disease** S/S:  Mild pain, worsens after meal  **Recurrent parotid/ submandibular swelling after meal** Dx: ** Clinical  Sialogram/ USG** Tx: - **Hydration, sialogogues e.g. cevimeline, massage, heat** - **Antibiotics** during acute attacks - **Excision** of the gland
48
# * Sialolithiasis Which gland most affected Clinical presentation Complications Diagnosis Tx
Gland: **80% submandibular gland** (more mucous, higher Ca content), 20% parotid S/S:  Recurrent swelling  Pain worse with eating Complications:  Sialadenitis  Ductal ectasia  Benign Stricture CT: submandibular stones only (radio- opaque), parotid gland stones are radiolucent Tx: - **Hydration, Sialagogues (cevimeline)**, conservative for spontaneous passage - Remove stone: **Transoral excision, Sialoendoscopy** - **Gland excision**: recurrent stones, multiple stones, proximal stones (inaccessible)
49
# * Sjogren's syndrome - Demographics - Pathogenesis - Differentiate primary vs secondary cause
- Demographics : F>M, usually 3rd & 4th decade - Pathogenesis: autoimmune disease: **lymphocyte- mediated destruction of exocrine glands, e.g. salivary, lacrimal** - Differentiate primary vs secondary cause Primary - no a/w other autoimmune diseases Secondary - a/w autoimmune diseases e.g. SLE
50
# * Sjogren's syndrome Clinical presentation Diagnostic tests
S/S: - Eyes: **Keratoconjunctivitis sicca** (dry eyes), injected cornea, conjunctivitis - **Xerostomia (dry mouth)** - Diffuse, tender, fluctuating enlargement of parotid and submandibular glands - Constitutional: fatigue, low-grade fever Dx tests: - Blood test: High **ESR, CRP** Serology (similar to SLE): **ANA, Rheumatoid factor, Anti-Ro/ SS-A, Anti-LA/SS-B antibodies** - **Biopsy of sub-labial minor salivary glands**: gland destruction with lymphocytes infiltration
51
# * Sjogren's syndrome Treatment options
No cure, only supportive Tx  **Artificial saliva, adequate hydration**  **Eye drops, glasses**  **pilocarpine** for tear and saliva production  **Lubricants and moisturizers**  Monitor for **lymphoma in submandibular and parotid gland** (44-fold increased risk):
52
# * Compare the distribution of cancer in major salivary gland + proportion of benign vs malignant
Distribution (the smaller the salivary gland, the less chance of a tumor, but the higher chance of a malignant tumor):  **Parotid: 80% overall; 80% benign, 80% pleomorphic adenoma**  Submandibular: 15% overall; 50% benign  Sublingual/minor: 5% overall; 40% benign
53
# * List benign tumors of the major salivary glands
Benign: **Pleomorphic adenoma** -**Warthin's tumor**/ Papillary cystadenoma lymphomatosum -**Oncocytoma** -**Monomorphic adenoma** -**Basal cell adenoma** - Myoepithelioma
54
# * List malignant tumors of the major salivary glands
**Mucoepidermoid carcinoma** **Adenoid cystic carcinoma** **Squamous cell carcinoma** Lymphoepithelial- like carcinoma (LELC) Acinic cell carcinoma **Carcinoma ex- pleomorphic adenomav(from Mucoepidermoid carcinoma**
55
# * Pleomorphic adenoma - Demographics - S/S - Which glands most affected - Biological behavior - Tx
- Demographics: middle aged women - S/S: **Slow-growing, painless mass, massive** Mostly occurs in superficial lobe at the tail of parotid glands **Also occurs in submandibular and minor salivary glands** Rarely in sublingual gland - Biological behavior **Benign with 10% malignant potential (carcinoma ex- pleomorphic adenoma)** - Tx Complete surgical excision: - **Parotidectomy with facial nerve preservation** - **Submandibular gland excision** - **Wide local excision of minor salivary glands** **Radiotherapy**: Prevent recurrence/ Tumor spillage/ Recurrent tumor
56
# * Warthin's tumor/ papillary cystadenoma lymphomatosum - Demographics - S/S - Which gland most affected - Biological behavior
- Demographics: Old male, smokers - S/S: Slow-growing, painless, **Cystic mass, soft** - Which gland most affected: Parotid glands, rarely bilateral, **Multifocal** - Biological behavior Benign, **no malignant potential** Arise from intraparotid LN
57
# / Parotidectomy - Extent of excision - Approach technique
Excision of tumour with a cuff of normal parotid tissue, with facial nerve dissection Excisional biopsy of parotid tumour **Modified Blair’s incision, aka lazy S incision**: scar from preauricular area, string around ear lobe, down to mastoid area, back to neck
58
Early complications of parotidectomy and submandibulectomy
 **Bleeding**/ haematoma (bruise over the area  **Nerve injury:** Parotidectomy: Facial nerve palsy Submandibulectomy: Lingual nerve, Marginal mandibular nerve, Hypoglossal nerve  **Wound infection/ abscess** from mouth mucosa  **Salivary fistula**: commonly parotidectomy
59
Late complications of parotidectomy and submandibulectomy
**Recurrence** Hypertrophic scar/**keloid scar** **Frey’s syndrome – gustatory sweating/ parotid area becomes red and swollen after eating** Sunken parotid area, **cosmetic problem** (asymmetrical face) Submandibulectomy: Permanent nerve damage
60
# / Pathogenesis of Frey's syndrome
common in parotidectomy: - when patient eats, parotid area will sweat because secretory parasympathetic nerve has no end organ - nerve aberrantly innervates the skin and sweat gland - causes sweat instead of salivary secretion - parotid area becomes red and swollen after eating Very rare in submandibulectomy as whole gland is excised including the capsule, and the nerve is ligated
61
# * Pt presents with Long-standing, painless parotid mass with sudden enlargement Most likely neoplastic ddx
Carcinoma ex- pleomorphic adenoma High grade Mucoepidermoid carcinoma
62
# * Pt presents with pain in parotid area, paraesthesia over tongue and some facial weakness Most likely neoplastic Dx
Adenoid cystic carcinoma in Submandibular gland
63
# * Pt presents with slow-growing, painless mass over parotid glands Most likely neoplastic ddx
Low grade Mucoepidermoid carcinoma Acinic cell carcinoma
64
# * Mucoepidermoid carcinoma - Demographic - Most affected gland - Presentation - histology - Tx
- Demographic: **children, middle-aged women** - Most affected gland:**Parotid gland**(45-70%), 18% in palate - Presentation: Low-grade= **slow-growing, painless mass** High-grade: **rapidly enlarging +/- painful oral cavity ulcers** - histology: Glandular, mucus-secreting and sequamous components - Tx: localized = **gland excision** LN = **neck dissection** High grade = **radiotherapy**
65
# * Adenoid cystic carcinoma - Demographic - Most affected gland - Presentation - Tx
- Demographic: 5th decade, M=F - **Most affected gland: submandibular, sublingual and minor salivary glands** (cf mucoepidermoid carcinoma at parotid) - Presentation: Asymptomatic enlarging mass **Invading nerves:** - Pain in parotid area (greater auricular nerve) - Paraesthesia, numbness of tongue (lingual nerve) - Facial nerve palsy weakness/ paralysis - Hypoglossal nerve paralysis **Distant metastasis to LUNGS** - Tx: Complete local excision perineural invasion common - postoperative radiotherapy
66
# / Acinic cell carcinoma - Demographic - Most affected gland - Presentation - Tx
- Demographic: pediatrics, 5th decade female predominant - Most affected gland: unilateral parotid - Presentation: Slow growing, often painless mass, no nerve palsy - Tx  Complete local excision  +/- postoperative radiotherapy
67
# / Carcinoma ex- pleomorphic adenoma - Demographic - Most affected gland - Biological behavior - Presentation - Tx
- Demographic: old age, no sex predominant - Most affected gland: Parotid - Presentation Longstanding painless mass that undergoes sudden enlargement - Biological behavior: Malignant degeneration of pleomorphic adenoma  Poorly circumscribed, invasive mass  Infiltrative, hemorrhagic, necrotic  25% with neck node involvement - Tx  Radical excision  Neck dissection (25% with lymph node involvement at presentation)  Postoperative radiotherapy
68
# / Squamous cell carcinoma of salivary glands - Demographic - Origin of neoplastic cells
- Demographic: rare, 7th - 8th decade male Neoplasm from: - Direct extension of skin SCC (overlying parotid region; less common) - Metastatic SCC to intraglandular lymph nodes, usually from scalp SCC (skin cancer) - High-grade mucoepidermoid carcinoma
69
# / Lymphoepithelial- like carcinoma (LELC) Histology Tx
Undifferentiated carcinoma:  Histology exactly like NPC  EBV-related (tumor cells = EBER-RNA +ve Surgery + post-op radiotherapy to primary and neck
70
# * Most common and 2nd most common salivary gland neoplasms Most common pediatric salivary gland neoplasms Most common parotid tumor to cause facial paralysis
**Mucoepidermoid carcinoma = most common** **Adenoid cystic carcinoma = 2nd most** Pediatrics: Mucoepidermoid carcinoma Acinic cell carcinoma Facial paralysis High grade Adenoid cystic carcinoma (at submandibular gland)