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Malignant Salivary Gland Pathologies, Tumors & Its Treatment Plan by Dr. Aditya Tiwari.

Malignant Salivary Gland Pathologies, Tumors & Its Treatment Plan by Dr. Aditya Tiwari.

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Malignant Salivary Gland Pathologies, Tumors & Its Treatment Plan by Dr. Aditya Tiwari.

  1. 1. By Dr. Aditya Tiwari Resident, Dept. of ENT.JNMC Malignant Salivary Gland PathologIes
  2. 2. Salivary gland • Major salivary glands:- a. Parotid gland b. Submandibular gland c. Sublingual gland • Minor salivary gland 600 – 1,000 minor salivary gland distributed throughout the mucosa of the upper aerodigestive tract (most common in the soft and hard palate). • Malignant neoplasms of constitutes large collection of highly heterogeneous tumors that exhibit a wide spectrum of biologic behaviour, ranging from slow growth & indolence to highly aggressive behaviour & rapid fatality. • Malignant tumors of the salivary gland are relatively infrequent. • Cure rates are very poor for most histological types.
  3. 3. Surgical Pathology • Salivary gland tumors are relatively rare 2.5-3/100,000/yr. • Account for 5% of HNF malignancies. • 70-90% salivary tumors in parotid gland. • Malignant parotid tumors: Mucoepidermoid Ca. > Ca ex pleomorphic adenoma > Acinic cell Ca > Adenoid cystic Ca. • Malignant submandibular gland tumors: Adenoidcystic Ca. > Mucoepidermoid Ca. Nerve involvementHypoglossal N > Trigeminal Nerve > Facial Nerve. • Intraoral salivary tumors are mostly benign Comman malignant tumors are Mucoepidermoid Ca. > Adenoid cystic Ca. > PLGA  Palate is the MC site. • Minor salivary tumors F>M  Except adenoidcystic Ca. ( M=F) • Sublingual gland tumors Rare  MC adenoidcystic Ca.
  4. 4. General features of salivary gland tumors in adults & children ETIOLOGY 1) Smoking, 2) Alcohol consumption, 3) Ionizing radiations 4) Aflatoxins (mainly Aflatoxin B1), 4) Diet 5) Race mainly Eskimos 7) EBV infection. 8) Altered humoral immunity. Polyunsaturated fatty acids (PUFA) seem to exert a beneficial effect. Adults Childrens Occurs primarily in older adults. Rare in general. (only 1.7-3%) F>M except Warthin tumor & high grade Ca. InfantsHaemangioma & Lymphangioma MC Older children Epithelial tumors MC Epithelial (80%) tumors predominates. Malignant tumors are comman (60%) among the epithelial tumors. Benign tumor are more comman (75%) epithelial tumors. Most malignant tumors are low grade. Smaller the salivary gland, higher the proportion of malignant tumors Tumor mortality & morbidity are low.
  5. 5. THE CELL & MOLECULAR BIOLOGY •PCNA (proliferating cell nuclear antigen) immunoreactivity is high in malignancy. •ki67 antibodies  Provides a useful diagnostic tool. •Ki67 Has prognostic significance in Adenoid Cystic Ca. •Bcl2 & apoptotic index Good prognostic markers. •Bax is proapoptotic, decreased Bcl2 & increased Bax leading to increased apoptosis. •Cytokeratin14 is over expressed •Fibroblast growth factor (FGF) 1 and 2 over expressed. •NO has tumour promoting activity Inducible nitric oxide synthase plays important role in tumourogenesis.
  6. 6. Increased VEGF may be associated. METALLOTHIONEIN  May be a marker of differentiation in malignant salivary tumours. Increased Estrogen & progesterone receptors. Mucoepidermoid Carcinoma  Positive for a variety of Cytokeratin & also Vimentin, α1 Antichymotrypsin, S100, Leu N1. Adenoid Cystic Ca  Ki67 antibody, p53 Mdm2 raised Viruses implicated include  HHV8, HPV, CMV
  7. 7. Cellular origin for salivary gland tumour • Clear understanding • Two major theories of histogenesis 1) The bicellular reserve cell theory 2) The multicellular theory The Bicellular reserve cell theory • Basal cells of the excretory or intercalated duct can acts as a reserve cell with the potential for differentiation into a variety of intercalated cells. • Excretrory duct cell:- 1) Squamous cell carcinoma 2) Mucoepidermoid carcinoma • Intercalated duct cell:- 1) Mixed tumours, 2) Warthin tumour 3) Oncocytoma, 4) Adenoid cystic carcinoma 5) Oncocytic carcinoma
  8. 8. The multicellular theory • Salivary neoplasm arise from already differentiated cells along the salivary gland unit. 1) Oncocytic tumours Striated ductal cells 2) Acinous cell tumour Acinar cell 3) Sq & mucoepidermoid Excretory ductal cell 4) Mixed tumour Intercalated ductal cell & myoepithelial cells
  9. 9. WHO CLASSIFICATION BY SOBIN & SHEIFERT • 7 Categories: 1) Adenomas, 2) Carcinomas 3) Malignant melanoma 4) Non epithelial tumours 5) Secondary tumour 6) Undifferentiated tumours 7) Tumour like lesions • Histologically, carcinomas are probably best classified as below 1) Acinic cell Ca. 2) Mucoepidermoid Ca. 3) Adenoid cystic Ca. 4) Adenocarcinoma 5) Polymorphous low-grade adenocarcinoma 6) Papillary cystadenoCa. 7) Squamous cell carcinoma 8) Mucinous adenocarcinoma 9) Carcinoma ex pleomorphic adenoma; 10) Malignant mixed tumour; 11) Undifferentiated carcinoma.
  10. 10. MUCOEPIDERMOID CARCINOMA • Stewart, Foote & Becker- 1945 • Mucus secreting cells & epidermoid cells epithelial type. • Most common malignant salivary gland tumor in adult & childrens  29 – 34% • Parotid gland MC involved. (80-90%), Intraorally MC Palate Pathogenesis-: 1) Entrapment of retromolar mucous glands within the mandible Neoplastic transformation. 2) Developmentally Remnants of the submaxillary gland within mandible 3) Neoplastic transformation of the mucus secreting cells C/F:- 1) Appears as asymptomatic swelling, F>M 3rd -5th decade. 2) Aware of lession for yr or less. 3) Fluctuant & blue/red color.
  11. 11. Low grade malignancy 1) Slowly enlarging, painless, <5mm 2) Not comp. encapsulated 3) Often contain cyst with viscoid, high ratio of mucous cells 4) Closely resembles to mucocele 5) Intraoral lessions buccal mucosa, tongue, retromolar area 6) C/S:- solid white mass High grade malignancy 1) Grows rapidly with pain & infiltrate 2) FN palsy Parotid tumors 3) Trismus, ear drainage, dysphagia, ulceration & numbness of adj. area 4) Metastises to regional LN 5) Lung, bone, brain metastasis 6) C/S - mucinous fluid & high ratio of epidermoid cells Histologically:- Three cell type :- 1) Epidermoid cell, 2) Mucus cell 3) Intermediate cell
  12. 12. Brandwein Mucoepidermoid Carcinoma Criteria Features Points Intracystic component < 25% 2 Tumor front invades in small nest & island 2 Pronounced nuclear atypia 2 Lymphatic and/or vascular invasion 3 Bony invasion 3 >4 mitoses/10 HPF 3 Perineural spread 3 Necrosis 3 Grade 1 0 Grade 2 2-3 Grade 3 ≥4
  13. 13. • Low-grade tumours 5 yr survival of 96% & high-grade tumours Asso. with a death rate 10 times this. • The extent & grade of a tumour dictate the treatment. •TREATMENT :- • 1) For the most favorable tumours Superficial parotidectomy with facial nerve preservation, if possible, • 2) Radical excision is necessary for pts with large &/or high-grade lesions. • 3) Asso. elective ND to include level 2 & 3 for the No neck would also be appropriate. • 4) With more severe neck disease RND. • 5) High grade tumours Require post op RT.
  14. 14. ADENOID CYSTIC CARCINOMA • Slow growing, aggressive neoplasm. 2nd MC malignant tumor. • Slow-growing mass (tumour doubling time around an year) • 10%- non sq Ca in H & N. , 15%- all salivary gland neoplasm • Comman malignant tumor- submandibular, sublingual & minor salivary , 2/3rd – occurs in minor salivary glands. • C/F:- 1) MC seen in females 5th-6th decade. Local recurraance comman (30-50%). • 2) Parotid, submaxillary, acc. palate & tongue gland- MC involved. 3) Early local pain (surface ulceration), FN palsy, local invasion & fixation to deeper structure. LN metastasis 10%-30%. 4) Tendancy to spread through perineural spaces (20%-30%) • C/S :- Solid and well-circumscribed but unencapsulated.
  15. 15. • Perineural spread 50% Axial & circumferential pattern along the involved nerve & furthur spread can occur- antegrade & retrograde fashion. • Commanly involved nerves- Facial nerve, mandibular & maxillary nerve Pathway for invasion of the skull base • Tumor cell may reach trigeminal..pterigopalatine ganglion & cavernous sinus. • Spread along Haversial canal of bone with little bone erosion. • More frequent- advanced, recurrent & high grade tumors.
  16. 16. 3 Histological types Cribriform(40%) > Solid(25%) > Tubular (20%) • Solid Variant Worst prognosis, rarely cured & 100% recurrence seen at primary site at 30 yrs. • Distant metastases, particularly to the lung is characteristic. 70 % at 5 yrs and 100 % at 10 yrs. • IOC:- MRI of the primary site & CT scans of the lungs and liver and an isotope bone scan. 1) Sweese cheese pattern 2) Basaloid epith. cell nests 3) Intermediate prognosis. 1) Basaloid pattern 2) Sheets of cells with few or no luminal spaces 3) Worst prognosis 4) Least comman 1) Trabecular 2) More glandular architecture 3) Best prognosis
  17. 17. •TREATMENT:- 1) Radical primary surgery Best survival rates at 20 yrs. 2) Postoperative irradiation Integral part of treatment. 3) No prophylactic neck dissection required (like in mucoepidermoid ca) 4) Limited role of chemotherapy Cisplatin + Doxorubicin. 5) Skip lesions in the facial nerve  Frozen section and on later paraffin section histology, certainly take place. 6) If gross or frozen section histology involvement of a nerve is found at operation, the nerve should be sacrificed & an immediate nerve graft carried out in the case of the facial nerve
  18. 18. CARCINOMA EX PLEOMORPHIC ADENOMA (Malignant mixed tumor) • 2nd MC parotid gland tumor Malignant form of pleomorphic Ca. • Primary malignant tumor involving both epithelial and mesenchymal element of the mixed tumor • Pre-exicting benign mixed tumor • Typical history of slowly growing mass demonstrating sudden increase in the growth, • Tumor Patterns:- 1) Noninvasive, 2) Minimally invasive:- < 1.5 mm penetration of the malignant component into extracapsular tissue 3) Invasive:- > 1.5 mm of invasion from the tumor capsule into adjacent tissues.
  19. 19. • 3 type:- 1) Ca. in pleomorphic adenoma 2) Carcinosarcoma. 3) Metastasing peomorphic adenoma • Cervical metastasis Pain • Malignant transformation Men > 40 years , tumours of the deep parotid lobe, solitary nodules >2 cm diameter & patients with a h/o a previous operation. TREATMENT:- Aggressive Tumour 1) Total parotidectomy with facial nerve conservation is ideal 2) facial nerve is sacrified if involved. 3) Post operative radiotherapy is must. 4) Invasion of <1 cm 5 yr survival approx 100% 5) Invasion of >1 cm 5 yr survival is halved. Poor prognosis.
  20. 20. Acinic cell carcinoma • Shows serous acinar cell differentiation characterized by cytoplasmic zymogen secretory granules. • 3rd most comman malignant Ca. of parotid gland. • Low malignancy. M:F=3:2, mainly in middle ages (44yrs) • Tumor may be multifocal or B/L. • Clinically – Painless lump, resembles pleomorphic adenoma in gross appearance. • Encapsulated & lobulated. Chiefly occurs Parotid (80%) • Most comman intraoral site Lips & buccal mucosa • Slowly growing, mobile or fixed mass of variable duration.
  21. 21. Histological pattern:- •Local recurrence & distal metastasis. •Has the best survival rate of any salivary cancer •Excision of a facial nerve is not justified unless it is grossly involved. •It is regarded as at the more benign end of the spectrum of malignant salivary disease. Microcystic follicular Papillary cystic Solid
  22. 22. Polymorphous Low-Grade Adenocarcinoma • Synonyms:- Terminal duct carcinoma, Lobular carcinoma. • Characterized by cytologic uniformity, morphologic diversity, an highly infiltrative growth locally, and low metastatic potential. • 2ND most common malignant intraoral tumor of the salivary glands. Palate (60-70%) > buccal mucosa (16%) > upper lip, retromolar area, base of tongue. • F:M = 2:1 & comman in 5th to 7th decade. • A painless mass in the palate is the most common presentation. • Gross - firm, circumscribed, but non-encapsulated, yellow tan lobulated nodule, average size 2.2cms. • Characteristic infiltrative growth.
  23. 23. • The main microscopic patterns are:- 1) lobular 2) papillary or papillary–cystic 3) Cribriform areas, sometimes resembling those in adenoid cystic carcinoma; and 4) trabecular or small, ductlike. • Variability of growth pattern is the most consistent architectural feature of the tumor Low power view showing histologic diversity within the tumor. Mainly solid and tubular growth patterns with focal cribriform and papillary areas Papillary configurations of columnar or cuboidal cells Polymorphous low-grade adenocarcinoma ‘‘Indian-file’’ growth pattern D/D:- 1) Pleomorphic carcinoma 2) adenoid cystic carcinoma
  24. 24. Squamous cell carcinoma • Primary salivary gland SCC is very rare(<1%) • The tumour must arise from the gland itself and not from lymph nodes within the gland. • There must be no regional or adjacent tumour especially of the skin • Parotid (80%), submandibular gland(20%) • Age : 60 to 65years, M:F= 2:1. • History of previous radiotherapy. • Risk factors for locoregional metastasis from cutaneous Sq. cell Ca 1) Tumor location in the area of the forehead, temples, eyelids, cheek, and auricle 2) Resection of the tumor without healthy margins, with narrow safety margins (tumor recurrence) 3) Tumor size >1.5 cm dia 4) Tumor thickness > 4mm 5) Low differentiation of tumor 6) Perineural invasion 7) Patientʼs age (> 70 years) 8) Immunosuppression
  25. 25. Salivary duct carcinoma • An aggressive adenocarcinoma which resembles high-grade breast ductal carcinoma” • Consist of solid, papillary cystic, and cribriform patterns. • M>F, after 50 years of age. • Site- parotid(~80%). • Present with a rapidly enlarging parotid mass associated with facial nerve palsy , pain and cervical lymphadenopathy. • Differential Diagnosis : 1) Metastasis : Breast 2) Oncocytic adenocarcinoma 3) High grade mucoepidermoid Ca. 4) Papillarycystic acinic cell ca 5) Cystadenocarcinoma.
  26. 26. Secondary (metastatic) tumors • Hematogenous metastasis – lung, kidney & breast • Parotid gland most comman site • Lymphatic spread from cutaneous malignancy of head & neck • <10% -Malignant parotid tumors,40%-melanomas,40% -Sq. cell ca. • 2/3rd of metastatic sq. cell Ca to parotid occurs within 1st yr after T/t of the primary skin cancer.
  27. 27. The malignant parotid tumor can be classified into: 1) High-grade aggressive behaviour, local invasion & LN metastasis.- 1) High grade mucoepidermoid carcinoma 2) Adenoid cystic carcinoma 3) Ca. ex phelomorphic adenoma 4) Adenocarcinoma 5) Squamous cell carcinoma 6) Undifferentiated carcinoma 2) Low-grade malignancy:- 1) low grade mucoepidermoid carcinoma 2) PLGA 3) Basal cell carcinoma 4) Acinic cell carcinoma 5) low grade adenocarcinoma 3) Intermediate grade:- 1) Intermediate grade mucoepidermoid carcinoma 2) Intermediate grade adenocarcinoma 3) Oncocytic carcinoma
  28. 28. TNM classification of carcinomas of the major salivary glands • Tx = Primary tumor cannot be assessed • T0 = No evidence of primary tumor • T1 = Tumor < 2 cm, no extraparenchymal extension • T2 = Tumor > 2 cm, < 4 cm, no extra parenchymal extension • T3 = Tumor > 4 cm or extraparenchymal extension (or both) • T4a = Tumor invades skin, mandible, ear canal, facial nerve, or any of these structures • T4b = Tumor invades skull base or pterygoid plates, or encases carotid artery • N0 =No cervical nodes metastasis • N1 =Single I/L LN < 3 cm • N2a =Single I/L LN >3cm & ≤ 6cm • N2b =Multiple I/L LN metastases, each ≤ 6 cm • N2c = B/L or contralateral LN metastases, each ≤ 6 cm • N3= Single or multiple LN metastases > 6 cm • MX =Distant metastases cannot be assessed • M0 =No distant metastases • M1 =Distant metastases present
  29. 29. Evaluation of patient A] History:- Important points in the history: 1) Mass (duration, rate of the growth, presence of pain) 2) Facial paralysis, B/L 3) Cervical lymphadenopathies 4) Eyes and joints symptoms 5) H/O exposure to radiation 6) Ipsilateral weakness or numbness of tongue B] Examination:- 1) Size of the mass 2) Overlying skin, Skin fixation, mobility 3) Lymphadenopathies 4) Cranial nerves essp. CN V,VII,
  30. 30. C] Investigations:- 1) Plain X ray 2) X ray chest To R/O secondaries. 3) OPG To R/O mandibular involvement. 4) Open biopsy Rarely used due to risk of recurrence & FN damage Useful HP guidance for use of palliative CTRT, poor surgical candidate, obvious malignancy. 5) Sialography:- a) C/I:-Acute infection, Iodine allergy, Multiple myeloma. b) Limitation:- Mass < 2mm, Deep lobe pathology. 6) Radiosialography Tc99 To detect mass lession & parenchyma function No use in ductal system study. 7) Color doppler sonography Noninvasive  Evaluates vascular anatomy. 8) PET Differentiate benign from malignant lessions.
  31. 31. Main investigations 9] FNAC:- 1) Accuracy95-98% 2) Diff benign from malignant dis. 2) The key to successful FNAC is immediate evaluation of the specimen for adequacy. 10] Ultrasound:- 1) Ideal tool for the initial assessment of superficially located tumors of the parotid and submandibular gland Distinguish intrinsic from extrinsic neoplasm 2) USG f/o malignant tumors include ill-defined margins, heterogeneous architecture, subcutaneous invasion, & the presence of LN metastases.
  32. 32. 11] C.T. & MRI:- 1) Effective modalities for imaging the size, the local, and the regional extension of the primary tumor and the neck metastasis & to differentiate intra from extra glandular mass. 2) CT IOC for subtle cortical involvement & bone destruction. 3) MRI IOC for bone marrow invasion. 3) MRIIOC for detecting perineural spread. 4) Contrast-enhanced MRI IOC for intracranial invasion. T1-weighted MRI shows enlargement & enhancement of the rt mandibular nerve (thick arrows), extending into the foramen ovale. Histology confirmed perineural spread. The normal lf mandibular nerve (short arrows) noted forcomparison. MRI of adenoid cystic carcinoma arising in the deep lobe of the right parotid gland. Disadvantage Of MRI :- 1) Less sensitive in cystic lessions. 2) Inability to detect calcification.
  33. 33. • C.T. saliography • Quantitative DCE-MRI, DW-MRI, and MRS New & evolving techniques for differentiating between benign and malignant salivary gland neoplasms. • FDG-PET/CT For local extent of the tumor and to detect locoregional & distant metastases. • Stage T N M • I T1 N0 M0 • II T2 N0 M0 • III T3 N0 M0 • T1-3 N1 M0 • IVa T1-3 N2 M0 • T4a N0-2 M0 • IVb T4b Any N M0 • Any T N3 M0 • IVc Any T Any N M1 Prognostic factors 1) Histopathological daignosis 2) Facial nerve paralysis 3) Skin involvement 4) Stage 5) Location 6) Incedence of recurrence 7) Distant metastasis 8) Radiotherapeutic sensitivity 9) Chemotherapeutic sensitivity
  34. 34. T/t plan of Parotid gland neoplasm
  36. 36. UNTREATED RESECTABLE Clinically benign <4cm (T1, T2) Clinically suspicious of cancer >4cm or deep lobe Complete surgical excision Benign Low grade mucoepidermoid Intermediate or high grade Follow up RT CT/MRI Base of the skull or clavicle Consider FNA Surgical resection Benign Cancer Follow up Superficial lobe Deep lobe N0 N+ N0 N+ Parotidectomy Parotidectomy + comprehensive neck dissection Total Parotidectomy Total Parotidectomy + comprehensive neck dissection
  37. 37. INCOMPLETELY RESECTED H & P CT/MRI Pathology Review Negative Physical Exam + imaging Gross residual disease on physical examination or imaging Adjuvant RT Follow up Surgical Resection if possible Non Surgical resection possible Adjuvant RT Definitive RT Follow up
  38. 38. CANCER SUPERFICIAL LOBE DEEP LOBE Completely excised Pariotidectomy No adverse characteristics Adverse characteristics Incompletely excised gross residual disease No further surgical resection possible Adjuvant RT Definitive RT Surgery ± adjuvant RT RT if feasible or clinical trial or single agent chemotherapy or best supportive care Rescetable Not Rescetable Chest X-ray annually TSH annually if thyroid irradiated Physical examination year 1 (every 1-3 mon) year 2 (every 2-4 mon) yr 3-5 (every 4-6 mon) ≥5 (every 6-12 mon)
  39. 39. SURGICAL MANAGEMENT OF PARAPHARYNGEAL SPACE SALIVARY GLAND NEOPLASMS PARAPHARYNGEAL SPACE Primary salivary gland neoplasm Parotid neoplasm that extend from the deep lobe Transcervical submandibular approach Superficial parotidectomy with facial nerve identification resection of deep lobe and paraharyngeal tumor a) Massive or recurrent benign neoplasms and invasive malignant neoplasm – Anterior mandibulotomy and mandibular swing. b) Complete tumor excision – Transcervical transoral approach
  40. 40. T/t plan of locoregional recurrence
  41. 41. T/t modality depending upon grading • Excision of the tumor with cuff of a normal tissue. • Facial nerve is preserved. • Regional lymph node evaluated at the time of surgery. • No post-op radio therapy unless the resection margin is not clear • Total parotidectomy with excision of the first node (digastric & submandibular nodes). • Facial nerve involvement: A) Patient with facial paralysis pre-op. Resection of the facial nerve with primary grafting. B) Patient with normal facial function pre-op. Resect the tumor of the facial and post- operative wide field radiation. Group 1: T1 and T2NO low-grade malignancy Low grade epidermoid tumour, acinic cell ca. Group 2: T1 and T2NO high- grade malignancy
  42. 42. • Radiacal parotidectomy (sacrifice Of CN VII with immediate reconstruction) • Modified radical neck dissection • Wide field PORT. • Radical parotidectomy with MRND and resection of masseter muscle, part of the mandible or mastoid or ear canal as required. • Resection of the facial nerve with the tumor and primary grafting. • Followed by wide field PORT. Group 3: T3NO or any N+ high- grade or recurrent cancer Group 4: Include all T4 tumor T1 & T2 LOW GRADE T1 & T2 HIGH GRADE STAGE T3 STAGE T4 Submandibular gland excision 1) Wide excision 2) Preserve nerve unless involved 2) PORT 1) Wide excision with neck dissection 2) PORT 1) Surgery to fit extent of disease 2) PORT
  43. 43. Indications of PORT 1) High-grade tumor 2) Deep lobe cancers 3) All T3 and T4 cancers 4) Recurrent disease 5) Documented LN metastasis 6) Extraparotid extension 7)Gross/microscopic residual disease 8) Tumor involving or close to the facial nerve Indications of neck dissection 1) Clinically cervical Lympadenopathies (15%). 2) Parotid tumor bigger than 4cm Occult metastasis risk >20%. 3) High grade malignancy Occult metastasis risk >25%.
  44. 44. Chemotherapy Treatment • Useful in pallation & in inoperable cases. Combination regimen have not proven better results AdenoCa. like tumors i.e. Adenoid cystic Ca., Acinic cell Ca., Ca. ex polymorphic Ca Epidermoid like tumor i.e. Sq. cell CA Mucoepidermoid Ca. Adriamycine Cisplatinum 5-flurouracil Methotrexate Cisplatin 2 groups
  45. 45. Points to remember in parotid surgery A] Pre-op evaluation: Patient general condition, all routine investigation B] Consenting patients for possible facial weakness. C] Operating in bloodless field by: 1) Hypotensive technique 2) Head end elevation 3) Delicate tissue handling 4) Proper hemostasis D] Using facial nerve monitoring during operation and at the end of operation. E] Exposure of the eye and the operative side of the face. F] Modified Blair’s incision. G] Landmark for the facial nerve Acute Late Facial nerve palsy Sensory deficit Bleeding or hematoma Cosmetic deformity Seroma Frey’s syndrome Salivary fistula COMPLICATIONS OF PAROTID SURGERY
  46. 46. Facial nerve marker during surgery • . 2) Posterior belly of digastric muscle:- The facial nerve is superior to the upper border of the belly of the digastric muscle 1) Tragal cartilage (pointer):- always point to the facial nerve. The facial nerve is 1 cm. inferior &1cm. medial to the pointer
  47. 47. 4)Retrograde inferior approach to the facial nerve:- The lower branch of the facial nerve invariably can be found immediately ext to the post. facial vein as it exits the lower pole of the parotid gland. 3)Tympanomastoid fissure – FN is 4 mm inferior to the tympanomastoid fissure as it exit from the stylomastoid foramen.
  48. 48. • Prognostic factors

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Malignant Salivary Gland Pathologies, Tumors & Its Treatment Plan by Dr. Aditya Tiwari.


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