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MBBS IV - Junior Clerkship WCS > JC101 (ENT) - Facial nerve palsy and salivary gland diseases > Flashcards

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

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

A

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

A

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

A
  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

A

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

A

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

A
  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

A

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

A

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
Q

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Parotid gland duct

  • Name
  • Size
  • Course
  • Opening
A

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

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26
Q

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Submandibular gland duct

  • Name
  • Size
  • Course
  • Opening
A

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)
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27
Q

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Submandibular gland ducts

  • Opening
A

~15 ducts (no true duct):

 Half open into submandibular duct

 Half open directly on sublingual fold and papilla

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28
Q

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Compare the presentation of inflammatory vs neoplastic salivary gland disease

  • swelling
  • pain
  • facial nerve palsy
  • LN
  • Signs of infection
A

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

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29
Q

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Outline P/E for salivary gland lesions

A

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
Q

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Conditions that mimic parotid gland swelling

How to rule out

A

 Masseter hypertrophy
 Neck lymph nodes
 Lipoma
 Vascular malformations

R/o with ultrasound

31
Q

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Conditions that mimic submandibular gland swelling

How to rule out?

A

 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
Q

*

First-line investigations for salivary gland diseases

A
  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
Q

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Ultrasound for salivary gland diseases

  • Functions
A

 Confirm origin of mass, location of tumor
 Enlarged neck lymph nodes
 Stones
 Tumor vs. inflammation
 Malignant vs. benign (not always accurate)
 Dilated ducts

34
Q

/

Sialogram for salivary gland diseases

  • Functions
  • Limitations
A

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
Q

/

MRI for salivary gland disease

  • Function
  • Limitation
A

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
Q

/

CT/ CT sialogram for salivary gland disease

Functions
Limitations

A

 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
Q

/

FNA for salivary gland diseases

Functions
Limitations

A

 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
Q

*

Biopsies for salivary gland diseases

  • Types of biopsy
  • Limitations
A

Trucut
Incisional - minor salivary glands only (risk of tumor spillage for parotid)
Excisional - parotidectomy, submandibulectomy

39
Q

*

Ddx inflammatory causes of parotid gland enlargement

A

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
Q

/

Causes of bilateral parotid enlargement

A

 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
Q

*

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

A

Acute parotitis

42
Q

*

Pt presents with high fever, bilateral parotid swelling and pain, testicular discomfort

Most likely Dx

A

Viral infection of parotid e.g. Mumps

43
Q

*

Pt presents with mild parotid pain that’s worse after meal, and intermittent swelling over the parotid glands

Most likely Dx

A

Chronic sialadenitis e.g. stone obstruction, stasis and infection

44
Q

*

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

A

Sjogren’s syndrome

45
Q

*

Acute parotitis

Pathogenesis
Clinical features
Tx

A

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
Q

*

Viral infection of parotid and submandibular glands

  • Causative pathogens
  • Clinical presentation
  • Diagnosis
A

Pathogen:
Mumps (commonest), but now vaccinated
 Coxsackie virus
 CMV
 Influenza

S/S:
High fever
 Usuallybilateral parotid and submandibular enlargement
 Mumps also affects other exocrine glands: pancreas, testes

Diagnosis:
 Clinica picture (high fever + symmetrical swelling)
 Serology

47
Q

*

Chronic sialadenitis

  • 2 main causes
  • General clinical features
  • Diagnosis
  • General Tx
A

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
Q

*

Sialolithiasis

Which gland most affected
Clinical presentation
Complications
Diagnosis
Tx

A

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
Q

*

Sjogren’s syndrome

  • Demographics
  • Pathogenesis
  • Differentiate primary vs secondary cause
A
  • 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
Q

*

Sjogren’s syndrome

Clinical presentation
Diagnostic tests

A

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
Q

*

Sjogren’s syndrome

Treatment options

A

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
Q

*

Compare the distribution of cancer in major salivary gland + proportion of benign vs malignant

A

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
Q

*

List benign tumors of the major salivary glands

A

Benign:

Pleomorphic adenoma
-Warthin’s tumor/ Papillary cystadenoma lymphomatosum
-Oncocytoma
-Monomorphic adenoma
-Basal cell adenoma
- Myoepithelioma

54
Q

*

List malignant tumors of the major salivary glands

A

Mucoepidermoid carcinoma
Adenoid cystic carcinoma
Squamous cell carcinoma
Lymphoepithelial- like carcinoma (LELC)
Acinic cell carcinoma
Carcinoma ex- pleomorphic adenomav(from Mucoepidermoid carcinoma

55
Q

*

Pleomorphic adenoma

  • Demographics
  • S/S
  • Which glands most affected
  • Biological behavior
  • Tx
A
  • 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
Q

*

Warthin’s tumor/ papillary cystadenoma lymphomatosum

  • Demographics
  • S/S
  • Which gland most affected
  • Biological behavior
A
  • 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
Q

/

Parotidectomy

  • Extent of excision
  • Approach technique
A

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
Q

Early complications of parotidectomy and submandibulectomy

A

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
Q

Late complications of parotidectomy and submandibulectomy

A

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
Q

/

Pathogenesis of Frey’s syndrome

A

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
Q

*

Pt presents with Long-standing, painless parotid mass with sudden enlargement

Most likely neoplastic ddx

A

Carcinoma ex- pleomorphic adenoma

High grade Mucoepidermoid carcinoma

62
Q

*

Pt presents with pain in parotid area, paraesthesia over tongue and some facial weakness

Most likely neoplastic Dx

A

Adenoid cystic carcinoma in Submandibular gland

63
Q

*

Pt presents with slow-growing, painless mass over parotid glands

Most likely neoplastic ddx

A

Low grade Mucoepidermoid carcinoma

Acinic cell carcinoma

64
Q

*

Mucoepidermoid carcinoma

  • Demographic
  • Most affected gland
  • Presentation
  • histology
  • Tx
A
  • 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
Q

*

Adenoid cystic carcinoma

  • Demographic
  • Most affected gland
  • Presentation
  • Tx
A
  • 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
Q

/

Acinic cell carcinoma

  • Demographic
  • Most affected gland
  • Presentation
  • Tx
A
  • 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
Q

/

Carcinoma ex- pleomorphic adenoma

  • Demographic
  • Most affected gland
  • Biological behavior
  • Presentation
  • Tx
A
  • 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
Q

/

Squamous cell carcinoma of salivary glands

  • Demographic
  • Origin of neoplastic cells
A
  • 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
Q

/

Lymphoepithelial- like carcinoma (LELC)

Histology
Tx

A

Undifferentiated carcinoma:
 Histology exactly like NPC
 EBV-related (tumor cells = EBER-RNA +ve

Surgery + post-op radiotherapy to primary and neck

70
Q

*

Most common and 2nd most common salivary gland neoplasms

Most common pediatric salivary gland neoplasms

Most common parotid tumor to cause facial paralysis

A

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)

MBBS IV - Junior Clerkship WCS (131 decks)

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