Professional Documents
Culture Documents
Deepak GOyal
Introduction
Classification
Benign Malignant
Pleomorphic adenoma
• Mucoepidermoid carcinoma
Warthin’s tumor
• Adenoid cystic carcinoma
Oncocytoma
• Carinoma ex- pleomorphic adenoma
Lymphangioma
• Acinic cell ca
Haemangioma
• Adenocarcinoma
canalicular adenoma,
• Salivary ductal carcinoma
basal cell adenoma
• Squamous cell carcinoma
myoepithelioma
• Non-hodgkin’s lymphoma
EPIDEMIOLOGY
Benign tumors account for 63% to 78% of all salivary gland neoplasms.
Genetic predisposition
Tobacco
Chemical carcinogens
Viruses
PLEOMORPHIC ADENOMA
4th-6th decades
M:F = 1:3-4
PLEOMORPHIC ADENOMA
Encapsulated
There are frequently multiple foci of recurrence that may continue to manifest
over several years.
Warthin’s tumor(papillary cystadenoma lymphomatosum )
2nd most common after pleomorphic adenoma
10% bilateral
Usually Fluctuant, slow growing
Never malignant
6th decade
No gender predilection
Surface telangiectasia
Nerve involvement
mucin producing cells & epithelial cells of epidermoid variety & according to that classified into
Low grade
Intermediate
High grade
Perineural spread
Treatment
Complete local excision
Tendency for perineural invasion: facial nerve sacrifice
Postoperative RT
Prognosis
Local recurrence: 42%
Indolent course: 5-year survival 75%, 20-year survival 13%
ACINIC CELL CARCINOMA
Mostly in parotid
Primary treatment is complete surgical resection with neck dissection limited to the therapeutic
setting.
Ranging from low grade well differentiated to high grade invasive lesions
Common in major glands
Originate from excretory or striated ducts
Cystic or solid, may be papillary or non-papillary in growth pattern
Prognosis depend on grade
SQUAMOUS CELL CARCINOMA
Rare to be primary & common to be secondary from intraparotid lymph node or direct
involvement
85% are N H L
Hematogenous metastasis are rare & majority from lung, kidney & breast
USG
X ray chest
OPG To R/O mandibular involvement.
CT SCAN
MRI
USG
Distinguish intrinsic from extrinsic tumors
It can be used to differentiate solid from cystic masses in the salivary glands
USG guided FNAC
CT/MRI
Anatomical localization
Local, regional ,distant invasion
MRI IS BETTER ??
Excellent assessment of margins
Deep extension and infiltration
Bone marrow invasion
Perineural spread
Intracranial extension
Fine-Needle Aspiration Biopsy
Confirms possibility
Lymphoma/inflammatory masses.
Cutting into the tumour should be absolutely avoided as it can lead to tumor spillage
Surgery
Benign tumors
Superficial parotidectomy
If the tumor originates from a minor salivary gland, the tumor and a cuff of normal
tissue should be excised.
Surgery
Malignancies
The mainstay of treatment for salivary carcinomas is surgical resection with or without postoperative
radiotherapy
The extent of surgery is dependent on the size and site of the tumour
As a general rule, every effort should be made to preserve a nerve which was functioning normally
preoperatively
Surgery
preoperative paralysis,
cases of recurrent malignancy
gross encasement and infiltration of the nerve
Surgery
Parotid Gland:
Most T1/T2 lesions lateral to the nerve are suitable for a superficial parotidectomy with adequate
margin 1.5cm
Larger and deep lobe tumours usually require a total conservative parotidectomy with preservation of
the facial nerve
Patients with high grade and extensive disease (i.e. skin involvement or facial palsy) may require
extended radical parotidectomy
Superficial parotidectomy:
Removal of
Both lobes of parotid
Facial nerve
Mandibular ramus
Masseter muscle
Infratemporal fossa dissection
Subtotal petrosectomy
Complications of parotid surgery
HEMATOMA
Salivary fistulas
Frey’s syndrome
Sialocele
A prophylactic selective neck dissection should be considered for patients with high-stage or high-
grade
Radiotherapy
Primary treatment for salivary carcinomas is limited to unresectable tumours
Given in large tumours to reduce the size and make it better operable, i.e. to down stage the disease
Prognosis
Advanced stage, higher histologic grade poor prognosis