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PAROTID GLAND NEOPLASM

Dillip Kumar Samal


Parotid Gland
Major salivary gland
Embryology- Ectodermal origin
It is anterior to and below the lower half of the ear,
superficial, posterior, and deep to the ramus of the
mandible
It extends from the zygomatic arch down to the lower
border of the mandible.
Posteriorly it covers the anterior part of the
sternocleidomastoid muscle and continues anteriorly to
halfway across the masseter muscle.
Anatomy
Anatomy
Parotid duct leaves the anterior edge of the parotid gland
midway between the zygomatic arch and the corner of the
mouth.
It crosses in a transverse direction and, cross the medial
border of the masseter muscle, turns deeply into the buccal
fat pad and pierces the buccinator muscle.
It enters the inside of the mouth near the second upper
molar tooth.
Anatomy
Covered by investing fascia of neck & contain lymphnode
mainly in superficial lobes.
Structures within the gland :
Facial nerve
Retromandibular vein
External carotid artery
Parotid lymphnodes
Anatomy
Anatomy
Deep lobe lie in parapharyngeal space.

Anterior : Infra-temporal fossa


Posterior : Carotid sheath & Styloid process
Medial : Superior constrictor muscle of pharynx, which
separates gland from oropharynx and tonsil.
Anatomy
Blood Supply:
-Superficial temporal artery
-Retro mandibular vein

Lymphati drainage
-Parotid & Deep cervical lymphnode
Anatomy
Nerve Supply:

Parasympathetic:
Inferior Salivatory nucleus CN IX
Lesser Petrosal Nerve Otic ganglion
Auriculotemporal nerve Parotid gland

Sympathetic :
Sympathetic trunk Superior cervical ganglion
External carotid artery plexus Parotid gland
Sensory innervation of the parotid gland is provided by the
auriculotemporal nerve, which is a branch of the mandibular nerve[V3].
CLASSIFICATIONS
A. Benign Tumour
1. Pleomorphic Adenoma
2. Myoepithelioma
3. Oncocytoma
4. Warthins Tumour
5. Basal cell Adenoma
6. Canalicular Adenoma
7. Sebaceous Adenoma
8. Ductal papilloma:
1. Inverted ductal papilloma
2. Intraductal papilloma
3. Sialodenoma paplliferum
9. Cystadenoma
1. Papillary cystadenoma
2. Mucinous cystadenoma
CLASSIFICATIONS
B. Carcinoma:
1. Acinic cell carcinoma
2. Mucoepidermoid carcinoma
3. Adenoid cystic carcinoma
4. Polymorphus low grade adenocarcinoma
5. Basal cell adenocarcinoma
6. Sebaceous carcinoma
7. Papillary cystadenocarcinoma
8. Mucinous adeno carcinoma
9. Oncocytic carcinoma
10. Adenocarcinoma
11. Squamous cell carcinoma
12. Small cell carcinoma
13. Undifferentiated carcinoma
CLASSIFICATIONS
C. Miscellaneous:
1. Non-epithelial tumours
2. Malignant lymphoma
3. Secondary tumours
4. Unclassified tumours
Histogenesis:
I. Multi-cellular theory
Each type of neoplasm is thought to ariginate from distinctive
cell type within the salivary gland.
1. Ductal cell- Warthins tumour & Oncocytic Tumour
2. Acinar cell- Acinic cell tumour
3. Intercalated duct & myoepithelial cell Mixed tumour

II. Bicellular Theory


The basal cell of excretory & intercalated duct act as stem
cells.
1. Intercalated duct stem cell: adenomatoid tumour including
pleomorphic adenoma and oncocytic tumors.
2. Excretory duct stem cell: squamous cell carcinoma &
mucoepidermoid carcinoma
AETIOLOGY
Radiation:

Exposure to ionising radiation increases the risk of


development of salivary gland neoplasm (both benign and
malignant).
Risk is higher for malignant tumors , especially
mucoepidermoid carcinoma.
Among benign neoplasm, Warthins tumor showed
maximum dose-response-related risk.
AETIOLOGY
Viral:

Epstein-Barr Virus has consistent association of with


lymphoepithelial carcinoma of the salivary gland ,
especially in asian population.
No evidence of causal role of EBV in other primary
salivary gland neoplasm.
AETIOLOGY

Genetic factors:

Many genetic alternation may be responsible for


increased likelihood of developing salivary gland
neoplasm, includes-
Allelic loss and point mutation.
Structural rearrangement (most commonly
translocations)
Monosomy & polysomy .
AETIOLOGY
Other factors:

Warthins tumor is strongly associated with cigarette smoking.


Occupational exposure to silica dust- linked to 2.5 fold increase
risk of salivary gland cancer.
Others-rubber workers exposed to nitrosamines.
Women with h/o early menarche and nulliparity had increased
risk of salivary gland carcinoma.
Incidence
Salivary gland tumors - 3% - 4% of all head & neck
neoplasm.
70% originate in parotid gland.
> 75% of them are Benign.
Benign neoplasm constitutes 54 % of all tumors.
Plemorphic adenoma constitutes 84% of benign tumors &
45% of all salivary gland neoplasm.
Warthins tumour- 2nd MC benign tumor (~12%).
MC benign tumor of minor salivary gland- Pleomorphic
adenoma.
Clinical presentations:
Usually present as slowly growing painless swelling,
whether benign or malignant.
Benign tumors of the parotid gland are usually well-
defined, nontender, and freely mobile.
They are commonly located in the "tail" of the parotid
gland, but may present anywhere.
Tumors can originate entirely from the deep lobe or extend
from the superficial to the deep lobe through the relatively
narrow stylomandibular tunnel, giving the appearance of a
dumbbell-shaped tumor
Clinical presentations:

Dumbbell tumor enters parapharyngeal space through stylomandibular


membrane between the mandible and the stylomandibular ligament.
Clinical presentations
Patients presenting with a mass in the parotid gland should be
asked about a history of cancer of the scalp or facial skin.
A sudden increase in size indicates-
malignant transformation of previous benign lesion,
inflammation,
cystic degeneration, Most commonly in Warthins Tumor
Malignanancy indicators:-
Facial nerve paresis or paralysis.
Pain
Fixation of mass to the overlying skin or underlying
structures
Cervical adenopathy
Fine-Needle aspiration
Biopsy
FNAB is safe, simple to perform, and relatively inexpersive.

Diagnostic accuracy is higher for benign than malignant


tumors.

Sensitivity ranges from 85.5%- 99%

Specificity ranges from 96.3% - 100%

The most common source of diagnostic error of FNAB is


inadequate sampling.
Fine-Needle aspiration
Biopsy
Advantages :
Important to distinguish benign vs. malignant nature of
neoplasm
Preoperative patient counseling
Surgical planning
Can avoid surgical excision- in cases of lymphoma and
inflammatory pathology
More Conservative approach can be adopted benign
tumors in elderly and high-surgical-risk patients.
Imaging modalities
Computed Tomography And Magnetic Resonance Imaging-
Provides accurate delineation of location & extent of the
tumor.
Its relation to major neurovascular structure
Intra or Extraglandular
Perineural spread.
Skull base invasion.
Intracranial extension.
Imaging modalities
MRI is the radiological modality more often recommended
to acess salivary gland neoplasm, if not contraindicated.
But most of the time cant provide histologic diagnosis
(Except rarely i.e; in cases of Lipoma)
Benign tumors have well-defined margins , where as
malignant tumors have irregular margins.
Imaging modalities
Advantages of Computed Tomography:
Less expensive
Better availability than MRI.
Bone destruction of mandible or skull base is best
visualised on CT ,i.e; particularly useful for evaluating
cortical bone erosion.
It is particularly helpful in assessing salivary gland masses
if sialolithiasis is considered to be a component of etiology.
An axial CT with
intravenous contrast
demonstrating a large,
rounded, well-defined mass
with smooth borders in the
parotid gland. The mass was
nonenhancing and had the
same density as the
subcutaneous fat. These
findings were
pathognomonic of parotid
lipoma. superficial
parotidectomy was
performed, and the diagnosis
was confirmed.
Imaging modalities
Magnetic Resonance Imaging:
Benign and malignant neoplasms of parotid gland are well
visualised on T 1-weighted images, because they are easily
distinguished from the fatty parenchyma of the gland,
which are hyperintense.
Benign epithelial neoplasm(such as pleomorphic adenoma)
and low-grade malignancies have low T1- weighted and
high T2-weighted signal intensities.
High-grade carcinoma shows low-to-intermediatesignal
intensities on both T1-weighted images and T2-weighted
imaging
Imaging modalities
Use of contrast material such as gadolinium and fat
saturation of T1-weighted images useful in assessing bone
involvement and perineural spread.

Enlarged foramina at the skull base and the presence of


hyperintense enhanced tumor tissue are suggestive of
perineural spread.
Imaging modalities
Advantages :-
MRI signal characteristics may be diagnostic-
Warthins tumor when parotid mass is B/L , especially if it is
non-enhancing.
A intermediate to lowT2 signal signal mass with or without
invasion of sorrounding tissue plane, is more likely to be
malignant i.e; Adenoid cystic carcinoma or Mucoepidermoid
carcinoma
MRI is superior in demonostrating internal architecture of
salivary gland tumors and to delineate tumor from normal
salivary gland
Bone marrow involvement is better picked-up with MRI.
Imaging modalities
MRI characteristics of Parapharyngeal space Tumors:

Deep lobe parotid tumors and minor salivary gland tumors of


parapharyngeal space ,lie in pre-styloid compartment anterior to
carotid artery and displace the parapharyngeal fat medially.
Deep lobe parotid tumors are connected to the parotid gland at
least in one imaging section, whereas minor salivary gland tumors
are completely sorrounded by fat.
Neurogenic tumors and Glomous tumors lie in the post-styloid
compartment, posterior to carotid artery, which is displaced
anteriorly.
Neurogenic tumors usually enhance intensely with Gadolinium ,
whereas glomous tumors have characteristic serpigenous flow
voids (salt and pepper appearance ) on MRI
Imaging modalities

New MR Technologies:

Dynamic contrast enhanced MRI


Diffusion weighted MRI
Proton MR spectroscopy
Ultrasonography
Inexpensive, non-invasive, simple
Differentiate solid from cystic lesion
USG guidance enhance accuracy of FNAB in non-palpable
tumors

Color Doppler Sonography:


Used to evaluate vascular anatomy of salivary glands.
Distinguish between physiologic alteration occurs during
salivary stimulation in normal subject and flow alteration occurs
in diseased glands.
Positron Emission
Tomography
Salivary glands have variable and inconsistent uptake of F-
18 fluorodeoxyglucose, (FDG) which is most commonly
used radiotracer with PET Scans.
So it is unreliable in both tumor detection and
distinguishing benign from malignant lesion.
Pleomorphic Adenoma
Benign mixed tumor
Most common neoplasms of salivary gland
F > M
75% of all benign tumors of major salivary gland
Originates from uncommitted reserve cell of the
intercalated duct that has the potential to differentiate into
epithelial and myoepithelial component.
In parotid gland-90% originate superficial to facial nerve
- 10% originates from deeep lobe and
usually located deep to stylomandibular ligament.
Pleomorphic Adenoma
When arises from minor salivary gland of parapharyngeal
space occupy the prestyloid compartment and may displace
the oropharynx medially.
Pleomorphic adenoma of minor salivary glands arises most
commonly from palate,2nd most common site is upper lip.
These are the MC benign tumors of lacrimal gland also.
Pleomorphic Adenoma
Pathologically, solitary, firm, round tumor.
Pleomorphic adenoma of major salivary glands have a
capsule with varying thickness and completeness (where as
in minor salivary gland, they are usully non-encapsulated.)
1/4th of tumors demonstrate satellite nodules or
pseudopodia.
Epithelial component: may take the form of ducts, nests,
cords or solid sheets of cells
Myoepithelial component: responsible for characteristic
myxoid or chondroid stroma.
Pleomorphic adenoma of the deep lobe of
a parotid gland, causing medial
displacement of the palate and tonsil.
Pleomorphic Adenoma
Pleomorphic adenoma - deep lobe of
the parotid gland and lies medial to the
stylomandibular tunnel.

Pleomorphic adenomas originating


from the minor salivary glands of the
parapharyngeal space have a similar
appearance on CT but are not
connected to the parotid gland.

Salivary gland tumors of the


parapharyngeal space will occupy the
prestyloid compartment and displace
the carotid artery posteriorly.
Pleomorphic Adenoma
Recurrent pleomorphic Adenoma:
Uncommon, but challenging problem
Multicentric pattern is characteristic of recurrent
pleomorphic Adenoma
Surgical excision is mainstay of treatment
Pts who undergone previous surgery are increased risk
for facial nerve injury, and as well as recurrence with
revision surgery.
Neutron Radiotherapy offers excellent local control and
survival rates in recurrence cases, who are not surgical
candidates even in presence of gross residual disease.
Pleomorphic Adenoma

Malignant transformation:
Rare and occurs most frequently in pts with long
standing tumors.
Risk of malignant transformation 1.5% within 1st 5 yrs
of diagnosis, increased to 10% if observed for >15 yrs.
Cases of benign pleomorphic adenoma metastasizing
to cervical lymphnodes has been reported.
Basal Cell Adenoma

Most commonly occors in parotid gland and minor


salivary gland of upper lip
Well circumscribed, solid tumor
In parotid, it is well circumscribed, where as in minor
salivary gland, it is non-capsulated usually
Four Histologic variety:-
Solid ,
Trabecular ,
Tubular , and
Membranous
Basal Cell Adenoma

D/D : Solid variety of Adenoid cystic carcinoma


Difference:
Lack of true invasion of surrounding tissue
Lack of perineural invasion
Vascular stroma
Peripheral palisading of outer layer of basaloid cells.
T/t is surgical excision with cuff of normal
surrounding tissue
Warthins Tumor
Papillary Cystadenoma lymphomatosum
or Adenolymphoma
2nd MC benign salivary gland neoplasm
10% of all parotid tumor
Found almost exclusively in parotid gland
M > F, More in whites.
B/L in 10% cases and may be simultaneous.
Associated with cigarette smoking, may be due to
irritation of ductal epithelium by tobacco smoke, which
initiates tumorigenesis.
Warthins Tumor
Presentation: slow-growing, painless mass often in superficial
lobe of parotid gland near the angle of mandible.
Gross: -Multiple large cystic appearance, with fluid filled
spaces.
Microscopy: Papillae of eosinophilic epithelia projecting into cystic
spaces and lymphoid matrices are pathognomonic histologic features.
Typical cells- Oncocytes ( cells with granular eosinophilic
cytoplasm)- have abundant mitochondria

Treatment: usually parotidectomy with facial nerve preservation.


Inadequate excision or tumor multictrity may explain
recurrence.
Oncocytoma
< 1% of salivary gand tumors.
Parotid is the most frequent site.
Slow-growing , painless mass.
6th decade.
M:F = 1:1.
Cell of origin: Oncocytes- large epithelial cell with
granular eosinophilic cytoplasm
Oncocytoma
Gross: Well circumscribed and encapsulated
Microscopy: Oncocytes.
Concentration of mitochondria differentiates oncocytoma
from other tumors.
True oncocytoma contains no lymphoid tissue.( The extensive
lymphoid tissue typical of warthins tumour is never
encountered)
D/D : Adenoid cystic crcinoma
Mucoepidermoid carcinoma
Adenocarcinoma
Metastatic thyroid & renal cell carcinoma
Treatment: Surgery
Hemangioma
Juvenile hemangioma are MC tumors of infancy.
More common in parotid than submandibular gland.
F > M
C/F : Asymptomatic, unilateral and compressible mass.
Usually involute completely, but may take several years.
Malignant tumors
Malignant neoplasms of the salivary glands constitutes 3% of all
head and neck malignancies.
Salivary gland tumors in children are more likely to be malignant.
The superficial lobe is the portion of gland lateral to plane of the
facial nerve and contains 10- 20 nodes on average.
The deep lobe lies medial to plane of facial nerve and extends in
to parapharyngeal space.
Parapharyngeal space devided in to :
Prestyloid ( anterolateral)
poststyloid ( posterolateral) compartment by a fascial layer
that extends from styloid process to Tensor veli palati ms.
Malignant tumors
Deep lobe tumors when involve:

Prestyloid compartment- submucosal bulging mass in


oropharynx and/or nasopharynx
Poststyloid compartment-Cranial nerve neuropathy( IX,
X,XI, XII)
Infratemporal fossa- Trismus.
2003 AJCC TNM STAGING FOR MAJOR SALIVARY
GLAND MALIGNANCY
TX Primary tumor cannot be assessed
T0 No evidence of primary tumor
T1 Tumor 2 cm or less
T2 Tumor 2-4 cm
T3 Tumor more than 4 cm or extraparenchymal extension
T4a Tumor invades skin, mandible, ear canal, or facial nerve
T4b Tumor invades skull base, pterygoid plates, or encases carotid artery
NX Regional lymph nodes cannot be assessed
N0 No regional lymph node metastasis
N1 Metastasis in a single ipsilateral lymph node 3 cm or less
N2a Metastasis in single ipsilateral lymph node 36 cm
N2b Metastasis in multiple ipsilateral lymph nodes <6 cm
N2c Metastasis in bilateral or contralateral lymph nodes <6 cm
N3 Metastasis in lymph node >6 cm
M0 No distant metastasis
M1 Distant metastasis
STAGE GROUPING FOR MAJOR SALIVARY
MALIGNANCY
Stage I T1 N0 M0
Stage II T2 N0 M0
Stage III T3 N0 M0
T1 N1 M0
T2 N1 M0
T3 N1 M0
Stage IVA T4a N0 M0 Stage IVB T4b AnyN M0
AnyT N3 M0
T4a N1 M0 Stage IVC AnyT AnyN M1
T1 N2 M0
T2 N2 M0
T3 N2 M0
T4a N2 M0
Malignant tumors
Relationship between site of primary tumor and frequency
of malignancy

Site Percentage of Percentage of


neoplasm Malignancy
parotid 73 % 15 %

Submandibular 10.7 % 37 %

Sublingual 0.3 % 85.7 %

Minor glands 14 % 46.4 %

Cummings 5th edition


Malignant tumors
Relative incidence of Malignant salivary neoplasm

Histologic Type Percent


Mucoepidermoid Carcinoma 34 %
Adenoid cystic carcinoma 22 %
Adenocarcinoma 18 %
Malignant mixed tumor 13 %
Acinic cell carcinoma 7%
Squamous cell carcinoma 4%
Others ( anaplastic etc. ) 3%

Cummings 5th edition


Mucoepidermoid
carcinoma
Most common salivary gland malignancy.
F > M.
Mean age : 45 yrs
Most common pediatric salivary gland carcinoma
MC presentation:
Painless slow growing mass.
Inraoral tumors may mimic a mucocele or vascular
lesion clinically by presenting as a blue red superficial
nodule.
Mucoepidermoid carcinoma
Gross: Have both solid and cystic component, often with
mucinous material within the cysts, imparts bluish colour to
the tumor
Mucoepidermoid
carcinoma
Microcopy : Hallmark is the presence of three types of
cells: Mucous, Squamoid (or Epidermoid), Intermediate
cell
Mucoepidermoid cancer is histologically classified:
low
intermediate
high grade.
A higher grade correlates with a poorer outcome.
Low-grade tumors have a higher percentage of mucinous
cells, whereas epithelial cells predominate in high-grade
tumors.
Low grade

intermediate grade

High grade
Mucoepidermoid
carcinoma
Differential diagnosis :

Necritising sialometaplasia ( particularly, when tumor


arising from mucosal sites )- non-neoplastic lesion of hard
palate
Adenosquamous carcinoma (aggesive variant of squamous
cell carcinoma.
Adenoid cystic carcinoma
Previously called Cylindroma
Overall 2nd most common malignancy
Most common in submandibular, sublingual and minor salivary glands
M = F
5th decade
Presentation:
Asymptomatic enlarging mass
Notorious for its infiltrative growth, slowly progressive behavior with
recurrences.
Perineural involvement- is characteristic of adenoid cystic carcinoma &
occur in 70-75%.
Adenoid cystic carcinoma

The palate is the most common site


for adenoid cystic carcinoma

Gross : Solid, light tan, firm and well-circumscribed,


unencapsulated tumor.

Microscopy : three growth pattern:


Tubular
Cribriform
Solid
Cribriform

Tubular

Solid pattern
Adenoid cystic carcinoma
Prognosis :

The cribriform pattern has a glandular architecture and is


reported to have the best prognosis.
The solid pattern is more epithelial in nature and is
associated with a poorer prognosis.
The tubular pattern has a clinical prognosis of intermediate
nature between the other two patterns.
Acinic Cell Carcinoma
1-3% of all salivary gland neoplasm.
~10 % of all parotid carcinoma
> 90% in parotid.
Wide age range, with peak in 3rd decade.
2nd most common childhood salivary gland
malignancy.
Presents : Slow growing mass , occasionally painful,
rarely associated with facial palsy.
Acinic Cell Carcinoma
Gross: Single, circumscribed, rubbery, solid mass with
1/3rd showing cystic degeneration.
Macroscopically: Four histological patterns identified
solid,
microcystic,
papillary-cystic
& follicular.
Small tumors can be easily missed because the acinar cells
are so well differentiated that they blend into the normal
surrounding tissue.
Most imp. D/D : Normal parotid gland
Acinic Cell Carcinoma
Low grade malignancy
But, 10-15% of these tumors -metastasize locally to
regional lymph nodes or distantly to lungs and bones.
Recurs in ~1/3rd cases.
T/t : Surgical resection with negative margins.
Malignant mixed
tumor
3-5 % of all salivary gland malignancies

Encompass three different salivary gland


malignancies:
1. True malignant mixed tumor ( or Carcinosarcoma)
2. Carcinoma ex-pleomorphic adenoma- MC
3. Metastasizing mixed tumor
Malignant mixed
tumor
True malignant mixed tumor ( or Carcinosarcoma)

Carcinomatous + sarcomatous component.


Sarcomatous component- usually chondrosarcoma or
osteosarcoma.
~1 % of all salivary gland malignancy.
Mean age : 58 yrs.
2/3rd cases in parotid gland.
Aggressive tumor with poor prognosis.
T/t : Wide local excision + radiotherapy.
Malignant mixed
tumor
Carcinoma ex-pleomorphic adenoma(MC variety)

Defined as a pleomorphic adenoma( or mixed tumor) with


which, or in which, a carcinoma is present.
Accounts for >95% of Malignant mixed tumor.
MC site- parotid gland.
Age group: Approx. 1 dacade later than the peak age for
pleomorphic adenoma-6th and 7th decade.
C/F : Long standing mass that suddenly undergoes rapid growth
over a pariod of several months.
Tm. Size can reach up to 25 cm
Carcinoma ex-pleomorphic adenoma

Axial CT demonstrating large


carcinoma expleomorphic tumor in the
superficial lobe of the parotid gland.
Malignant mixed
tumor
Carcinoma ex-pleomorphic adenoma
Prognosis and management:
1. Dependant on the type of cacinoma associated with the mixed
tumor
2. critical histologic feature i.e;

Non-invasive (intra-capsular) No risk of recurrence


or metastasis from a
completely resected
Minimally invasive (1.5mm beyond the capsule)tumor

Invasive (1.5 mm)- poor prognosis.

T/t: Wide resection with lymphnode dissection and radiation


theraphy is the t/t of choice
Malignant mixed
tumor
Metastasizing mixed tumor/pleomorphic adenoma

Least common form of Malignant mixed tumor.


Have a morphology of a pleomorphic adenoma with a
mixture of myoepithelial and duct like epithelial
components and myxoid or chondroid surrounding
matrix.
Metastasize to :
Local lymphnodes (30 % )
Bones (50 % )
Lungs (30 % )
The time interval between the primary tumor and detection of
metastatic disease is ~ 12 yrs.
Salivary duct carcinoma
It is the most aggressive salivary gland carcinoma.
Constitutes < 10 % of all salivary gland carcinoma.
M : F = 4 : 1
Usually in 6th decade
70 90 % in parotid gland.
Presents as rapidly growing parotid mass Facial nerve
involvement.
Salivary duct carcinoma

Infiltration to surroundig tissue - common


Vascular and perineural invasion - common.
High grade tumor.
30 % - 40 % of patients shows local recurrences
50 % - 75 % shows develop distant metastasis
Squamous cell carcinoma
Rarely to be primary.
Usually metastasized tumor to intraparotid lymph node from
skin cancers of head & neck or direct involvement from
adjacent tissue.
80% -90 % arise in parotid gland.
6th to 8th decade
H/o prior radiation therapy may present.
Aggressive tumor, shows perineural invasion with extension
of tumor tissue into periglandular soft tissue.
T/t: Radical surgery+ Neck dissection + Radiotherapy
Primary small cell carcinoma
Also called high-grade neuroendocrine carcinoma
~ 2 % of all salivary gland malignancy
MC in parotid gland.
Presents as :
Painless mass of several months
6th to 7th decade
Many with associated cervical lymphadenopathy
Facial nerve palsy
Prognosis poor
Metastasis occurs to Lymphnode as well as distant sites-
Liver, lung, brain and bones.
Metastatic tumor
Metastasis can occur to intraglandular or periglandular
lymphnodes.
Parotid gland contains an avg. of 20 intraparenchymal nodes,
(submandibular and sublingual gland- no nodes)
Usually from head and neck primaries.
Skin tumors like Squamous cell carcinoma and Melanoma
accounts for for 80% to 90 % of metastases
Non-cutaneus malignancy- Lung, kidney, breast, nasopharynx
Focused within the lymph nodes, but almost always have a
extracapsular extension with growth of tumor into adjacent
normal salivary gland tissue.
Lymphoma
Constitutes 5 % of extranodal lymphoma
2 % of all salivary gland tumor
MC is non-hodgkins lymphoma
Age group: 50 70 yrs.
MALT lymphoma can occur in the settings of lympho-
epithelial sialodenitis.
FNAC is helpful in diagnosis with high sesitivity and
specificity.
Epithelial-Myoepithelial
carcinoma
Moderately aggressive tumor
0.5 %- 1% of salivary gland neoplasm
Predominantly in parotid gland ( 80% )
Microscopic invasion to adjacent parenchyma present.
Recurrence rate 40 %
Shows both lympnode and systemic metastasis
T/t : Wide local excision Radiotherapy.
Factor associated with occult metastasis and/or poor
prognosis of salivary gland malignancies:

1. Tumors of submandibular and sublingual gland tend to


metastasize more frequently, than parotid gland.
2. T3, T4 lesions.
3. > 50 yrs of age.
4. Facial paralysis and pain are associated with lymph node
metastasis.
5. Histology:
High grade muco-epidermoid carcinoma
Undifferentiated carcinoma
Squamous cell carcinoma
Adenocarcinoma
Salivary duct carcinoma
Factor associated with occult metastasis and/or
poor prognosis of salivary gland malignancies:

6. Perineural invasion, local bone invasion


7. Positive resection margin
8. High Ki-67 and low p27 expression, especially in
adenoid cystic and mucoepidermoid carcinoma
9. HER-2 /neu overexpression in salivary duct
carcinoma and mucoepidermoid carcinoma
Treatment

principal treatment of salivary gland tumors is surgical


resection with save margins used either as single
modality or conjunction with adjuvant radiotherapy.
Surgery
When tumor is limited to lateral (or superficial) lobe, a
superficial parotidectomy is adequate treatment for low
grade well-encapsulated tumor, like Acinic cell
carcinoma.
If tumor is larger, a partial deep lobe resection can be
performed to include an adequate margin.
Total parotidectomy indicated in :
High grade malignant tumor with risk of metastasis
Any parotid malignancy with an indication of having
metastasized to intraglandular or cervical lymph node.
Primary malignancy originating in deep lobe itself.
Surgery
modified Blairs incision.

Modified face-lift incision


( Incision extends posteriorly
and inferiorly along the hairline,
unlike cervical extension in case
of Modified blairs incision)
Surgery

Facial nerve :

If pre-operative function is intact, most probably it is not


involved.
If pre-operative evaluation reveals facial paresis, means it is
involved and has to be resected
The nerve may be reconstructed later by:
primary neurorraphy or
by placing interposition graft, using either a segment of
Greater auricular nerve or Sural nerve.
Complications of
parotidectomy

Intra-operative complications :

Transection of facial nerve


Rupture of capsule of parotid tumor
Incomplete surgical resection of parotid tumor
Hemorrhage
Post-operative complications
Early

Facial nerve paralysis


Hemorrhage or haematoma
Infection
Skin flap necrosis
Cosmetic deformity
Trismus
Parotid fistula
Post-operative complications

Late

Facial synkinesis after facial palsy


Hypoesthesia of greater auricular nerve
Recurrent tumor
soft tissue defect
Hypertrophic scar or keloid
Freys syndrome
parotidectomy

Facial nerve injury:

Post-operative facial nerve dysfunction involving some or all


of the branches of the nerve is the most frequent early
complication of parotid gland surgery.
The incidence of facial nerve paralysis is higher with total,
than with superficial parotidectomy.
Revision parotidectomy or parotidectomies for parotid fistula
are generally associated with a higher incidence of facial
weakness.
parotidectomy
The branch of the facial nerve most at risk for injury during
parotidectomy is the marginal mandibular branch.

EMG monitoring in parotid surgery :


Laryngoscope, 119:22992305, 2009

Did not diminish either the incidence of postoperative facial


paralysis or the final facial outcome.
Nevertheless, the duration of surgery for superficial parotidectomy
could be reduced by using EMG monitoring.
parotidectomy
Frey syndrome :
ACTA OTORHINOLARYNGOL ITAL 25, 174-178,2005

Frey syndrome is a disorder characterized by unilateral


sweating and flushing of the facial skin in the area of the
parotid gland occurring during meals.

Evident usually 1-12 months after surgery.

Pathogenesis : Based on the aberrant regeneration of sectioned


parasympathetic secretomotor fibres of the auriculotemporal
nerve with inappropriate innervation of the cutaneous facial
sweat glands that are normally innervated by sympathetic
cholinergic fibres.
Complications of
parotidectomy
Frey syndrome :
The clinical incidence may as high as 50% (severe in 15%).
Gustatory sweating is detected in almost 100% of cases,
evaluated by means of a post-operative iodine-starch test
(Minor test)
Treatment :
Madical :
Systemic or topical application of various anticholinergic
agents (scopolamine,glycopyrrolate, diphemnanil-
methylsulfate) and
the use of stellate ganglion blockade have been unsuccessful.
Complications of
parotidectomy
Frey syndrome :
Surgical treatment : Includes-
cervical sympathectomy,
tympanic neurectomy,
sternocleidomastoid transfer and
dermis-fat grafts and the use of various materials, as
interpositional barriers
The outcome of these techniques has been disappointing since
only temporary relief is achieved.

Prophylactic measures, including the use of the


Superficial musculoaponeurotic system (SMAS) as a flap or
Superficial temporal artery fascial flap.- shows better result.
Complications of
parotidectomy
Frey syndrome :
Botulinum toxin injection:

BTX therapy, now the standard treatment.


Botulinum toxins prevent the release of acetylcholine at the
neuromuscular junction of striated muscles and thus produce
chemical denervation and paralysis of the muscles
There are two commercial product of BTX-A available: Botox
(Allergan Ltd, Ireland) and Dysport (Ipsen Ltd, UK). The dose
of botulinum toxin is expressed in mouse units (U).
Clinically, 1 U of Botox is equivalent to approximately 3 U of
Dysport.
Complications of
parotidectomy
Frey syndrome :
The mean dose is 30-50 U
The gustatory sweating usually ceases in the treated area,
within 48-72 hours. No significant adverse effects have
been described and only transient paresis of the orbicularis
oris
A marked long-lasting improvement, ranging from 11 to 36
months occur after a single injection.
Surgery
Advanced parotid tumor may require:
A partial mandibulectomy,
A lateral or partial temporal bone resection
Extended resection of pharyngeal mucosa
Resection of facial skin

PAROTID CANCER OCCULT NODAL 30 % of


INVOLVEMENT mets
( Armstrong and colleagues )
Parotid nodes 16 53
Level 1 3 10
Level 2 8 27
Level 3 7 23
Level 4 6 30
Level 5 1 3
Lymph node metastasis
Tumor with N0 neck:
Occult metastasis in N0 neck: 38% - 45 %
Seen more in high grade tumors and undifferentiated carcinoma,
but can be present in T1 or T2 lesions also.
So, selective ipsilateral neck dissection should be performed on all
patients with salivary gland malignancies- in view of recent studies.
Some advocated use of radiation therapy for N0 neck.
Tumors with N+ Neck:
Ipsilateral neck dissection should be performed with palpable or
radiographic enlarged lymph node.
Improves loco-regional control and survival
Ipsilateral modified radical neck dissection is indicated.
Radiation therapy
Adjuvent radiation therapy:

Adjuvant radiotherapy postoperatively is superior to


surgery alone & appears to improve locoregional control.
Especially recommended in cases:
Advanced stage of tumors
Presence of positive margins following resection
High grade tumors
Neural involvement
Bone involvement
Radiation therapy
Radiation of the neck :

The postoperative radiotherapy of the neck in cases where


lymphnode positive improves locoregional control and
survival rates.
In N0 neck cancer cases post-op radiation decreases nodal
recurences, as per the recent studies, because micro-metastasis
can occur even in T1 or T2 diseases also.
Radiation therapy
Neutron beam radiotherapy:

Salivary gland malignancies considered to be relatively radio-


resistant.
Fast neutrons deliver more energy, compared to
photons/electron radiotherapy and are more destructing, so can
be used in t/t of unresectable or recurrent tumors.
Shows significant improvement of locoregional control with
Neutron beam radiotherapy, but overall survival however
shows no difference, because of distant metastasis.
Chemotherapy
Currently limited to palliative treatment of
locally advanced , recurrent and metastatic
diseases.
Agents used :
Platinum based ( e.g; cisplatin, carboplatin,
etc )
Anthracyclin based ( e.g; mitoxantron )
Newer therapies:
Adenoid cystic carcinoma express c-KIT in >90 % cases and
expression of this correlated with tumor grade.
EGFR (Also known as ErbB1 ) is expressed in 79 % of parotid
malignancies.
Directed therapy against biologic targets :
Receptor tyrosin kinase such as c-KIT and
Members of ErbB family (EGFR, Her2/neu )
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