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Premanagement in
Salivary Gland TumorsDr Sasikumar SambasivamModerator: Dr Nidhi Patni
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Anatomy
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Anatomy
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y
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External carotid A
RetromandibularVein
Facial NerveSuperficialtemporal A
MaxillaryA
P.AuricularA
Superficialtemporal V
MaxillaryV
Post auricularVExternal
jugularCommon FacialV
FacialNerve
temporal
buccal
mandibular
cervical
zygomatic
Zygomaticotemporal
Cervicofacial
Parotid
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gland
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gland
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Ducts
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Neural Str.Major Gland Cranial Nerve Foramina of base of skull
ParotidSuperficial
Deep
7
9,10,11,12
Stylo mastoid foramen
Jugular foramen andHypoglossal canal
Sub mandibular V3,7 (mand and cervical br.),12
Foramen ovaleStylomastoid foramenHypoglossal canal
Sub lingual V3 Foramen ovale
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The Saliva
Serous (Parotid and Von Ebner)
Viscous (Sublingual & Minor )
Mixed (Submandibular &Sublingual)
Parotid-25 % of total saliva secretion Submandibular-60%
Sublingual-5%
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unc onsbriefing
Saliva
Anti-Bacterial
Buffering
Digestion
Mineral-
izationLubricat-ion&Visco-elasticity
TissueCoating
Anti-Fung
al
Anti
-Viral
Carbonic
anhydrases,Histatins
Amylases,Mucins,
Lipase
Cystatins,
Histatins,Proline-rich proteins,Statherins
Mucins,Statherins
Amylases,Cystatins, Mucins,
Proline-rich proteins,Statherins
Histati
ns
Cystatins,
Mucins
Amylases,
Cystatins,Histatins,Mucins,Peroxidases
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ymp o es oParotid
Peri and Intraparotid Level 1B,2,3, RPnodes; C/L nodes if T crosses midline
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ofSub Mandibular Level IB
Level2 Level 3
Sub Lingual Level IA Level
1B- Level 2
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p em o ogy
3-4% of all H & N neoplasms In gen
-Parotid>SubMandibular>SubLingual
Parotid: 80% benign, Submandibular: 50% benign
Sublingual : Most are malignant
Age factor:
Benign: 40 M>F; Malignant: 55yrs M=F
3% of all in Children ,half are malignant.
i l
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Aetiology Unknown
Radiation Induced(Modan et al)
Nutritional deficiency(A &C)
Infection EBV UV rays controversial
Cigarettes ,Alcohol, hair dyes, higher
educational level ? Ass. With Breast cancer(2.5 fold
increase)
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Pathology
Benign:
Pleomorphic Adenoma
Papillary Cystadenoma Lymphomatosum(Warthin Tumor)
Benign Lymphoepithelial Lesions (GodwinTumor)
Oncocytoma
Basal Cell Adenoma
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-types(WHO)
Acinic cell carcinomaMucoepidermoidcarcinomaAdenoid cystic carcinomaPolymorphous LG adenocaEpithelial-myoepithelial
caBasal cell adenoca
Sebaceous caPapillary cystadeno caMucinous adeno ca
Oncocytic carcinomaSalivary duct carcinoma
Adeno caMyoepithelial ca
Ca in pleomorphicadenomaSquamous cell
carcinomaSmall cell carcinoma
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g Low grade
Acinic cell ca
Muco epidermoid (LG)
High grade
Mucoepidermoid(HG) ca
Adeno ca / PD/Anaplastic
Malignant Mixed
Adenoid Cystic
Lymphoepithelioma(Eskimoma)
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.types :TYPE %
Parotid (n = 1778 cases)
Mucoepidermoid 32Adenocarcinoma 16
Malignant mixed 14
Adenoid cystic 11
Acinic 11
Undifferentiated and squamous 16
Submandibular (n = 383 cases)
Adenoid cystic 41
Acinic 17
Malignant mixed 12
Mucoepidermoid 10
Undifferentiated 9
Squamous 9
Adenocarcinoma 2
Data from Memorial Sloan-Kettering Cancer
en gn P eomorp ic
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en gn: P eomorp icadenoma
Parotid > Sub mandibular
Painless,slow growing ,Ipsilateral andmore in females
Has a pseudo capsule; Recurrence after
excision common 5-10% chance for malignant
transformationPapillary Cystadenoma
LymphomatosumWarthin tumor, confined to parotid(Tail)B/L in 10% ;more in older men;Recurrence rare after surgery
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conditions:Mucoepidermoid ca:
MC malignancy of SG;90% in parotids f/bHard palate and minor SGs.
Majority are slow growing
Most frequent SG tumor in children
Behavoiur WD vs PD
Adenocarcinoma:
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Malignant Mixed Tumors
From benign conditions like Pas
Pathlogically carcinosarcomas
Aggressive behaviour with 20% risk oflocal recc.
Propensity of LN mets >25%
Carcinoma Ex Pleomorphic
Adenoma
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Adenoid Cystic Carcinoma:
MC type in Submandibular and Minor SGs
Solid HP (Undiff)- more malignantbehaviour
Typical natural history
LN mets rare(
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Histology
Incidence
AgePredil.(Decade)
SexPredil.
Favored Site
NodeMets
7thNerveInv.
Recurr.DistantMets
Aciniccellcarcinoma
4 5th F > M Parotid 10 3 10-22 Rare
Adenoidcystic
carcinoma
2-5 5th-6th F = M
Minor
salivary15 26 High* 28
Mucoepidermoidcarcinoma
Lowgrade
1st-2nd 8 17
17-20 4th-5th M > F None 60 33
Highgrade
6th High* 75
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Histology
Incidence
AgePredil.(Decade)
SexPredil.
Favored Site
NodeMets
7thNerveInv.
RecurrDistantMets
Malignantmixedtumor
4 7th M > F
Parotidandsubmaxillaryglands
33 14 30-40 31
Squamous cellcarcinoma
0.1-3 None None
Parotidsandsalivaryduct
High* High* 70 High*
Adenocarcinoma
2.8 5th-6th None Parotid 50 9 67 19
Undifferentiatedcarcinoma
3 7th-8th F > M None 50 23 High* 30
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SpreadHistologic Subtypes (%)
Anaplastic 86
Epidermoid 21
Adenocarcinoma 22
Mucoepidermoid 14
Malignant mixed 16
Acinic 2
Adenoid cystic 2
Oncocytoma 0
Data from Armstronget al
Swellings related
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Swellings relatedto SGs
Mucocoele
Ranula
Necrotising Sialometaplasia
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Presentation Painless slow growing mass in most of
benign.
1/3rd of parotid ca CN 7 inv. But only10-20 % present with pain
Multiple CN inv in case of PNI tumors
Parotid masses mostly in tail.
Most malignant salivary gland tumors areseen in patients 5060 years old, 2% inchil-dren
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n ca ors omalignancy
Facial nerve involvement
Indurations / ulceration of skin , mucousmembrane
Lymph node metastasis
Rapid tumor growth
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massMetastases to intraparotid nodes/ Lymphoma
Reactive adenopathy
Fatty tail of parotid
Chronic parotitis
Sarcoidosis
HIV infection
Calculus in duct with obstruction
Neoplasms of mandible
Cysts (dermoid, bronchial cleft)
Prominent transverse process of C1 vertebra
Hemangioma, lipoma, lymphangioma
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History Local invasion is the initial route
,depending on location and histologictype. In Parotid ca -fixation to structuresin 20%.
Skin invasion is more often seen inparotid tumors (10%), compared withsubmandibular tumors (3%)
Approximately 25-35% of patients with a
malignant parotid salivary gland tumorpresent with facial palsy from cranialnerve invasion.
Lymph node involvement for parotid
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History LN mets Parotid-18%,SM-28%,
Tumors from oral cavity presents withcervical node metastases of less than10%.
Nasopharyngeal SG tumors have a highrisk of occult metastases (50%)
The risk of + findings in the neck may be
based on a combination of T-stage andhistology.The highest risk -for SCC, UDC,and salivary duct cancer
Distant Mets lung>bone >liver.
k
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Work up History and clinical examination esp.
CN,trismus Basic Investigations-CBC , CXR
FNAC
CT or *MRI Indications: (1) deep lobeparotid tumors, (2) neurologicallysymptomatic tumors, (3) recurrent
tumors, and (4) large size (5) Minor SGtumors
In secondary dep. in SGT -- work up for
the primary.
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-Malignancy
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NX Cannot be assessed
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N0 No LN mets
N1 I/L single 3 - 6 cm
b I/L multiple < = 6 cm
c B/L, C/L 6 cm
M0 No Distant Mets
M1 Distant Mets
Stage 1 T1 N1 M0
Stage 2 T2 N0 M0
Stage 3 T3 N0 MO T1-T3 N1 M0
Stage 4 A T4a N0/ N1 M0 T1-T4a N2 M0
Stage 4 B T4b Any N M0 Any T N 3 M0
Stage 4 C Any T Any N M1
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Descriptors
Residual Tumor (R)
RX: Presence ofresidual tumor
cannot be assessedR0: No residual
rognos c
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rognos cFactors
Grade , postsurgical residual disease &
LN status.High grade tumors- 49% LN mets.
Size of LN
EC Extn from LN Clinical location of Cervical LN
ECS -clinical and pathological
Larger T size & CN inv.--poor prognosis.
Adenoid cystic, ductal, andundifferentiated carcinoma -highest
rates of distant mets.
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on
Spiro et al. (434 Patients, MSKCC) 90% treated surgically
Cause specific 5yr cure rate 44%,10y-
32%,15y-21% Mortality -51% due to original cancer
Adenoid cystic- poorest prog, about 20%
surv w/o recurrence Adeno ca- IM outlook, about 35%w/o
recurrence
Mucoepidermoid ca-Best control rate, about
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Thank