CLINICO PATHOLOGICAL STUDY AND

MANAGEMENT OF PAROTID TUMOURS

By

Dr. PEDDI MANJUNATH MBBS

A dissertation submitted to the Rajiv Gandhi University of Health Sciences, Bangalore In

partial fulfillment of the requirements for the degree of the

M. S. (GENERAL SURGERY)

Under the guidance of

Dr. K. SESHAGIRI RAO M. S.

DEPARTMENT OF GENERAL SURGERY

BANGALORE MEDICAL COLLEGE

BANGALORE.

2006

i

RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, KARNATAKA

DECLARATION BY THE CANDIDATE

I hereby declare that this dissertation entitled “CLINICOPATHOLOGICAL

STUDY AND MANAGEMENT OF PAROTID TUMOURS” is a bonafide and

genuine research work carried out by me under the guidance of

Dr. K. SESHAGIRI RAO M. S., Assistant Professor of Surgery, Bangalore Medical

College, Bangalore.

Signature of the Candidate

Name: Dr. PEDDI MANJUNATH

Place: Bangalore

Date:

ii

CERTIFICATE BY THE GUIDE

This is to certify that this dissertation titled “CLINICOPATHOLOGICAL

STUDY AND MANAGEMENT OF PAROTID TUMOURS” is a bonafide research

work done by Dr. PEDDI MANJUNATH in partial fulfillment of the requirement for

the degree of M. S. in General Surgery, Bangalore Medical College.

Signature of the Guide Name: Dr. K. SESHAGIRI RAO MS Assistant Professor, Bangalore Medical College Bangalore.

Place: Bangalore

Date:

iii

ENDORSEMENT BY THE HOD, PRINCIPAL/HEAD OF THE

INSTITUTION

This is to certify that this dissertation entitled “CLINICOPATHOLOGICAL

STUDY AND MANAGEMENT OF PAROTID TUMOURS” is a bonafide research

work done by Dr. PEDDI MANJUNATH. Postgraduate Student in General Surgery,

under the guidance of Dr. K. SESHAGIRI RAO, Assistant Professor, Department of

General Surgery, Bangalore Medical College, Bangalore.

Seal and Signature of the HOD Seal and Signature of the Principal

Dr. T. K. LAKSHMIKANTH MS Dr. T. RAJESHWARI MS Professor and HOD Principal Department of General Surgery Bangalore Medical College Bangalore Medical College Bangalore. Bangalore.

Date: Date:

Place: Place:

iv

COPYRIGHT

DECLARATION BY THE CANDIDATE

I herby declare that the Rajiv Gandhi University of Health Sciences, Karnataka

shall have the rights to preserve, use and disseminate this dissertation/thesis in print or

electronic format for the academic/ research purpose.

Date: Signature of the Candidate

Place: Name:

© Rajiv Gandhi University of Health Sciences, Karnataka

v

ACKNOWLEDGEMENT

With the most sincere and deepest sense of gratitude, I thank

Dr. K SESHAGIRI RAO M. S., Assistant Professor of Surgery, Bangalore Medical

College, for his patience, constant encouragement, guidance and constructive criticism.

His valuable suggestions and timely advice were of immense help to me throughout all

phases of this study.

I extend my sincere thanks to Dr. T. K. LAKSHMIKANTH M. S., Professor and

Head of the Department of Surgery, Bangalore Medical College, Bangalore, for his

valuable guidance, encouragement and suggestion during this dissertation.

I express my heartfelt gratitude to Prof. Dr N. Srinivasan,

Dr. A. P. Vilas, Dr. B. S. Shivaswamy, Dr. T. Durganna, Dr. Shankarappa M., Dr.

Chikkannachar, Dr. Z. Sharieff, Dr. Rajiv Shetty, Dr. S. I. S. Khadri,

Dr. Shivananda, Dr. P. R. Thippeswamy Naik, Dr. Shanmukappa,

Dr. M. K. Ramesh, Dr. Harindranath, Dr. Shashikala and all the teaching faculties for

their timely advice and encouragement in preparing this dissertation.

I thank Dr. Avinash, Dr. Prasad, Dr. Prabhakar T and all my friends and

interns for having helped me and being my constant source of moral support.

I also thank Mr. A. S. Madhukeshwara, for his editing and processing of this

dissertation.

I will be failing in duty, if I do not express my gratitude to all the patients, who

were the subjects of this study. My sincere thanks to them for being my study subjects.

Date: Signature of the Candidate

Place: Name:

vi

LIST OF ABBREVIATIONS USED

C/S - Cut section

CT - Computed Tomography

FNAC - Fine needle aspiration cytology

H/o - History of

MRI - Magnetic Resonance Imaging

HPE - Histopathological examination

vii

ABSTRACT

BACKGROUND

Parotid gland is the largest salivary gland. Tumors arising from the parotid

constitute 3-4% of all the head and neck tumors. But they have created much interest

because of the engulfment of the facial nerve and proximity of the vessels and debate

because of their remarkable variability in presentation and behavior of the tumor.

Face and the facial expression recognize a person, this is carried by the facial

nerve as facial nerve is embedded in parotid gland identification and preservation of the

facial nerve during surgery is very important. In view of this, we need to study the

management of parotid gland tumors.

AIMS AND OBJECTIVES

• To study the age and sex distribution

• To study the various modes of presentation of parotid tumors.

• To compare the FNAC of parotid tumor with the biopsy post operations.

• To evaluate the various modes of surgery and to minimize the postoperative

complications.

METHODS

The study is conducted in Victoria hospital attached to Bangalore medical

college from Jan 2003 to Mar 2005. 30 cases had been studied who are presented with

swelling in the parotid region. Pediatric patients, tumor like condition and infectious

viii

causes of swelling are excluded. All patients underwent pre operative work up and

surgery. Few patients are subjected for postoperative radiotherapy. Follow up period

ranging from 3 months to 24 months.

RESULTS

Benign tumors are more common than the malignant tumors. Pleomorphic

tumors are the most common benign tumors (70%) followed by warthins tumor. Males

are most commonly affected during 3rd to 5th decade. the most common malignant tumor

is malignant mixed tumor(80%) among the malignant tumors .Temporary facial nerve

palsy is the most common post operative complication.

KEYWORDS:

Parotid tumors, Pleomorphic adenoma, Facial nerve, Mixed Malignant tumor, Frey’s

syndrome.

ix

TABLE OF CONTENTS

Sl. No. Particulars Page Nos.

1. INTRODUCTION 1

2. OBJECTIVES 2

3. REVIEW OF LITERATURE

• History 3

• Embryology 6

• Anatomy 7

• Physiology 12

• Histology 14

• Classification and staging of parotid Tumours 16

• Etiopathogenesis and Clinical features 20

• Individual Parotid Tumours 24

• Investigations 41

• Management 44

4. METHODOLOGY 64

5. OBSERVATION AND RESULTS 66

6. DISCUSSION 76

7. CONCLUSION 80

8. SUMMARY 83

9. BIBLIOGRAPHY 84

10. ANNEXURES

• PROFORMA 87

• MASTER CHART 92

• KEY TO MASTER CHART 93

x

LIST OF TABLES

Page Nos.

1. Age and Sex incidence in parotid tumours 66

2. Distribution of tumours 67

3. Incidence of benign and malignant parotid tumours 68

4. Distribution of benign tumours 69

5. Distribution malignant tumours 69

6 Distribution of side of the tumour 69

7. Clinical presentation of parotid tumours 70

8. Incidence in relation to duration of the mass 72

9. Correlation of FNAC with histopathological examination 72

10. Types of surgical treatment adopted in the study 73

11. Complications following surgery 74

12. Comparison of FNAC and HPE 77

xi

LIST OF FIGURES

Sl. No.

Page Nos.

1. Relations of parotid gland 9

2 Branching pattern of Facial Nerve 9

3 Microscopic appearance of benign mixed tumor. Epithelial and myothelial cells can be easily distinguished. 25

4 Benign mixed tumour. The myoepithelial cells are undergoing cartilaginous metaplasia 26

5 Low power appearances of Warthin’s tumour - Germinal centers are very prominent. 27

6 High power field showing Acinic cell carcinoma 34

7 Benign mixed tumour (left) with areas of malignant transformation in the form of poorly differentiated carcinoma (right) 36

8 Pleomorphic adenoma- lateral view 43

9 Malignant mixed tumour-lateral view 43

10 Incision 48

11 Raising anterior skin flap 49

12 Mobilization of parotid tumour (Plemorphic adenoma) 50

13 Showing facial nerve after superficial parotidectomy 52

14 Specimen of plemorphic adenoma 53

xii

INTRODUCTION

The analogue of the parotid gland is the first gland to form in humans. Lesions of

the parotid gland are fairly easy to recognize mainly because of the location and limited

number of structures present here.

Salivary glands tumours are less commonly encountered in surgical practice

constitute 3-4 % of head and neck tumours. The incidence of parotid gland tumours is

between 1-3 / 1, 00,000 per year, approximately 75 – 85% of the salivary gland neoplasm

occur in parotid gland of which 70 – 80% is benign and 80% benign tumours are

plemorphic adenoma. 80 % of parotid tumours are located in the superficial lobe. Deep

lobe neoplasms are considered to have a greater incidence of malignancy. Although

mostly observed in adults. Salivary gland tumors occur is all age and both sex. They

exhibit a wide variety of behaviour and widely diversified histology. In this part of the

world, the problem of these tumours is more troublesome in management because of their

late presentation, poor economic condition and lack of awareness of health among the

general population.

It is recommended that increased community awareness of early referral of

parotid mass is necessary, as surgical treatment is the form of superficial parotidectomy,

which ideal procedure for such lumps. Surgery performed by experienced surgeon with a

special interest in parotid surgery carries minimal morbidity.

1

OBJECTIVES

• To study the age and sex distribution.

• To study the various modes of presentation of parotid tumours.

• To compare the FNAC of parotid tumour with the biopsy post operations.

• To evaluate the various modes of surgery and to minimize the postoperative

complications.

2

REVIEW OF LITERATURE

History

Riolan (1648): First to recognize the Glandular substance of parotid glands.

Niels Stenson (1960)1: Dissected sheep’s head and discovered the direct of

parotid gland.

Lorenzo – Heister (1765): Described the earliest parotidectomy performed but no

importance was given to facial N. or vascular network within gland.

Berrandi (1802): outlined the first surgical plans of parotidectomy.

Heyfelder (1825): was able to avoid facial paralysis while performing

parotidectomy.

Mc Fairland (1930)2: Drew the attention to the high recurrence associated with

enucleation.

Karolinske (1960): Popularized the use of FNAC in parotid tumours in Karolinska

Institute of Stockholm.

Patey (1940)3: recognized that frequent recurrence after enucleation was the result

of capsular defect.

3

Bailey (1941)4: stressed importance of capsule and anatomy of VII cranial nerve

in parotid gland.

Patey (1954)5: Fully defined and described conservative radical parotidectomy.

Berg and associates (1968): noted increase in incidence of major salivary gland

cancer and breast cancer following irradiation.

Hobbsely described the superficial parotidectomy.6

David M. Patey (1969): Reclassified the parotid tumors based on Foot and

Frassels.

Frazell (1968): Prognosis varies according to histological type of tumor.

S E Afify et al (1992)7: reported that for any malignant parotid tumor radical

resection with radical neck dissection must be undertaken followed by radical

postoperative radiotherapy.

Richard L. Fabian (1994)8: reported salivary neoplasms are encountered at all

ages. But majority of benign tumors occurs in 3rd and 4th decade of life, whereas

malignant tumors occur in 5th and 6th decade.

4

Gordon T. Deans (1995)9: studied and reported that superficial parotidectomy is

advised for not benign lesions confined to superficial lobe although enucleation may be

considered to select cases with small mobile lesions.

McGurk M and Hussan K (1997)10: studied FNAC can distinguish benign from

malignant parotid disease in 93% of patients. The management of discrete, apparently

benign, parotid lump whether adenoma or carcinoma is essentially same.

Joseph Califano et al (1999)11: reported that approximately 80% salivary gland

tumors are found in the parotid gland 10 to 15% in submandibular gland of 5-10% in

sublingual gland. Approximately 85% of parotid neoplasms all benign and majority of

sublingual and minor salivary gland are malignant.

5

EMBRYOLOGY

The embryology of the parotid gland is incompletely understood, as there is some

debate over the question of germ cell origin of parotid glands. The stomodial plate has an

anterior ectodermal layer and posterior endodermal layer some embryologists believe it is

of endodermal origin, but however others argue that frequent presence of sebaceous

gland in the parotid gland points out to ectodermal origin.

Parotid is the first among the salivary glands to appear about 6th week of

intrauterine life. The gland appears as an epithelial in growth near the angle of the mouth

on the inner surface of either cheek. It runs dorsally from the angle of the mouth between

the angle of the mandibular arch and maxillary process as it grows backwards the ramus

of the mandible it becomes a hollowed tube at this level, which eventually becomes the

parotid duct opening into the oral cavity. The peripheral epithelium branches and

differentiates into the body of the parotid gland. Condensation of mesenchyme

surrounding the developing parotid occurs later in embryonic life. So lymphnode may

become entrapped in the parotid gland. Sebaceous glands are rarely found in the parotid

gland. The acinar cells occur from preexisting acini and other cells of ductal origin. The

origin of myoepithelial cells is not known.

As the gland arborises posteriorly, the facial nerve migrates anteriorly through it.

Since parotid ductal branching and facial nerve migration occurs before the condensation

of the mesenchyme. The gland and the nerve develop an intimate relationship.12

6

ANATOMY

The Parotid Gland

The parotid gland is the largest of the major salivary gland. The parotid gland is

an irregular wedge shaped organ that envelops the post border of ascending ramus of

mandible. On its superficial surface extends medially to cover a portion of the masseter

muscle. The body of the gland fills the space between the mandible and surface bounded

by external auditory meatus and the mastoid process. Deep to ascending ramus, the gland

extends forward to a variable degree, lying in contact with the medial pterygoid muscle.

Just below the condylar neck, above the attachment of the medial pterygoid to the bone

the gland extends between the two. In the region of the condyle, the gland lies between

the capsule of the temporomandibular joint and sternocleidomastoid muscle, the gland

lies directly on the posterior belly of digastrics, muscle, styloid process, and stylohyoid

muscle. These structures separate the gland from Internal carotid artery, Internal jugular

vein and cranial nerves IX to XII. Practically these anatomic entities form the parotid

bed, which is related to the so-called deep lobe of the parotid gland.

Superficial surface of gland is covered by skin and superficial fascia. The

investing layer of deep cervical fascia splits to surround the gland with tough fascial

capsule.

Anteromedial surface is grooved by the posterior border of mandibular ramus.

The parotid duct and facial nerve branches emerge from anteromedial surface and run

7

forwards deep to anterior border. The terminal branches of external carotid artery

(superficial temporal and maxillary) leave this surface.

Posteromedial surface is in contact with mastoid process. The external carotid

artery enters the gland through the lower part of this surface. The facial trunk enters the

gland between mastoid and styloid process.

Although not found in every gland, 3 – 5 process of parotid gland exist. Making it

extremely difficulty to perform a total parotidectomy. 3 superficial processes:

(a) Condylar process: near the temporomandibular joint.

(b) Metal process: In the medial area of the incisura of external auditory canal.

(c) Posterior process: Projecting between the mastoid and S.C.M. muscle.

2 deep process gland processes: which rests of vaginal process of the tympanic

portion of the temporal bone. Stylomandibular process projects anteromedially above the

stylomandibular leg.

The facial nerve passes through the parotid gland tissue dividing the gland into

superficial and deed lobe, which are not distinct structures. Superficial to the facial nerve

comprises 80% of gland and deep lobe (deep to facial nerve) makes up 20 % of parotid

tissue.

The facial nerve enters the posterior surface of the gland approximately 1 cm after

exiting the skull. It is superficial to the external carotid A and post facial vein. The nerve

branches into an upper temporofacial division, which take vertical course, and a lower

8

cervicofacial division, which is a transverse continuation of the main trunk. The point of

branching is called pes anserinus. From the pes, the nerve branches into 5 branches

1) Temporal, 2) Zygomatic, 3) Buccal, 4) Mandibular and 5) Cervical.

Fig.1 Relations of parotid gland

Fig. 2 Branching pattern of facial nerve

9

Parotid Duct (of stenses), about 5 cm long, passes from the anterolateral edge of

parotid gland over the masseter muscle. At the arterial margin of muscle and enter the

oral cavity, the duct opens on the mucous membrane of the cheek opposite the second

upper molar tooth; it pierces the buccinators further back and runs forwards beneath the

mucous membrane to its orifice. It follows a line from the floor of the external auditory

meatus to just above the commissure of the lips.

The wall of the parotid duct is thick, with an external fibrous layer containing

non-striated muscle and a mucosa lined by columnar epitheliums. Its caliber is about

3mm, but smaller at its oral orifice.12

Accessory parotid gland usually lies on the necessities between the duct and the

zygomatic arch. Several ducts open from it into parotid duct. It and the duct lie on the

aponeurotic part of the surface of the master muscle.

Blood supply: The parotid arterial supply is from external carotid artery and its

terminal branches namely maxillary and superficial tumor artery. The veins drain to

external jugular vein through its tributaries.

Lymph Drainage

Lymph drains to the preauricular (Parotid) nodes within the parotid sheaths and

hence nodes of the upper group of deep cervical nodes.

10

Nerve supply

The parotid gland is innervated by sympathetic and parasympathetic fibers. The

function of sympathetic fiber is most likely vasoconstrictions and the function of the

parasympathetic fibres (IX) is most likely secretary.13

Sympathetic (vasoconstrictor) fibres reach the gland from the superior cervical

ganglion by way of the plexus on the external carotid and middle meningeal arteries.

Parasympathetic fibres (Secretomotor) arise from cell bodies in the otic Ganglion

and reach the Gland by hitch hiking along the auriculotemoporal nerve. [As it passes

backwards along the mandibular neck and ascends behind the TMJ]. The auricotemporal

nerve in is in contact with the anteromedial surface of the Gland, which is penetrated by

filamentous from the nerve. The preganglionic fibres arise from cell bodies is the inferior

salivary nucleus in the medulla, and travel by way of the IX cranial nerve. It’s tympanic

the tympanic plexus and lesser petrosal nerve to otic ganglion.

11

PHYSIOLOGY

Saliva

Saliva includes the combined secretion of all major and minor salivary gland.

About 1500 ml of saliva is secreted per day. The patient of saliva from resting gland is

slightly less than 7.0 but during active secretion is approaches 8.0.14

Composition of Saliva

Saliva contains chiefly water, proteins, glycoprotein (enzyme and antibiotics) and

electrolytes. The 2 enzymes are lingual lipase (secreted by the glands on the tough and

ptyalin (salivary α-amylase) secreted by the salivary glands. It has very high potassium

concentration about 7 times that of blood and a sodium concentration about 1/10 that of

blood, a bicarbonate concentration about 3 times that of blood and significant amounts of

calcium, phosphorus, chloride, thiocyanate and urea.

Functions of Saliva

1. Moistening of oral mucosa

2. Moistening dry foods to aid swallowing.

3. Providing a medium for dissolved and suspended food materials that chemically

stimulate task buds.

4. Buffering of the contents of oral cavity through its high concentrating bicarbonate

ions.

5. Digestion of carbohydrate by the digestive enzymes α-amylase that breaks the

1-4 glycoside bonds and continues to act is the esophagus and stomach.

12

6. Controlling the bacterial flora of the oral cavity because of the presence of the

antibacterial enzyme lysozyme.

7. As a source of calcium and phosphate ions essential for normal tooth development

and maintenance.

8. Immunologic functions of saliva – IGA.

Control of salivary secretions

Although food ingestion is the most common for salivations, the sight of food or

even thoughts of food can stimulate salivation. Autonomic stimulation can very the

composition of saliva. Sympathetic stimulation causes secretion of viscous saliva rich in

protein i.e. enzymes. Parasympathetic stimulation causes secretion of copious watery

saliva that serves principally as a lubricant buffer.

13

HISTOLOGY

The parotid gland secretes serous fluid. The mature parotid gland unit begins as

serious acinus which empty into an intercalate duct, which in turn leads to a striated duct

that empties into an excretory duct. The excretory duct forms the collecting tubes for

saliva. Each parotid gland segment has specialized functional and morphological

characteristics.

Acinar cells are highly differentiated cells and responsible for production of

serious secretions. These cells contain well-developed endoplasmic reticulum and Golgi

bodies with abundant secretary granules and unmyelinated nerve terminals with

numerous synaptic vesicles just between the acinar cells indicating autonomic

innervation. The cubodial cells of the intercalated ducts are relatively undifferentiated.

The myoepithelial cells (Zimmerman’s cells) are located around the periphery of

the acini and intercalated duct. They appear to have the ability to contact and expel saliva

from the acini. The myoepithelial cells also seem to play an important role in the

transport and basement membrane function. The cells of the striated ducts are well

differentiated and show features common to the renal proximal tubule cells. These cells

play an important role in water and electrolyte transportation.

The basal cells of the intercalated and excretory ducts act are reserve cells for the

more differentiated cells of the salivary gland unit. Basal cells of the excretory duct give

rise to columnar and squamous cells of excretory duct and intercalated duct cells give rise

14

to acinar cells, other intercalated duct cells and myoepithelial cells. Therefore these two

cells are not only responsible for normal parotid gland development, but also for tumour

formation. It is now generally accepted that parotid gland tumours arise from one of these

two cells and data from both light and electron microscope studies support this theory.15

15

CLASSIFICATION AND STAGING OF PAROTID TUMOURS

REVISED WHO CLASSIFICATION OF SALIVARY GLAND TUMOURS (1992) 16

ICD – O

I. ADENOMAS

1.1 Pleomorphic adenoma 8940/0

1.2 Myoepithelioma (Myoepithelial adenoma) 8982/0

1.3 Basal Cell adenoma 8147/0

1.4 Warthin’s Tumour (Adenolymphoma) 8561/0

1.5 Oncocytoma (Oncocytic Adenoma) 8290/0

1.6 Canalicular Adenoma

1.7 Sebaceous Adenoma 8410/0

1.8 Ductal Papilloma

a. Inverted ductal papilloma 8503/0

b. Intra-ductal papilloma 8503/C

c. Sialadenoma papilliferum 8260/0

1.9 Cystadenoma 8440/0

a. Papillary Cystadenoma 8450/0

b. Mucinous Cystadenoma 8470/0

II. CARCINOMAS

2.1 Acinic Cell Carcinoma 8550/3

2.2 Muco-epidermoid carcinoma 8430/3

2.3 Adenoid Cystic Carcinoma 8200/3

2.4 Polymorphous low grade adenocarcinoma (terminal duct adenocarcinoma)

2.5 Epithelial-myoepithelial carcinoma 8562/3

16

2.6 Basal Cell Adenocarcinoma 8147/3

2.7 Sebaceous Carcinoma 8410/3

2.8 Papillary cystadenocarcinoma 8450/3

2.9 Mucinous adeno carcinoma 8480/3

2.10 Oncocytic carcinoma 8290/3

2.11 Salivary duct carcinoma 8500/3

2.12 Adenocarcinoma 8410/3

2.13 Malignant myoepithelioma (Myoepithelial Carcinoma) 8982/3

2.14 Carcinoma in pleomorphic adenoma (Malignant mixed tumour)

8941/3

2.15 Squamous cell carcinoma 8070/3

2.16 Small cell carcinoma

2.17 Undifferentiated carcinoma

2.18 Other carcinomas

III. NON-EPITHELIAL TUMOURS

IV. MALIGNANT LYMPHOMAS

V. SECONDARY TUMOURS

VI. UNDIFFERENTIATED TUMOURS

VII. TUMOUR LIKE LESIONS

7.1 Sialadenosis (sialosis) 71000

7.2 Oncocytosis 73050

7.3 Necrotizing sialometaplasia (salivary gland infarction) 73220

7.4 Benign lympho – epithelial lesion 72240

7.5 Salivary duct cysts 33400

7.6 Chronic sclerosing sialadenitis of submandibular gland (kuttner tumour)

45000

7.7 Cystic lymphoid hyperplasia in AIDS

17

TNM CLASSIFICATION OF SALIVARY GLAND TUMOURS (1997) 17:

T Primary Tumour.

TX Primary Tumour cannot be assessed.

T0 No evidence of Primary Tumour.

T1 Tumour 2 Cm or less in greatest dimension without extra parenchymal extension.

T2 Tumour more than 2 cms but not more than 4 cms in greatest dimension without extra – parenchymal extension.

T3 Tumour having extra – parenchymal extension without seventh nerve involvement and / or more than 4 cm but more than 6 cm in greatest dimension.

T4 Tumour invades base of the skull, seventh nerve and / or exceeds 6 cm in greatest dimension.

N Regional lymph nodes.

Nx Regional lymph nodes cannot be assessed.

No No regional lymph node metastasis.

N1 Metastasis in a single ipsilateral lymph node, 3 cm or less in greatest dimension.

N2 Metastasis in a single ipsilateral lymph node, more than 3 cm but not more than 6 cm in greatest dimension or in multiple ipsilateral lymph nodes, none more than 6 cm in greatest dimension, or in bilateral or contralateral lymph nodes, none more than 6 cm in greatest dimension.

N3 Metastasis in a lymphnode more than 6 cm in greatest dimension.

M Distant metastasis.

Mx Distant metastasis cannot be assessed.

M0 No distant metastasis.

M1 Distant metastasis.

18

Stage Grouping

Stage I T1 N0 M0

T2 N0 M0

Stage II T3 N0 M0

Stage III T1 N1 M0

T2 N1 M0

Stage IV T4 N0 M0

T3 N1 M0

T4 N1 M0

Any T N2 M0

Any T N3 M0

Any T Any N M1

19

ETIOPATHOGENESIS AND CLINICAL FEATURES OF

PAROTID TUMOURS

Salivary neoplasms are distinctly rare and of interest to the specialist surgeon and

pathologist. They vary in the degree of malignancy. At the lower end of the scale is

adenolymphomas, which is completely innocent, followed by mixed tumour, which is

classified as innocent but whose potentials for infiltration, implantation and

carcinomatous change warrant its preferable classification as a tumour of low-grade

malignancy. Next comes the mucoepidernoid carcinoma and the cylindroma, which

show definite malignant characteristics. Finally there are carcinomas, which are

extremely malignant tumours with marked tendency to infiltrate and metastasis.

Fortunately most of the parotid tumours are of low-grade malignancy and the progress

potentially controlled if treated properly.

Salivary gland tumour constitutes 3% of head and neck tumours of the parotid

gland tumours 70-80% are benign tumours, of which 80% are pleomorphic adenoma.18

Individuals with blood group ‘A’ are more susceptible to tumours of parotid gland

(Osberone and De-George 1962). Associations of radiation to head and neck area and

parotid gland tumour formation have been reported. An epidemiological survey

undertaken in survivors of the atomic blast has revealed an increase in malignant parotid

tumours. The incidence of parotid tumours in Eskimos has been attributed to vitamin ‘A’

deficiency (Rove et 1970).

20

Multiple studies have demonstrated an association of development of Warthin’s

tumour and smoking. Initial studies have demonstrated a high incidence of allelic loss on

chromosomal also 12q in Pleomorphic adenoma.19

The current classification of neoplasm is based on the characteristic of neoplastic

cells to mimic morphologically its cell of origin. In the case of parotid the suggested

possibility is the bicellular theory of origin, according to this, neoplasms generate from

two undifferentiated reserve cells i.e. excretory duct reserve cells and the intercalated

duct reserve cells. The squamous cell and mucoepidermoid carcinoma arises from

excretory duct reserve cells. Acini cell carcinoma, adenocarcinoma and oncocytic

tumours from intercalated duct reserve cells.

Clinical evaluation

Symptoms

Mass

Majority of parotid neoplasms manifest as painless masses in the periauricular

region, typically in front or below the ear.

Pain

When the signs and symptoms of inflammation are absent, pain may be a sign of

neoplastic involvement. There is a general agreement however that pain represents an

adverse finding in a patient with malignancy of the parotid gland.

21

Facial nerve weakness

A parotid mass in association with paralysis or weakness of any or all branches of

the facial nerve should be assumed to be malignant until proved otherwise. The incidence

of facial nerve weakness at the time of presentation in patients with parotid malignances

ranges from 10-15%.

Signs

Local invasion

Physical finding indicative of extension beyond the capsule of the parotid are

regarded as signs of a poor prognosis. These findings would include fixation of the

overlying skin or involvement of neighbouring structures, such as the external auditory

canal, mastoid tip, zygomatic arch, mandible, masseter muscle, pterygoid muscles or

sternomastoid.

Adenopathy

The presence of enlarged cervical lymph nodes generally signals malignant

disease of the parotid gland, assuming in inflammatory signs are absent. Regional

metastasis correlates strongly with a diminished overall survival.

Physical evaluation

The presence of a suspected parotid mass requires a thorough history and physical

examination. Important questions include duration of the mass, associated pain

masticatory pain, intraoral drainage, fluctuation in size, history of antecedent facial,

auricular or scalp lesions and facial nerve dysfunction.

22

A complete head and neck examination is essential. Lesions of the scalp, eyelids,

temporal region and ear have the capability to metastasize to the parotid gland. Likewise

lesions of the nasopharynx, middle ear, and soft palate also have this potential. The mass

itself should be inspected and palpated for evidence of skin fixation and invasion of

adjacent structures. The temporomandibular joint should be examined for signs of direct

tumour extension. The mastoid tip must be palpated to determine whether there may be

difficulty freeing the tumour from this structure. Fixation to the tip will likely change the

scope of the surgery and should be identified pre-operatively so that radiological imaging

can be undertaken to further define the extent of the invasion. Parotid neoplasms may

involve the ear canal secondarily via the fissures of santorini. Even when the skin is

intact, there may be subtle signs of subcutaneous invasion such as oedema or induration

of the canal skin.

Oral cavity examination should include inspection of stenson’s duct for evidence

of abnormal or purulent drainage. These findings are more often associated with

inflammatory disease. Trismus should be identified because it may be indicative of

invasion of the masseter or pterygoid muscles. The oropharynx must be carefully

evaluated for signs of para pharyngeal space involvement. Typically this will be

manifested by a submucosal bulge in the soft palate or tonsillar regions.20

23

INDIVIDUAL PAROTID TUMOURS

Clinical features & pathology

Benign Tumours of the Parotid Gland

Pleomorphic Adenoma (Benign Mixed Tumour)

Most common tumour of the parotid gland, consisting 80% of all the parotid

neoplasms and 75% of the benign tumours of the parotid gland.

Pathology

Gross

Well circumscribed round to oval firm mass, bulges when incised, C/s. Tumour is

lobulated, grey white and translucent. Myxoid and rarely cystic areas are seen.

Haemorrhage and necrosis are uncommon and should raise the suspicion of malignancy.

Microscopy

The tumour capsule is in fact penetrated by numerous ‘psuedopods’ of tumour

that extend beyond the clinically evident capsule. There are wide ranges of histological

findings that have been described in pleomorphic adenomas. There is often significant

variability from one microscopic field to another. Mixed tumours demonstrate differing

degrees of epithelial and mesenchymal elements. Some tumours are very cellular,

whereas others show a prominence of myxoid, chondroid or fibrous tissue. The epithelial

component of basophilic small cells may show a trabecular pattern coursing through a

stroma composed of mesenchymal tissues displaying myxoid, chondroid or fibrous

features.

24

Clinical features

Any age group-commonly in the 3rd and 4th decade, F>M, H/o Slow growing mass

present for months and years which is mobile, firm and circumscribed. Facial nerve

paralysis or weakness is rare in untreated benign mixed tumours. Most tumours are

located in the tail of the parotid gland, although they can involve other parts of the gland.

10% of the pleomorphic adenomas occur in the deep lobe of the parotid gland. Incidence

of recurrence after parotidectomy in pleomorphic adenoma is 5%. Incidence of

malignant transformation is 3 – 15%. Except for recurrence prognosis is excellent.

Recurrence in pleomorphic adenoma may be due to (1) Inadequate surgery (Enucleation)

(2) Inadvertant spillage (3) Tumour removal with inadequate margin (4) Multicentricity.

Fig 3. Microscopic appearance of benign mixed tumor. Epithelial and myothelial

cells can be easily distinguished.

25

Fig 4. Benign mixed tumour. The myoepithelial cells are undergoing cartilaginous

metaplasia

Warthin’s Tumour

[Adenolymphoma] [Papillary cystadenoma lymphomatosum]

Second most frequent benign neoplasm arising from the parotid gland. Accounts

for 10% of the benign tumours arising from the parotid gland. The pathophysiology is

directly related to the embryology of the parotid gland. Although the parotid is the first

salivary gland to develop, it is the last to become encapsulated. During this encapsulation

process, lymph nodes are entrapped in the substance of the gland, and these are believed

to be the origin of this neoplasm. It has the propensity for being bilateral (2-6%) and

multicentric.

26

Pathology

Gross

Located in the superficial areas of the parotid average about 3cm in size, well

circumscribed. C/S – Lobulated mass, usually brown in colour, which is multicystic, the

cyst contains mucoid fluid.

Microscopy

Two histological components must be identified for diagnosis an eosinophilic

epithelium (oncocytes) and a lymphoid stroma. The epithelium is double layered with

inner layer cuboidal and outer zone of tall columnar-layered cells. The lymphoid stroma

has similar lymph follicles and sometimes a connective tissue capsule.

Fig 5. Low power appearances of warthin’s tumour. Germinal centers are very

prominent.

27

Clinical feature

Age group is 55- 60 yrs; M: F = 5:1; Common in males than females. Presents as

a slowly growing mass, often of several years duration. Pain is rarely a complaint.

Bilaterality [and/or multicentricity] is not rare. Characteristically arises in the inferior

pole of the parotid gland and occasionally originates in the lymph nodes adjacent to that

part of thegland.20, 22

Monomorphic Adenoma

Monomorphic adenoma describes a group of parotid tumours derived from

intercalated duct cell. These lesions manifest as purely epithelial or purely mesenchymal

growth pattern. Most classifications include the purely epithelial lesions as monomorphic

adenoma and diagnose mesenchymal varieties as myoepitheloma. Constitute 2% of the

parotid tumours.

Pathology

Gross

Tumours are rarely larger than 3cms and often encapsulated and are tan in colour.

Microscopy

The monomorphic adenomas are divided based on predominant histological

pattern-tubular adenoma, trabecular adenoma, canalicular adenoma, membranous

adenoma and basal cell adenoma. Basal cell adenoma is the most common monomorphic

adenoma and likely represent the isocellular counterpart of pleomorphic adenoma. Basal

28

cell adenoma is composed of basal cells, which are isomorphic with basophilic nuclei and

cytoplasm. The parenchyma and stroma are well demonstrated by a basal membrane.

Clinical features

Affects adults in 5-7th decade; F>M. Usually manifest as slow growing

asymptomatic masses.23

Oncocytomas

Oncocytomas are benign tumours characterized by their unique composition of

oncocytes [Eosinophilic cells] with granular cytoplasm. Oncocytes are thought to be a

product of aging and are seldom seen in patients below 50 years. Formerly referred to as

oxophilic cell adenomas.

Pathology

Gross

Round to oval but may be coarsely nodular. They appear encapsulated and may be

homogenous or lobulated. C/S is brownish red, brownish pink or pale pink.

Microscopy

Oncocytes exhibit bright pink cytoplasm with comparatively small rounded

nuclei. The cell outlines are distinct, and the cytoplasm is finely granular under higher

magnification.

29

Clinical Features

Accounts for 1% of the parotid neoplasm. Manifest as painless masses, usually

occurring in those older than 50 years of age with no sex predilection.20

Sebaceous Adenoma

Neoplasms of sebaceous cell type is rare in parotid gland.

Pathology

Gross

Appear as firm and yellow grey with focal small cysts.

Microscopy – The tumour contains sebaceous gland strewn in a background of benign

lymphoid tissue. Keratin and sebum are produced and may distend tumour ducts.

Clinical Features

Manifests as asymptomatic masses in the parotid gland.

Malignant Tumours of the Parotid Gland

Muco-Epidermoid Tumour

Most common malignancy of the parotid gland, comprise between 25-50% of the

parotid cancers. Arise from the parotid gland duct cells, which have the potential to

differentiate into mucous, squamous and intermediate cells. High-grade tumours have a

high recurrence rate (15-75%). Based on the pathological findings classified into high,

intermediate and low grade.16

30

Pathology

Gross

Low-grade tumours are small, ovoid well circumscribed and often at least

partially encapsulated. Some tumours are cystic and contain clear or mucinous fluid.

High-grade tumours show more evidence of infiltration to be cystic and more often

appear as a dense gray white mass lacking a distinct capsule.

Microscopy

In muco-epidermoid carcinoma 6 cell types are identified-material cells,

intermediate cells, epidermoid cells, clear cells, columnar cells, mucous cells. Stromal

hyalinization, fibrous and inflammatory cell reaction may be present in these tumours.

Low-grade

Low-grade tumours are dominated with columnar and mucin forming cells. There

are cystic or glandular spaces. Pleomorphism and mitosis are rare.

Intermediate grade

Intermediate grade lesions are more cellular with epidermoid and intermediate

cells being more frequent. Cystic spaces are less evident, occasional mitosis with slight to

moderate pleomorphism seen.

High-grade

Shows a highly infiltrative nature and demonstrate a predominance of squamous

cells, with less cystic formation and limited number of mucous cells.

31

Clinical Features

Usually occur in adults, females more affected than males. Most common

malignant parotid tumour in childhood. Durations of symptoms is variable (1 – 6 years)

Facial nerve is rarely noted on presentation but is an indication of a high-grade cancer.

Mostly they are slow growing and invade local tissues to a limited degree and only

occasionally metastasize to lymph nodes, lungs and skin.

ADENOID CYSTIC CARCINOMA (Cylindromatous carcinoma)

Accounts for 15% of parotid malignancies. Characterized by the presence of

cribiform pattern giving rise to a sieve like “Swiss Cheese” or cylindromatous pattern.

Pathology

Gross

Ill-defined or circumscribed mass of grey white tissue, size ranges from 0.5 – 0.6

cms.

Microscopy

Hallmark is sieve like or cribiform pattern of growth. The cells are arranged in

4 patterns – cribiform, cylindromatous, solid and tubular. The chief histologic feature is

that of small darkly straining cells with little cytoplasm arranged in cords. Between these

are acellular regions that contain mucous or hyaline material. The spaces ultra-

structurally are psuedocysts – perineural invasion is a common finding in these tumours.

32

Clinical Features

Rare in children’s and usually diagnosed in the fifth decade of life. Sex incidence

is equal. Most common presenting symptom is mass in the region of the parotid gland.

Pain is common and usually correlates with facial nerve involvement. They are slowly

growing tumours and may be present for years. However sooner or later, pain, areas of

anaesthesia of the skin and paralysis of muscles appear due to involvement of the related

nerves. Involvement of regional lymph nodes is found in 10-15% of cases. Distant

metastasis to lung and bone occurs late in the course of the disease.16

Acinic Cell Carcinoma

Constitutes 6-12% of the parotid malignancies. Second most common salivary

gland malignancy in childhood. Bilateral in 3% of the cases and multifocal tumours can

be seen. Generally regarded as a low-grade malignancy.

Pathology

Gross

May be cystic or solid. Most common parotid gland tumour to present as a cystic

mass. The cyst may comprise only a small portion of the tumour or may be large with

only small solid or papillary foci.

Microscopy

They are composed of uniformly round or polygonal cells with dark eccentric

nuclei. The cells are generally basophilic and there is generally very little stroma. There

is abundant cytoplasm, which is most often finely granular but in some cases may be

33

clear. The arrangement of these cells may be quite variable. Described pattern include

solid, papillary, cystic, follicular and microcystic.

Fig 6. High Power Field showing Acinic Cell Carcinoma

Clinical Features

Affects all ages from childhood to the elderly, F>M ; common in 4-5th decade.

Presents with lump in the parotid region. Pain and nerve dysfunction is rarely

noted on initial presentation.16

34

Adenocarcinoma

Accounts for 10-14% of the parotid malignancies.

Pathology

Gross

3 cm to very large size with infiltrative edges. Necrosis and cystic degeneration

are common.

Microscopy

Resembles gastro-intestinal carcinoma with much production and even signet ring

cells.

Clinical Features

Occur in adults and at an early stage, produce obvious signs of malignancy.

These are fixation, resorption of adjacent bone, pain, anaesthesia of skin or mucous

membrane and paralysis of muscles. Facial nerve irritability occurs first and muscle

spasm can be produced if the tissues over the nerve are trapped. The risk of lymph node

metastasis is 24 – 36%. 16

Malignant mixed tumours – Includes: 24

(1) A neoplasm with the basic pattern of mixed tumour, but in which all the epithelial

elements are malignant.

(2) A true carcino-sarcoma where in both a carcinoma and recognizable

mesenchymal malignancy co-exists.

(3) A metastasizing benign mixed tumour.

(4) Carcinoma occurring in or in association with a recognizable benign mixed

tumour.

35

First three are rare and most cases designated malignant mixed tumour represent

carcinomas arising in benign mixed tumour. Carcinoma arising in mixed tumour

comprises about 7 – 17% of parotid malignancies.

Pathology

Gross

Size ranges from 2-25 cms. Tumour may be obviously invasive or may grossly

resemble a circumscribed benign mixed tumour. Necrosis, haemorrhage and cyst

formation is common.

Microscopy

There is histological evidence of destructive and infiltrative growth of a malignant

neoplasm and admits this process there is pre-existing neoplasm with the features of a

benign mixed tumour.

Fig 7. Benign mixed tumour (Left) with areas of malignant transformation in the

form of poorly differentiated carcinoma. (Right)

36

Clinical Features

Occur in the sixth or seventh decade. Occur primarily in the parotid gland.

Females are affected more than males. Long history of slow growing parotid swelling,

with recent rapid growth brings them to medical attention. Pain, skin ulceration, facial

nerve weakness, attachment to skin, and telangiectasia can occur and should lead the

clinician to suspect malignancy in a mixed tumour. The malignant component may be

characteristic of adenocarcinoma, squamous cell carcinoma or undifferentiated

carcinoma.16

Squamous Cell Carcinoma

It represents 1% of all the parotid malignancies. Primarily squamous cell

carcinoma of the parotid gland is a diagnosis of exclusion.16

Pathology

Gross

Unencapsulated, infiltrative, firm, greyish white mass with variable amounts of

cavitation and glandular infiltration may be seen.

Microscopy

Characteristic features include intracellular keratinisation, intra-cellular bridges

and keratin pearl formation. Only after exhaustive pathologic evaluation including

special strains, electron microscopy and histochemical studies, should a primary

neoplasm of the parotid gland be labelled as squamous cell carcinoma.

37

Clinical Features

The history needs to include any previous treatment of skin lesions and if these

were excised, the original histology should be sought. Complete head and neck

examination is mandatory to search for any primary. Cancers of the temporal region,

lateral facial skin, eyelids, scalp and primaries in the nasopharynx and palate have the

capability to spread to the parotid gland. At an early stage, it produces obvious signs of

malignancy.

Undifferentiated carcinomas

The term has been used to classify those lesions that do not conform to the

designations listed in the preceding discussion. Occur in older patients and are regarded

as highly aggressive malignancies.

Pathology

Typically they demonstrate increased mitotic figures with a significant degree of

cellular pleomorphism. Because of the bizarre cells and the lack of organization into a

recognizable arrangement, there is great difficulty is distinguishing the origins of the

tumour, thus it is placed into the undifferentiated category.

Clinical Features

This tumour at an early stage produce signs of malignancy. These are fixation,

resorption of the adjacent bone, pain, anaesthesia of the skin or mucous membrane,

paralysis of the muscle, and facial nerve paralysis.

38

Malignant lymphoma

Primary malignant lymphoma of salivary glands is rare and virtually always

occurs in parotid gland. Divided into 2 sub groups

(1) Arising in the intra parotid and paraparotid nodes

(2) Salivary parenchyma.

Primary nodal lymphoma presenting as a parotid lesion is often a stage I lesion

and is associated with a good prognosis. Parenchymal lymphomas usually arise in the

setting of lympho epithelial lesions with or without Sjogren’s syndrome.

Pathology

Gross

Firm, non-encapsulated masses of variable size.

Microscopy

All types of lymphomas have been reported.

Clinical Features

Occur in the 5-6th decade of life, F>M, H/O Sjogrens syndrome or arthritis is

elicited in majority of patients.

Metastatic tumours of the Parotid Gland

Reach the gland by direct spread, lymphatic or haematogenous spread. Malignant

melanoma and squamous cell carcinoma of the mucosa of the upper aero-digestive tract

39

via the lymphatics account for 80% of the parotid metastasis. Haematogeous spread is

most often from carcinoma of the lung, kidney, breast and colon.

Non-epithelial tumours

Vascular lesions

Include venous ecstasies, cavernous hemangiomas, hemangioendothelioma,

lymphangiomas or cystic hygroma of the neck. These tumours usually occur in children.

40

INVESTIGATIONS IN A CASE OF PAROTID TUMOUR

1. Routine investigation: Hb, BT, CT, TC, DC, RBS, Blood urea, serum creatinine,

Chest Screening, ECG, ESR, and blood grouping.

2. X ray of the part: To detect calcification of the parotid gland, thickening of the

mandible.

3. FNAC of the parotid gland: Although FNAC has been discouraged in the past

because of the potential for seedling, thin needle (22 gauge) technique has proved

to be very safe and also accurate when done by an experienced cytopathologist.

The finding of a benign tumour in FNAC will steer the surgeon towards

conservative management. When FNAC is suspicious for malignancy, imaging

may be helpful in determining the structures that are involved by tumour and thus

help in planning of the surgery, as well as in the counselling of the patient.20, 30

4. Ultrasound of the parotid gland: May be done to delineate whether the mass is

cystic or solid. It is seldom done because other studies yield more useful

information.

5. Radio-nuclide scan using technetium pertechnate: Warthins tumour and

oncocytoma produce hot spots on radio-nuclide scan because the oncocytes which

are present in these tumours have the ability to concentrate these substances at

greater levels than normal parotid tissue.26

6. CT Scanning: This is the gold standard for investigation of parotid tumours. The

important thing to assess in the work up of a parotid tumour is its extension into

the deep lobe, its relation to the facial nerve, involvement of the bone, extension

into the parapharyngeal space.27, 29

41

7. MRI [Magnetic Resonance Imaging]: Has no significant advantage over CT at

the moment but its overall advantage is the lack of ionizing radiation. For parotid

tumours, the contrast between the tumour and surrounding tissue is greater than

with CT scanning but tissue details is less well defined.27

8. Sialography: It is seldom indicated in parotid gland neoplasms because it may

cause inflammation or infection. Extravasation of the dye may cause a severe

inflammatory reaction, preventing a clear demarcation of tumour margins and

may also delay the planned surgical procedure.

9. CT SAILOGRAPHY: It is found that useful in tumor mapping preparation for

surgery. Specifically the tumors location in relationship to deep lobe the facial

nerve and the Para pharyngeal space can be assessed. CT sailography cannot

definitely diagnose or rule out the malignancy to avoid the need for surgery.24

10. Frozen section: evaluation of efficacy and usefulness of frozen section study

yielded varying results. It is utilized to assess the margins of resection.

42

Fig 8. Pleomorphic Adenoma- Lateral View

Fig 9. Malignant Mixed Tumour-Lateral View

43

MANAGEMENT OF PAROTID TUMOURS

MANAGEMENT OF BENIGN PAROTID TUMOURS

Superficial parotidectomy is the treatment of choice of benign tumours of the

parotid gland, except when the tumour involves the deep lobe where total conservative

parotidectomy is done. In case of a recurrent pleomorphic adenoma, total parotidectomy

with preservation of the facial nerve function is the ideal treatment. Postoperative

radiotherapy is recommended if the lesion encases the nerve, for recurrent lesions, and

when complete gross tumour removal is not possible. The management of haemangiomas

and lymphangiomas in children is principally observational. Most of them involute. If

aggressive growth continues after the age of 2 or 3, a parotidectomy may be appropriate.

MANAGEMENT OF MALIGNANT PAROTID TUMOUR

Histological grade and clinical staging are the two most important determinants of

survival. By combining the T classification and histopathological diagnosis 4 groups are

identified. As we pass from group 1 to group 4, increasing severity of disease is matched

with progressively more aggressive therapy.17

44

Management of malignant tumours

Tumour Type Treatment

Group I T1 & T2, N0, Low grade (low

grade muco-epidermoid tumour,

Acinic cell tumour)

Superficial or total parotidectomy with

preservation of facial nerve. Nodal

sampling sos neck dissection (N+ RND)

Group II T1 & T2, N0, High grade

(Adenocarcinoma, Malignant

mixed tumour, Undifferentiated

carcinoma, Squamous carcinoma,

Adenoid cystic carcinoma, High

muco-epidermoid carcinoma)

Total parotidectomy with preservation of

the facial nerve Nodal sampling sos neck

dissection (N+ RND) Post op radio -

therapy for primary and neck.

Group III T3, N0/N+ and any recurrent

tumour not in group IV

Radical parotidectomy sacrificing the

facial nerve with immediate

reconstruction. Nodal sampling sos

dissection (N+ RND)

Post op radio therapy for primary and

neck

Group IV T4 Radical parotidectomy sacrificing facial

nerve with immediate reconstruction with

resection of the skin, mandible, muscles

& mastoid tip as indicated.

Nodal sampling sos dissection (N+ RND)

Post op radio therapy for primary and

neck.

45

Role of Surgery in Parotid Tumours

Specific Surgical Procedures

1. Superficial Parotidectomy – signifies removal of that portion of the gland that

lies superficial to the facial nerve.

2. Total Conservative Parotidectomy – Refers to excision of the superficial lobe of

the parotid gland followed by removal of the deep lobe of the parotid gland. In

this procedure the facial nerve is left intact.

3. Radical Parotidectomy – The entire gland along with the facial nerve and its

branches are resected. This may imply enbloc resection but not in all cases.28, 31

Preoperative preparations

The possible risk of transient or permanent paralysis of the facial nerve and its

branches should be discussed with patients especially when there is clinical suspicion of

malignancy and elective sacrifice of the main trunk or a major branch is likely. Transient

weakness may be due to handling or stretching of the nerve or its branches during

operation due to haemotoma or local oedema. Hair should be shaved from the

periauricular skin for a distance commensurate with closure of the lines of the lines of

incision.

Anaesthesia

Morphine 10 mg and promethiazine 25mg produces very adequate pre-operative

sedation for patients undergoing parotidectomy coupled with the additional anti-emetic

effect of promethiazine. Anaesthesia by endotracheal tube is mandatory. This follows

the usual sleep dose of thiopentone and succinylcholine. Preference should be given to a

46

relaxant intermittent positive pressure respiration technique, which removes any

possibility of straining with its attendant congestion during the course of operation.

Anaesthesia in maintained with vecuronium and halothane.

This produces a mild degree of hypotension, which is aided by head up tilt of the

table. Despite the apnea produced by these two drugs, there is still sufficient tone in the

facial muscles to respond to the surgeon’s use of a nerve stimulator during the parotid

dissection.

Position of the patient

The patient is placed in a supine position on the operating table with the head of

the table elevated by an angle of 15 degree to reduce venous engorgement. The head of

the patient should be placed on a rubber ring, to maintain its position and rotated towards

the contralateral side.

Immediate preoperative preparation

Pads should be applied to the lower limbs for use of diathermy and an electrical

nerve stimulator. Cleansing of the skin of the face, pinna and upper neck is done in a

routine way with an aqueous antiseptic solution since spillage of an alcoholic preparation

into the eye will cause conjunctivitis. The external auditory canal may be packed with

sterile ribbon gauze to prevent accumulation of blood that might predispose to otitis

external. The head, face should be allowed in order to check movement of the muscles of

facial expression in response to stimulation of the facial nerve.

47

The incision

The incision begins as a vertical limb in the pre-auricular skin just in front of the

pinna and extends up to the level of the zygoma. It is continued downwards, passing

backwards below the pinna and behind the angle of the mandible to curve forwards in the

second upper cervical skin crease as far as the tip of the hyoid bone.

Fig 10. Incision

Exploration of the Parotid Gland

The skin incision is deepened through the subcutaneous tissues down to the

capsule of parotid gland. First the anterior skin flap is raised by sharp scissor dissection

following the plane of capsule as far as the anterior border of the gland in the mid cheek.

Second the postero-inferior flap is reflected off the mastoid process and upper fibres of

the sternomastoid muscle in order to expose the thin lingula of the parotid tissue that

overlaps these structures. Third the superior flap, including the lobule of the pinna is

reflected upwards as far as the cartilaginous plates, which form the floor of the external

auditory canal.

48

Mobilization of the posterior part of the gland by dissection with scissors begins

with elevation of the lingula of parotid tissue in order to expose the mastoid process and

tendinous attachment of sternomastoid muscle. The lingula can be lifted forwards with

mosquito artery forceps provided that they do not impinge on the tumour. The posterior

border of the gland is carefully dissected away from the sternomastoid muscle. Absolute

haemostasis should be maintained with diathermy so that bleeding does not interfere with

recognition of the facial nerve. The great auricular nerve is divided as it ascends on the

surface of the sternomastoid. The gland is mobilized down to the level of the posterior

belly of the digastic muscle where the styloid process can be felt deep to this muscle.

Fig 11. Raising anterior skin flap

49

Fig 12. Mobilisation of parotid tumour (Plemorphic Adenoma)

Facial nerve identifications

Efforts at this point should focus on localization of the extratemporal portion of

the facial nerve. The most constant landmark for the facial nerve is at the stylomastoid

foramen, between the styloid and mastoid process. During routine parotidectomy,

however, complete access to this region is difficult. The following landmarks and

techniques can be used for identification of the facial nerve trunk during superficial and

total parotidectomy.

Tragal “Cartilaginous Pointer”: Because of the inherent shape of the tragal

cartilage, it takes the form of a pointer, leading the surgeon to the main trunk of the facial

nerve, proximal to the pes. The main trunk of the facial nerve may be located

approximately 1 to 1.5 cm deep and inferior to the tragal pointer.

50

Tympanomastoid Suture: The next landmark that may be used is to trace the

tympanomastoid suture line medially, approximately 6 to 8 mm deep, as this leads to the

main trunk of the facial nerve.

Digastric Muscle: The posterior belly of the digastric muscle may be used

alternatively to guide the surgeon close to the exit from the stylomastoid foramen, as the

nerve trunk is found just superior to the posterior cephalic margin of the muscle.

Styloid Process: The base of the styloid process is 5 to 8 mm deep to the

tympanomastoid suture line. The facial nerve trunk lies on the posterolateral aspect of the

styloid process near its base.

Retrograde Dissection: Identification of the lower branches of the facial nerve,

namely the cervical or marginal mandibular branches, is useful id the surgeon must rely

on retrograde dissection to find the pes anserinus. This should be unusual. The cervical

branch of the facial nerve located lateral to the posterior division of the retromandibular

vein. Tracing the external jugular vein superiorly to the posterior division of the

retromandibular vein will lead to the point where the cervical branch crosses the vein.

The marginal branch can be found crossing the facial vein by tracing the vein superiorly

from the neck. The buccal branches can be identified with careful dissection near the

Stensen’s duct, which lies at an imaginary line drawn between the tragus and philtrum of

the upper lip, midway between the corner of the mouth and zygomatic arch (or,

approximately 1 cm below the lower border of the arch). The buccal branches usually lie

just superior to the ducts. The zygomaticotemporal branches can be identified as they

51

ascend over the zygomatic arch midway between the tragus and lateral canthus of the

eye, and anterior to the superficial temporal artery. These branches can be traced

proximally to the pes.

Cortical Mastoidectomy: As a last resort, a mastoidectomy may be performed to

identify the intratemporal mastoid course of the facial nerve and then follow it out of the

mastoid as it exits the stylomastoid foramen.28

Once the facial nerve is located, the main trunk is traced out to the pes anserinus,

and the dissection may follow either the upper or lower division. The parotid tissue is

lifted off each branch of the facial nerve sequentially, using fine clamps and sharp

dissection, while taking care not to interrupt the capsule of the tumor. Finally, the parotid

duct is ligated and transected, freeing the tumor of the deep portion of the gland.

After removal of the tumor, haemostasis is achieved carefully with bipolar cautery. Drain

placement and pressure dressing then is applied to prevent postoperative Haematoma.

Fig 13. Showing facial nerve after superficial parotidectomy

52

Fig 14. Specimen of plemorphic adenoma

Superficial parotidectomy

The main trunk of facial nerve is identified and isolated as already described. The

upper and lower divisions and the named branches are exposed by tunneling along each

in turn. A pair of mosquito forceps is well suited to this purpose. Tunneling must be

done with care and the communicating tissue between superficial and deep parts of the

parotid divided successively within the field of vision produced by this maneuver. This

allows the superficial parotid tissue to be lifted away gradually exposing the full

anatomical distribution of the facial nerve. Meticulous haemostasis must be maintained

at all times in order to allow identification and visualization of the branches of the nerve.

Dissection is continued as far as the anterior border of the gland, when the whole

superficial lobe can be removed. After excision is complete, haemostasis should be

completed. Function of all branches of the facial nerve should be checked with the nerve

stimulation before closure. The operative field is drained with suction drain, the skin

incision closed and the wound dressed.

53

Conservative total parotidectomy28

Superficial parotidectomy is the essential first step in removal of deep lobe

tumour, in order to obtain adequate access. Once the superficial tissue has been excised,

the branches of the facial nerve overlying the tumour must be carefully mobilized. The

course of each branch is followed in turn and the nerve elevated by gentle retraction with

nerve hooks. The nerve is lifted forwards and the deeply situated tumour is then removed

by meticulous extra capsular dissection.

Occasionally, if the tumour is very posteriorly situated its surface is immediately

visible once the posterior border of the gland has been separated from the sternomastoid

muscle. Under such circumstances, superficial parotidectomy is not always necessary and

a local approach to the tumour can then be made. The deep parotid tissue is approximated

with interrupted catgut sutures. A suction drain is placed down to the site of removal of

the tumour and brought out through the separate stab incision. The skin incision is closed

as described previously and a light pressure dressing applied.

Radical parotidectomy28

The lingula of the parotid gland is reflected off the mastoid process and the

posterior border of the gland is separated from the sternomastoid muscle. The trunk of

the facial nerve or its main upper and lower divisions are isolated and divided.

Preservation of the first division of the facial nerve facilitates subsequent repair by

grafting, provided that it does not prejudice removal of the tumour. Markers either by

black silk ligatures or silver clips can aid identification after excision has been completed.

The plane of dissection is deepened down to the level of the posterior belly of the digastic

54

muscle. The parotid gland and the tumour are dissected forwards off the masseter muscle

and capsule of the temporomandibular joint. The termination of the external carotid

artery is found as it winds round the posterior border of the vertical ramus of the

mandible. It is divided and ligated at this level as also its branches as they are

encountered. Large venous tributaries, which follow the posterior facial vein, must be

similarly dealt with. If the tumour is adherent to the masseter muscle, then it may be

excised in part or in its entirety while, on occasions the vertical ramus of the mandible

may also have to be sacrificed. The parotid gland is reflected upwards as far as its

anterior border. The main parotid duct may be recognized as its turns medially to

penetrate the muscles of the cheek where it may be formerly ligated. If the parotid duct is

involved, it may be excised with cuff of muscle and mucosa. The mucosa is closed with

interrupted chromic catgut sutures. The transition from the substance of the parotid gland

to the fascia of the cheek and fibrofatty tissue is recognized easily and excision of the

gland is completed by dividing the remaining soft tissue attachment.

The facial nerve is best repaired with a cable graft-using segment of the greater

auricular nerve. If skin has not been sacrificed the site is drained and the incision closed

in a routine manner. Skin defects must be repaired using either local random flap,

provided they give sufficient surface area or regional axial flaps for larger defects.

Complications of Parotid Gland Surgeries28

1. Infection: wound infection following parotidectomy is uncommon.

2. Haemorrhage and haematoma: Significant bleeding is best avoided by careful

dissection, isolation and ligation of the vessels. Incidence of haematoma varies

55

from 0.8-16% following parotid gland surgery. Once the diagnosis of haematoma

is made, the patient is taken to the operating room for evaluation of the wound

and control of offending vessel.

3. Aesthetic Problems: Barely noticeable scar is possible with placement of the

incision in skin fold; gentle handling of the tissues and cosmetic wound closure in

which the epithelial edges are accurately approximated before the placement of

the skin sutures. Another source of aesthetic concern is the depression or hollow

resulting from the parotid gland resection, particularly following total

parotidectomy.

4. Sensory changes: Cutaneous anaesthesia and hypesthesia are very annoying

sequelae of parotid gland surgeries. Anaesthesia, hypesthesia and parasthesia

from greater auricular nerve transection occur routinely and should be discussed

with the patient. Recovery will take 6-9 months to occur.

5. Sialoceles and salivary fistulas: Incidence is 3-6.5% and 0.2-3.3% respectively.

Most are transient and respond to pressure dressings with repeated aspirations,

proving necessary in the case of sialoceles. Glycopyrolate assists in decreasing

the volume of secretions, thus facilitating closure. Removal of the deep lobe of

the parotid can be curative. Radiation therapy has been tried. Tympanic

neurectomy has been successful in treatment of chronic fistulas provided a

complete interruption of Jacobson nerve is performed. When wound care fails,

this procedure is the treatment of choice.

6. Frey’s syndrome (Gustatory sweating and flushing)21: It is thought that

following injury to the auriculotemporal nerve, post-ganglionic parasympathetic

56

fibres from the otic ganglion become united to sympathetic nerves from the

superior cervical ganglion destined to supply the vessels and sweat glands of the

skin.

Treatment of Frey’s Syndrome

1. Topical agents

a. Antiperspirants – Effective in milder cases

b. Anti-cholinergic preparations

Scopalamine, Glycopyrolate, Diphemanil, Methylsulfate,

2. Radiation therapy

Dose of 50 gy is needed to control gustatory sweating.

3. Surgical procedures

a. Skin excision – used for localised and relatively small areas

b. Auricular nerve section

c. Fascialata interposition

d. Tympanic neurectomy

e. Acellular human dermal (Allodelus) interposition

7. Facial nerve dysfunction: Transient weakness of a branch or branches of the

facial nerve is not uncommon. Permanent weakness may follow division of a

significant branch although distal cross linkage can maintain normal function. The

procedures used to rehabilitate the paralyzed face after injury to the facial nerve

may be arbitrarily divided into the following general categories.24, 25

57

Physiologic nerve repair or graft

1. Synergistic nerve crossover or substitution.

2. Dynamic reanimation

a. Alloplastic eyelid reanimation

b. Muscle transposition

3. Static supportive procedures

4. Other adjunctive procedures

1. Physiologic nerve repair or graft

In choosing a rehabilitative approach, it is axiomatic that restoration of facial

nerve continuity by direct repair or grafting be the procedure of choice when possible,

assuming it can be performed within 12 months of the injury. With physiologic

approaches, the facial muscles are reanimated by repairing or grafting the proximal centre

nerve stump to the distal segment. Time after injury and avoidance of tension at the

anastomotic site appear to be most important factors in determining the degree of success.

The best results are achieved when repair is performed within 30 days after injury. The

sural or the greater auricular nerve is most commonly used for grafting purposes. The

sural nerve is preferred to defects greater than 8 cm or when the greater auricular nerve is

unsuitable.

Under ideal circumstances, as with immediate repair of a facia nerve after surgical

injury, recovery is usually noted by the sixth month and continuous to improve for

2-5 years. In general the earlier the onset of recovery, the more completes the recovery.

Here microscopic epineural suture technique using 7-0 monofilament nylon is used.

58

2. Synergistic nerve crossover or substitution

When the central stump of the facial nerve is unavailable and the mimetic muscles

are still viable, hypoglossal facial crossover is the favoured technique, though it is not

without its drawbacks. The VII-> VII cross face nerve graft that connects the nonessential

midface branches to the contralateral facial nerve with a long sural nerve graft is another

less favoured and more complex technique in patients where the central stump of the

facial nerve on the injured side is not available.

Cross-face Grafts

It appears that cross face nerve grafting should not be used as a primary procedure

but rather as an adjunct to other procedures performed to restore facial function. The

obvious disadvantage of the procedure is that it sacrifices normal facial function for the

potential benefit of the paralyzed side.

Hypoglossal – Facial Anastomosis

Most surgeons prefer the hypoglossal facial anastomosis when the central stump

of the facial nerve is unavailable. The essence of the procedure is to attempt to improve a

devastating neurologic deficit at the expense of an inatrogenically created deficit of lesser

consequence. The requirement for the successful performance of a XII – VII substitution

are:

1. An intact extra cranial facial nerve.

2. Intact mimetic facial muscles.

3. An intact donor 12th nerve.

59

4. A patient who can physiologically and psychologically accept the neurologic

deficit created by sacrifice of the 12th nerve.

3. Dynamic Procedures: Eyelid reanimation and muscle transposition

When the facial nerve is unavailable or the mimetic muscles are absent, deficient

or fibrotic, alternatives to nerve grafting and crossover techniques must be used.

Techniques for rehabilitating the paralyzed face in the absence of the facial nerve include

both dynamic and static procedures. Dynamic procedures include regional muscle

transposition (i.e., temporalis, masseter, and various eyelid reanimating procedures

including gold weight lid loading and eyelid spring implantation) all of which are aimed

in restoration of the eyelid closure. Static procedures include fascial or alloplastic slings,

browlift, rhytidoplasty, canthoplasy and lid tightening.

Mouth Reanimation

Reanimation of the mouth has been most rewarding using the temporalis muscle

transposition. It is useful for long standing facial paralysis and has been used in selected

cases to augment results with the nerve grafts or XII –VII crossover. Symmetry and

voluntary smile are achieved in 3-6 weeks and continue to improve over a period of

1 year.

4. Adjunctive Static Procedures

A variety of adjunctive static suspension techniques may be used to enhance

facial symmetry in repose. The temporalis muscle itself creates a moderate degree of

static suspension in addition to providing dynamic reanimation to the mouth area. The

60

temporalis may be tightened or augmented with the use of fascia (i.e, gore-tex). The

same materials may be used to provide static suspension in patients whose temporalis is

unusable. Attachment to the midface and oral region requires over correction for long-

term success.

A face lift may be combined with any of the reanimating techniques discussed

and is quite useful for long standing facial paralysis accompanied by loss of skin tone and

sagging.

8. Tumour recurrence

In case of pleomorphic adenoma recurrence has declined from the range of

20-30% to 0.7 %, as superficial parotidectomy has become the standard procedure.

Role of radiotherapy in parotid tumours

In the past three decades, there has been an evolution in the role of radiotherapy in

management of parotid tumours. In most instances, it is used as an adjunctive treatment

after surgical resection of tumour. In selected patients, there may be a role for

radiotherapy as a primary curative modality or in the setting of palliation. In some

institutes once the diagnosis is established, a course of radiotherapy of which 2/3 is given

pre-operatively and 1/3 post-operatively. Surgery is timed for approximately 6 weeks

after conclusion of the pre-operative course to allow most of the radiation reaction to

subside and the post-operative course is begun once all the surgical wounds have healed

and the general condition of the patient allows it. The current indications for the use of

61

post-operative radiation in the setting of parotid malignancies are derived from

Guillamondegui and co-workers as modified by Johns.

1. High grade tumours

2. Recurrent lesions

3. Tumour of the deep lobe

4. Gross/microscopic residual disease

5. Tumour adjacent to facial nerve

6. Regional lymph node metastasis

7. Extra-parotid extension/perineural invasion

8. Any T3 parotid cancer

Technique

The majority of malignant parotid tumours will be adequately treated using two

angled wedge fields (anterolateral or posterolateral beams) the patient being placed

supine on the treatment couch and the posterolateral beam provided from an under couch

source. The supine position has been found to be the most comfortable and is well

tolerated by patients who are often unfit.

The wedge shaped volume, extends from the tip of the zygoma superiorly down to

the hyoid bone and from the anterior border of masseter to the mastoid, medially it

extends to the midline. It thus includes the entire parotid gland, the parotid duct, and the

parapharyngeal space an upper deep cervical lymph nodes as well covering the surgical

scar. The upper limit may need to be extended if there is base of the skull invasion, or

any likelihood of spread of an adenoid cystic carcinoma along the facial nerve into the

62

skull. If there is established lymph node involvement or if as in case of squamous or

undifferentiated tumours, there is a significant risk of occult nodal disease, the ipsilateral

lower neck should also be irradiated. When there is skin involvement by tumour 0.5 cm

of wax bolus is applied to the shell to circumvent the skin sparing effect of mega voltage

irradiation.

For postoperative radiation, a dose of 6,000 – 6,500 CGY range is given for

6 to 7 weeks. When using a split course of radiotherapy give pre-operatively course of

4,000-4,500 CGY in 4 weeks. Surgery is planned for 6 weeks after the completion of its

pre-operative radiotherapy. Once the surgical scar has healed and the patient’s general

condition allows, the remaining 2,000-2,500 CGY are given to the main volume. When

no surgery is contemplated, our aim is to irradiate the planned volume to 6,500 CGY in 6

– 7 weeks giving daily treatments of 200 CGY.17

ROLE OF CHEMOTHERAPY IN PAROTID TUMOURS

There is no established standard chemotherapy for treatment of parotid cancers

because of the lack of formal trails with adequate number of patients. The role of

chemotherapy in the management of the malignant parotid tumours is limited to disease

that is metastatic or locally advanced and unresectable. The most commonly used drugs

singly or in combination are cisplatin, 5 Flurouracil & doxorubicin.17

63

METHODOLOGY

This study was conducted from January 2003 to June 2005, over a period of

2 years and 6 months. 30 patients admitted to Victoria Hospital with parotid gland

neoplasms are included in this study.

All patients admitted were evaluated by documenting the history, thorough

clinical examination, routine laboratory investigations and specific investigations. In

history, importance was give to presenting complaints, duration of lump, rapid increased

in size, associated symptoms of facial nerve involvement, previous surgical treatment or

any medical problem.

Regarding physical examination, particulars mentioned in the proforma was

noted. Importance was given to the site, extent of the tumour, deep lobe enlargement and

fixity to the surrounding structures, facial nerve involvement and regional

lymphadenopathy. Associated medical conditions like diabetes, hypertension, and

anaemia were managed and controlled before surgery with physician’s advice.

As a part of general work up for surgery in all patients, haemoglobin level,

bleeding time, clotting time, urine, sugar albumin, microscopy, chest screening. ECG,

Blood urea, Serum creatinine, RBS was estimated. Specific investigations like FNAC, x-

ray of mandible, were done for all patients in the study group. CT scan, MRI was not

done for any of these patients in the study group, as there was no facility for these

investigations in this hospital and because of the poor economic background of these

64

patients. Sialography is not done for any of these patients because it may cause

inflammation or infection. Extravasation of the dye may cause a severe inflammatory

reaction preventing a clear demarcation of tumour margins and may also delay the

planned surgical procedure.

After evaluation of the tumour by clinical examination and specific investigations,

a surgical plan was formulated. The final decision was taken per operatively by the

surgeon. The specimen was sent for histopathology for final diagnosis and tumour typing.

The adjuvant treatment was decided depending on the final histopathological report.

Different modalities of treatment adopted in this study are

1. Surgery alone

2. Surgery and postoperative radiotherapy

Different surgical procedures adopted in this study are

1. Superficial parotidectomy

2. Total conservative parotidectomy

The follow up period of these patients ranged from 3 months to 1 year. Long term

follow up is necessary to study the tumour recurrence, which was not possible in this

study.

65

OBSERVATIONS AND RESULTS

Following observations were made in 30 patients who presented with parotid

gland neoplasms in this study.

Table 1

Age and Sex incidence in parotid tumours

Age Group

Total No. of Cases

% Pleomorphic Adenoma

Warthin’s Tumour

Basal cell Adenoma

Onocytoma Malignant Mixed Tumour

Acinic Cell Carcinoma

11-20 2 6.67 2 1

21-30 8 26.67 5 1

31-40 7 23.33 7 1

41-50 9 30.00 6 1 2 1

51-60 2 6.67 1

61-70 1 3.33 1

71-80 1 3.33 1

Total 30 100 21 2 1 1 4 1

The age incidence of the patients in the study group ranged from 14-72 years. The

malignant tumours occurred between the age group of 36-72 years. Most patients in this

series were in the 4th decade of life (44%). The mean age was 37.6 years for benign

tumours and 50.7 years for malignant tumours.

66

Distribution of tumours

Table 2

Distribution of tumours

Sex Total No. of Cases

% Pleomorphic Adenoma

Warthins Tumour

Basalcell Adenoma

Oncocytoma Malignant Mixed Tumour

Acinic Cell Carcinoma

Male 18 60 11 2 1 1 2 1

Female 12 40 10 2

Total 30 100 21 2 1 1 4 1

Sex Incidence

60%

40%

Male Female

In this series, 18 (60%) patients were male and 12 (40%) were female. M:F ratio

is 3:2. Benign tumours were common in males (M: F – 3:2). there was no sex

differentiation in malignant tumors (M:F-1:1).

67

Age & Sex Incidence in parotid tumours

01020304050607080

Pleomorp

hic Aden

oma

Warthins T

umour

Basalc

ell A

denoma

Oncocy

toma

Malignan

t Mixe

d Tumour

Acinic

Cell C

arcinoma

Individual tumours

Perc

enta

ge

Table 3

Incidence of benign and malignant parotid tumours

Sl. No.

Individual Tumours No. patients (n-30)

%

1 Pleomorphic Adenoma 21 70

2 Warthins Tumour 2 6.66

3 Basal Cell Adenoma 1 3.33

4 Oncocytoma 1 3.33

5 Malignant Mixed Tumour 4 13.33

6 Acinic cell carcinoma 1 3.33

Overall pleomorphic adenoma, constituted 70% of the tumour and among

malignant tumour, malignant mixed tumour constituted 13% of the tumours in the series.

68

Table 4

Distribution of benign tumours

Benign Tumours No of cases (n=25)

%

Pleomorphic Adenoma 21 84

Warthins Tumour 2 8

Basal Cell Adenoma 1 4

Oncocytoma 1 4

Table 5

Distribution malignant tumours

Malignant Tumours No of cases (n=5)

%

Malignant Mixed Tumour 4 80

Acinic cell Carcinoma 1 20

In this study, among the benign tumours pleomorphic adenoma constituted 84%

of the benign tumours and among the malignant tumours, malignant mixed tumour

constituted 80% of the malignant parotid tumours.

Side of the tumour

60% of the parotid tumours occurred in the left parotid gland in this series.

Table 6

Distribution of side of the tumour

Side of the Tumour No. Cases (n=30) %

Right Side 12 40

Left Side 18 60

69

Table 7

Clinical presentation of parotid tumours

Signs and Symptoms No. of Cases Overall %

Swelling 30 100

Pain 14 46.67

Fungating Mass 0 0

Symptoms of facial palsy - -

Cervical lymphadenopathy - -

Deep Lobe Enlargement 2 6.66

Fixity to Masseter/Mandible 2 6.66

Clinical presentation of parotid tumours

0

5

10

15

20

25

30

35

Swelling

Pain

Fungatin

g Mass

Symptom

s of fa

cial p

alsy

Cervica

l lymphad

enop

athy

Deep Lob

e Enlar

gemen

t

Fixity

to M

assete

r/Man

dible

Signs and Symptoms

No.

of c

ases

70

All patients presented with swelling in the parotid region. Features of rapid

growth, pain, fixity and associated facial paralysis were considered as signs of

malignancy. Hard in consistency is noted mostly in malignant tumour. Out of 30 patients,

14 patients presented with pain (46.67%) in swelling, out of which 9 were benign and

5 were malignant. Pain occurred in 100% of the patients with malignant tumours and

36% of the patients with benign tumours. Deep lope enlargement was seen in 2 patients

in this series and the tumour was fixed to masseter/mandible in 2 patients. No patient had

facial nerve paralysis at presentation of this series.

71

Table 8

Incidence in relation to duration of the mass

Signs and Symptoms No. of Cases Overall %

1 – 12 months 5 16.67

1 – 5 years 15 50.00

6 – 10 years 9 30.00

11 – 15 years 1 3.33

All patients presented with swelling in the parotid regions of which most cases

(66.6%) presented within 5 years after noticing the swelling.

Recurrent tumours

One recurrent tumour was operated in this series. It was acinic cell tumour.

FNAC & Histopathology

All 30 cases subjected to FNAC and were reported as parotid tumours. After

surgical excision or biopsy, all specimens were studied histopathologically and the table

below shows co-relation between FNAC reporting and histopathological diagnosis.

Table 9

Correlation of FNAC with histopathological examination

Diagnosed as Benign Diagnosed as Malignant

FNAC Biopsy FNAC Biopsy

28 25 2 3

72

Surgery

Surgery was performed in 30 patients, the type of surgery was chosen according

to clinical impression, FNAC and per-operative findings.

Table 10

Types of surgical treatment adopted in the study

Procedure No. of Cases %

Superficial Parotidectomy 25 83.33

Conservative Total Parotidectomy 5 16.67

Superficial parotidectomy was performed in 25 patients (83.33%), conservative

total parotidectomy in 5 patients (16.67%). In this study, radical parotidectomy and RND

was not done in any of the patients in this series.

Adjuvant treatment

Radiotherapy was given to 5 patients, with malignant tumour of the parotid gland,

5 patients were given post-operative radiotherapy. Out of theses 4 patients had malignant

mixed tumour and other one had acinic cell tumour. One patient who received

radiotherapy developed xeroxtomia, which was treated conservatively. No patient with

benign disease of the parotid was given radiotherapy. No patients were given

chemotherapy in this series.

73

Table 11

Complications following surgery

Complications Pleomorphic Adenoma

Warthins Tumour

Basal cell Adenoma

Oncocytoma Malignant Mixed

Tumour

Acini cell ca

Total (%)

Immediate post op facial nerve weakness

5 1 0 1 7 (28.33)

Permanent facial nerve weakness

3 0 1 1 5 (16.66)

Parotid fistula 2 0 2 (6.66)

Wound infection

2 2 4 (13.33)

Frey’s syndrome

1 1 (3.3)

Post operatively 7 patients developed facial nerve weakness, 5 patients had

pleomorphic adenoma. 1 patient had malignant mixed tumour, 1 patient had Warthins.

No facial nerve repair was done in this study. Out of 7 patients, in 3 patients facial nerve

weakness improved over 3-6 months. Permanent facial nerve weakness occurred in

15 patients (16.67%). 2 patients underwent lateral tarsoraphy to prevent eye

complications. Wound infection occurred in 4 patients and parotid fistula occurred in 2

patients with pleomorphic adenoma tumour who had undergone superficial

parotidectomy, which healed spontaneously within 3 months. No postoperative death was

encountered in this study.

74

Follow up

In this series follow up ranged form 3 months – 1 year. To know the recurrence of

a tumour long term follow up is necessary which was not possible in this study. In spite

of repeated postal reminders most of the patients in this study did not respond. During the

study period none of the operated patients came back with recurrent diseases.

75

DISCUSSION

In this study, most patients were in the 3rd and 5th decade of life. Malignant

tumours were common in the 4th and the 5th decade. Malignant tumours were encountered

more in the older age group in comparison to benign ones. The mean age group was

36.97 years for benign tumours and 49.6 years for malignant tumours.

Males were affected more than females in both benign and malignant tumours.

The duration of swelling was form 8 months to 12 years. The history of duration of the

swelling is not significant, as long-standing benign tumour may turn malignant. Rapid

growths, pain, change in the growth pattern, facial nerve involvement is significant. The

commonest site of parotid tumour was superficial lobe (100%). Deep lobe enlargement

was seen in 2 patients (6.67%) in this series.

All patients presented with history of swelling in the parotid region. 46.67% of

the patients presented with pain in the swelling, 6.6% with fixity to masseter/mandible.

No patient presented with facial nerve palsy. In this series 100% of the patients with

malignant parotid disease presented with pain. Potdar et al and Woods et al have reported

the incidence of pain and facial nerve paralysis in malignant neoplasms as 25-33% and

20-33% respectively. NO patient presented with cervical lymph node metastasis.

2 patients, one with malignant mixed tumour and other with Acini cells carcinoma

presented with fixity to masseter / mandible.

76

The safest and the most acceptable means of diagnosis is FNAC, though complete

surgical excision and histopathological examination was the final court of trial. In this

series, FNAC was carried out in all cases. In one occasion, the report was inadequate

tissue for diagnosis and in other occasion it was reported as supportive lesion. So these

two patients were not included in the correlation between FNAC and histopathology.

Table 12

Comparison of FNAC and HPE

Source No. of Patients

Histology (FNAC)

Accuracy Benign from

Malignant (%)

Exact overall Cytohistological Correlation (%)

Exact Cytohistological Correlation in

malignancies (%)

Kline et al 69 50 96 57 56

Koejan et al 52 29 86 79 83

Sismanis et al 51 51 91 74 60

Webb et al 66 50 98 92 92

Qizilabash et al 160 101 98 88 79

Present study 30 30 100 89.2 40

Overall Cytohistological Correlation (%)

0

20

40

60

80

100

Kline et al Koejan etal

Sismanis etal

Webb et al Qizilabashet al

Presentstudy

Source

Perc

enta

ge

77

In this study FNAC correctly diagnosed benign from malignant in 91.3% of the

cases. The exact cytohistological correlation in case of malignancy was 60%. The exact

overall cytohistological correlation was 89.2%, which is comparable to western literature.

In the series by Mcgurk & K. Hussain et al, the ability to distinguish benign from

malignant parotid gland tumour was 93%, but the definitive histological diagnosis could

be established in 77% of the cases. In the series by JMH Debeto & JJK Munting, the

accuracy of FNAC was 74% for overall parotid tumour and 81% for pleomorphic

adenoma.

Radiotherapy was given to 5 patients with malignant tumours of the parotid gland.

5 patients were given postoperative radiotherapy and 4 patients are presented with

malignant mixed carcinoma and one patient presented with recurrent Pleomorphic

adenoma it turned out to be acinic cell carcinoma. In the management of malignant

tumours, the usefulness of radiotherapy as an adjuvant to surgery has been accepted by

all authors.

Chemotherapy is of doubtful benefit in the management of malignant parotid

tumours and in this study it has not been given a trial.

Temporary Facial Weakness

In this study postoperative facial nerve weakness occurred in 7 patients (23.33%)

And in 3 patients facial nerve weakness recovered completely over 6 months. Reported

incidence of immediate postoperative facial weakness varies between 11-82% as per

western literature. Normal function usually returns within 3-6 months, but it may take

78

upto one year. It may be caused by nerve ischaemia, fatigue from excessive stimulation,

stretching or haematoma formation.

Permanent facial weakness

In this study, postoperatively 16.6% (No.5) of the patients developed permanent

facial weakness, which is comparable with the western literature (3 patients with

malignant mixed tumour and 1 patient with acini cell pleomorphic adenoma). Reported

incidence of permanent facial weakness in 0-17%, as per western literature.

Mehle et al & Lacourrey et al have reported 46% and 65% incidence of

immediate postoperative facial weakness. Permanent facial weakness was 4% in both the

series. Permanent facial weakness is slightly higher compared to western literature.

Source Permanent facial weakness JMH Debetes & JDK Munting et al32 7% Mehle et al and Laccourreye et al 4% Present study 16.67%

2 patients developed parotid fistula following superficial parotidectomy, which

healed spontaneously within 3 months. 4 patients developed wound infection in this

series.

In this study, pleomorphic adenoma was the commonest tumour encountered

constituting 70% of the parotid tumours. Among the benign parotid tumours pleomorphic

adenoma constituted about 84% of the benign parotid tumours. Among malignant

tumours the commonest was malignant mixed tumour constituting 80% of the malignant

tumours.

79

CONCLUSION

• 30 cases admitted in Victoria Hospital attached to Bangalore Medical College

from January 2003 to June 2005 over a period of 2½ years were included in this

study.

• Incidence is highest in the 3rd to 5th decade constituting 65% of the patients.

• Male to female ratio is 3:2.

• Benign tumours of the parotid constituted about 83.33% and malignant tumours

constituted 16.66% of the parotid neoplasms in the study.

• All patients presented with swelling in the parotid region.

• Pain was the second commonest symptom. Pain was noticed in 46.67% of the

patients. Pain in the swelling occurred in 100% of the malignant tumours and 36%

of the benign tumours.

• None of the patients in this series presented with facial nerve weakness or cervical

lymph node metastasis.

• 6.66% of the patients presented with enlargement of the deep lobe of the parotid

gland.

• Pleomorphic adenoma was the commonest tumour in this series constituting 70%

of the over all parotid tumours.

• Pleomorphic adenoma was the commonest benign tumour constituting 84% of the

benign tumours.

• Malignant mixed tumour was the commonest malignant tumour constituting 80%

of the malignant parotid tumours.

80

• FNAC was done in all patients. The overall accuracy of FNAC in this study was

86.9%, which is comparable to western literature.

• CT scan and MRI were not done for any of these patients in the study group. CT

scan is one of the most accurate preoperative methods of examination. MRI is

reported to give more detailed anatomical information and to define the position

of a parotid mass in relation to the facial nerve better.

• Sialography is seldom indicated in parotid gland neoplasms because it may cause

inflammation or infection. Sialography was routinely done previously in patients

with parotid gland neoplasms; Extravasation of the dye may cause a severe

inflammatory reaction, preventing a clear demarcation of tumour margins and

may also delay the planned surgical procedure.

• The treatment of choice for parotid neoplasms is surgery. This may or may not be

followed by radiotherapy.

• In this study, all patients with malignant tumours were given post-operative

radiotherapy. No patient with benign tumours of the parotid was given

radiotherapy.

• No patients in the study were give chemotherapy.

• Commonest postoperative complication is facial nerve weakness.

• The incidence of permanent facial nerve weakness was 16.6%. This is comparable

to western standard (0-17%). This has occurred mainly in patients with malignant

tumours and recurrent tumours. In this study no form of facial nerve repair was

done except lateral tarsoraphy to prevent eye complications.

81

• In view of the late presentation, in this series, which can adversely affect in

malignant tumours, increased community awareness for early referral is

mandatory.

• The adequacy of treatment cannot be commented because of the short follow up

of these patients in the study. The study group in this series is small, as compared

to large series in western literature; so statistical data in this series may not

represent the actual data quoted in the western literature.

82

SUMMARY

Clinicopathological study and management of parotid tumours, study carried out

in Victoria Hospital attached to Bangalore Medical College from January 2003 to March

2005. It is more common in males and it is seen in 3rd to 5th decade. Benign tumors are

more common than the malignant tumours (80:20). Pleomorphic adenoma is most

common benign tumors followed by Warthin’s tumour. Malignant mixed tumour is the

most common malignant tumour of parotid gland. All patients underwent preoperative

evaluation and surgery, adjunct chemotherapy for malignant tumors. FNAC is the simple

and sensitive for parotid tumours. It guides for the treatment of the tumour and

histopathology confirmed the disease. Temporary facial nerve palsy is most common

complication noted. We had one case of Frey’s syndrome as a postoperative complication

in our series.

83

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86

CASE PROFORMA

Name: IP No:

Age: DOA:

Sex: DOD:

Occupation: DOS:

Address:

CHIEF COMPLAINTS

Duration:

1. Swelling

2. Pain

3. Difficulty in chewing

4. Difficulty in opening mouth

5. Salivation: Normal/Increased/Decreased/Purulent/Otherwise

6. Recurrence of swelling

HISTORY OF PRESENTING COMPLAINTS

1. Swelling:

a. Situation of the swelling to start with and duration

b. Mode of onset: Sudden/Gradual

c. Progress of the swelling: slow/rapid

d. Increase in size of the swelling with intake of food.

87

2. Pain

a. Site

b. Nature

c. Time of onset

d. Radiation

3. Similar swelling

4. Loss of weight:

PAST HISTORY

FAMILY HISTORY Marital status:

PERSONAL HISTORY

a. Appetite

b. Sleep

c. Bowel/Bladder

d. Smoking

e. Alcohol intake

f. Diet

GENERAL PHYSICAL EXAMINATION

1. Anaemia : Present / Absent

2. Nutritional assessment

3. Lymphadenopathy

4. Icterus

5. Cyanosis

88

Vitals

a. Pulse Rate

b. BP

c. Respiratory Rate

LOCAL EXAMINATION

1. Inspection

a. Site: in relation to the lobule of the ear

Elevation of the ear lobule:

b. Size

c. Shape

d. Extent

e. Surface: Smooth / Lobulated

f. Skin over the swelling: scar/ulcer/signs of inflammation

g. Edge: well defined / diffuse

h. Pulsation over the swelling: present/ absent

2. Palpation

a. Local temperature

b. Tenderness

c. Site, size, shape and extent

d. Surface: Smooth / lobulated

e. Edge: well defined / diffuse

f. Consistency: soft /cystic/firm/hard

g. Mobility: freely mobile/restricted/fixed

h. Fixity to the skin or masseter or mandible

89

3. Examination of the facial nerve

Involved / Not Involved

4. Examination of the oral cavity:

a. Oral hygiene

b. Orifice of parotid duct

c. Discharge from the parotid duct

5. Examination of the regional lymph nodes: involved / not involved

6. Examination of the mandible: Involved / not involved

SYSTEMIC EXAMINATION

1. Per Abdominal examination

2. CVS

3. RS

Investigations

a. Hb, BT, CT

b. ESR

c. FBS, PPBS

d. Blood Urea

e. Serum Creatinine

f. Chest x-Ray

g. ECG

h. FNAC of the swelling

i. X ray of the part / Mandible

90

Treatment

1. Surgery :

a. Operative procedure:

b. Postoperative complications

c. Biopsy report

2. Radiotherapy

3. 3. Chemotherapy

Follow Up

91

KEYS TO MASTER CHART

DOA - Date of admission

DOD - Date of discharge

DOO - Date of operation

L - Left

L/N - Lymph node

MS - Masseter muscle

MD - Mandible

MMT - Malignant Mixed Tumour

PA - Pleomorphic Adenoma

R - Right

Rec. PA - Recurrent Pleomorphic adenoma

SP - Superficial parotidectomy

T - Temporary

TP - Total parotidectomy

WT - Warthin’s Tumour

MASTER CHARTSl

. No.

Nam

e

Age

Sex

IP N

O.

Occ

upat

ion

Add

ress

DO

A

DO

O

DO

D

Dur

atio

n

Clinical features

Ass

ocia

ted

Dis

ease

Clin

ical

Dia

gnos

is

FNA

C

Proc

edur

e

HPE

Complications

Swel

ling

Pain

Fixi

ty to

MS

& M

D

Dee

p lo

be

Faci

al n

erve

Faci

al n

erve

W. I

nf

Fist

ula

Frey

's s

yn

1 Mehrunisa 46 F 749401 Housewife Bangalore 3/9/2003 3/13/2003 3/21/2003 5 years R - 7x4 cm - - - - - PA PA SP PA - - - -

2 Puttalingamma 30 F 750262 Coolie Kanakapura 3/26/2006 3/31/2003 4/8/2003 8 years L - 3x3 cm + - - - - PA/LN PA SP PA - - + -

3 Chandramma 48 F 753302 Teacher Madikeri 6/12/2003 6/15/2003 6/26/2003 10 years L - 3x5 cm - - - - HTN PA PA SP PA -/0 - - -

4 Mukesh 35 M 755228 Coolie Bangalore 6/26/2003 6/30/2003 7/6/2003 7 years L - 4x3 cm + - - - TB PA PA SP PA -/T - - -

5 Mahadeva 50 M 755614 Agriculturist Channarayapatna 7/7/2003 7/17/2003 7/23/2003 2 years R - 8x5 cm + - - - TB PA PA SP WT -/T - - -

6 Radha 14 F 756706 Student Bangalore 7/25/2003 7/29/2003 8/4/2003 1 year L - 3x2 cm - - - - - PA PA SP PA - - - -

7 Shanmugamma 44 M 756450 Coolie Bangalore 7/30/2003 8/11/2003 8/19/2003 6 years L - 5x6 cm - - - - DM PA PA SP PA +/T + - -

8 Muniraju 45 M 759500 Agriculturist Bangalore 9/15/2003 9/24/2003 10/1/2003 9 months R - 3x7 cm + + - - - REC PAACINIC CELL CA TP

ACINIC CELL CA - - - -

9 Gulshan 25 F 758860 Housewife Bangalore 9/11/2003 9/15/2003 9/22/2003 7 years L - 2x6 cm - - - - ASTHAMA PA PA SP PA +/P - - -

10 Manikantan 55 M 767347 Agriculturist Hosur 3/2/2004 3/6/2004 3/14/2004 4 years L - 3x4 cm - - - - HTN PA PA SP PA - + - -

11 Muniyappa 25 M 716838 Agriculturist Mysore 3/8/2004 3/14/2004 3/20/2004 1 1/2 years L - 3x2 cm + - - - DM PA PA SP PA + - - -

12 Manjula 21 F 735892 Housewife Kolar 6/6/2004 6/9/2004 6/17/2004 4 years L - 4x4 cm + - - - - PA PA SP PA - - - -

13 Jamaluddin 30 M 743188 Coolie Tumkur 7/15/2004 7/18/2004 7/25/2004 8 years R - 12x5 cm - - - - - PA PA SP PA - - - -

14 Padma 32 F 742253 Housewife Bangalore 7/26/2004 7/30/2004 8/6/2004 10 years L - 3x7 cm - - - - - PA PA SP PA - - - -

15 Udayakumari 30 F 750351 Coolie Maddur 8/12/2004 8/16/2004 8/22/2004 2 years L - 4x5 cm + - - - - PA PA SP PA - - - -

16 Tersa 72 F 764321 Teacher Bangalore 9/7/2004 9/10/2004 9/20/2004 1 year R - 2x5 cm + - - - DM PA PA TP MMT +/P - -

17 Siddamma 45 F 774303 Coolie Kolar 9/21/2004 9/23/2004 9/30/2004 12 years R - 4x3 cm + + - - - PA MMT TP MMT +/T + - -

18 Satyanarayan 53 M 778890 Agriculturist Bangalore 9/28/2004 10/4/2004 10/10/2004 3 years L - 2x5 cm - - - - - PA PA SP PA - + - -

19 Girija 24 F 779425 Tailor Bidadi 11/30/2004 11/4/2004 10/11/2004 3 years R - 3x1 cm - - - - - PA PA SP PA - - - -

20 Shantamma 32 F 790821 Housewife Bangalore 11/11/2004 11/15/2004 11/22/2004 6 years L - 1x2 cm - - - - - PA PA SP PA - - + -

21 Iqbal Ahmed 36 M 784281 Coolie Kolar 12/11/2004 12/15/2004 1/20/2004 4 years R - 2x3 cm + - - - TB PA PA SP PA - - - -

22 Rajappa 42 M 789391 Agriculturist Bidadi 12/27/2004 12/29/2004 1/4/2005 2 years L - 5x7 cm - - - - - PA PA SP PA +/T - - -

23 Shivanna 39 M 713814 Teacher Magadi 1/17/2005 1/20/2005 1/27/2005 1year R - 3x4 cm + - - - HTN PA PA SP PA - - - +

24 Rajesh 16 M 718124 Student Bangalore 1/20/2005 1/24/2005 1/30/2005 8 months L - 1x2 cm - - - - - PA PA SPBASAL CELL ADENO CA - - - -

25 Nagaraj 30 M 729139 Coolie Bangalore 2/20/2005 2/24/2005 3/2/2005 5 years R - 2x3 cm + - - - - PA WT SP WT +/T - - -

26 Gangappa 36 M 734213 Agriculturist Tumkur 2/25/2005 2/28/2005 3/5/2005 9 years L - 5x7 cm + - + - - PA PA TP MMT +/P - - -

27 Satyaveerappa 39 M 736413 Agriculturist Anekal 3/1/2005 3/4/2005 3/10/2005 3 years R - 3x4 cm - - - - - PA PA SP PA - - - -

28 K.B. Nanjappa 43 M 739319 Coolie Bangalore 3/10/2005 3/12/2005 3/20/2005 2 years R - 2x5 cm - - - - - PA PA SP PA +/T - - -29 Wazeer 50 M 741214 Coolie Bangalore 3/18/2005 3/20/2005 3/26/2005 7 years L - 6x7 cm + - + - DM MMT M MT TP MMT +/P - - -

30 Ramanna 65 M 742639 Agriculturist Kanakapura 3/20/2005 3/22/2005 3/30/2005 2 years L - 1x2 cm - - - - - PA PA SP Oncocytoma - - - -