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

Seal and Signature of the Principal Dr. T. RAJESHWARI MS Principal Bangalore Medical College Bangalore.

Date: Place:

Date: 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: Place:

Signature of the Candidate Name:

Rajiv Gandhi University of Health Sciences, Karnataka

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: Place:

Signature of the Candidate Name:

vi

LIST OF ABBREVIATIONS USED

C/S CT FNAC H/o MRI HPE

Cut section Computed Tomography Fine needle aspiration cytology History of Magnetic Resonance Imaging 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, Freys syndrome.

ix

TABLE OF CONTENTS

Sl. No. 1. 2. 3. INTRODUCTION OBJECTIVES

Particulars

Page Nos. 1 2

REVIEW OF LITERATURE History Embryology Anatomy Physiology Histology Classification and staging of parotid Tumours Etiopathogenesis and Clinical features Individual Parotid Tumours Investigations Management 3 6 7 12 14 16 20 24 41 44 64 66 76 80 83 84

4. 5. 6. 7. 8. 9. 10.

METHODOLOGY OBSERVATION AND RESULTS DISCUSSION CONCLUSION SUMMARY BIBLIOGRAPHY ANNEXURES PROFORMA MASTER CHART KEY TO MASTER CHART

87 92 93

LIST OF TABLES

Page Nos. 1. 2. 3. 4. 5. 6 7. 8. 9. 10. 11. 12. Age and Sex incidence in parotid tumours Distribution of tumours Incidence of benign and malignant parotid tumours Distribution of benign tumours Distribution malignant tumours Distribution of side of the tumour Clinical presentation of parotid tumours Incidence in relation to duration of the mass Correlation of FNAC with histopathological examination Types of surgical treatment adopted in the study Complications following surgery Comparison of FNAC and HPE 66 67 68 69 69 69 70 72 72 73 74 77

xi

LIST OF FIGURES

Sl. No. 1. 2 3 4 5 6 7 8 9 10 11 12 13 14 Relations of parotid gland Branching pattern of Facial Nerve Microscopic appearance of benign mixed tumor. Epithelial and myothelial cells can be easily distinguished. Benign mixed tumour. The myoepithelial cells are undergoing cartilaginous metaplasia Low power appearances of Warthins tumour - Germinal centers are very prominent. High power field showing Acinic cell carcinoma Benign mixed tumour (left) with areas of malignant transformation in the form of poorly differentiated carcinoma (right) Pleomorphic adenoma- lateral view Malignant mixed tumour-lateral view Incision Raising anterior skin flap Mobilization of parotid tumour (Plemorphic adenoma) Showing facial nerve after superficial parotidectomy Specimen of plemorphic adenoma

Page Nos. 9 9 25 26 27 34 36 43 43 48 49 50 52 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.

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.

REVIEW OF LITERATURE
History Riolan (1648): First to recognize the Glandular substance of parotid glands.

Niels Stenson (1960)1: Dissected sheeps 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.

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.

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.

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

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

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) (b) (c) Condylar process: near the temporomandibular joint. Metal process: In the medial area of the incisura of external auditory canal. 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

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

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. Its 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 -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. 2. 3. Moistening of oral mucosa Moistening dry foods to aid swallowing. 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 -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 (Zimmermans 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. 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 ADENOMAS

Pleomorphic adenoma Myoepithelioma (Myoepithelial adenoma) Basal Cell adenoma Warthins Tumour (Adenolymphoma) Oncocytoma (Oncocytic Adenoma) Canalicular Adenoma Sebaceous Adenoma Ductal Papilloma a. Inverted ductal papilloma b. Intra-ductal papilloma c. Sialadenoma papilliferum

8940/0 8982/0 8147/0 8561/0 8290/0

8410/0

8503/0 8503/C 8260/0 8440/0 8450/0 8470/0

1.9

Cystadenoma a. Papillary Cystadenoma b. Mucinous Cystadenoma

II. 2.1 2.2 2.3 2.4

CARCINOMAS Acinic Cell Carcinoma Muco-epidermoid carcinoma Adenoid Cystic Carcinoma Polymorphous low grade adenocarcinoma (terminal duct adenocarcinoma) Epithelial-myoepithelial carcinoma
8562/3 8550/3 8430/3 8200/3

2.5

16

2.6 2.7 2.8 2.9 2.10 2.11 2.12 2.13 2.14

Basal Cell Adenocarcinoma Sebaceous Carcinoma Papillary cystadenocarcinoma Mucinous adeno carcinoma Oncocytic carcinoma Salivary duct carcinoma Adenocarcinoma Malignant myoepithelioma (Myoepithelial Carcinoma) Carcinoma in pleomorphic adenoma (Malignant mixed tumour) Squamous cell carcinoma Small cell carcinoma Undifferentiated carcinoma Other carcinomas NON-EPITHELIAL TUMOURS MALIGNANT LYMPHOMAS SECONDARY TUMOURS UNDIFFERENTIATED TUMOURS TUMOUR LIKE LESIONS Sialadenosis (sialosis) Oncocytosis Necrotizing sialometaplasia (salivary gland infarction) Benign lympho epithelial lesion Salivary duct cysts Chronic sclerosing sialadenitis of submandibular gland (kuttner tumour) Cystic lymphoid hyperplasia in AIDS

8147/3 8410/3 8450/3 8480/3 8290/3 8500/3 8410/3 8982/3 8941/3

2.15 2.16 2.17 2.18 III. IV. V. VI. VII.

8070/3

7.1 7.2 7.3 7.4 7.5 7.6 7.7

71000 73050 73220 72240 33400 45000

17

TNM CLASSIFICATION OF SALIVARY GLAND TUMOURS (1997) 17: T TX T0 T1 T2 T3 Primary Tumour. Primary Tumour cannot be assessed. No evidence of Primary Tumour. Tumour 2 Cm or less in greatest dimension without extra parenchymal extension. Tumour more than 2 cms but not more than 4 cms in greatest dimension without extra parenchymal extension. Tumour having extra parenchymal extension without seventh nerve involvement and / or more than 4 cm but more than 6 cm in greatest dimension. Tumour invades base of the skull, seventh nerve and / or exceeds 6 cm in greatest dimension. Regional lymph nodes. Regional lymph nodes cannot be assessed. No regional lymph node metastasis. Metastasis in a single ipsilateral lymph node, 3 cm or less in greatest dimension. 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. Metastasis in a lymphnode more than 6 cm in greatest dimension. Distant metastasis. Distant metastasis cannot be assessed. No distant metastasis. Distant metastasis.

T4 N Nx No N1 N2

N3 M Mx M0 M1

18

Stage Grouping Stage I T1 T2 Stage II Stage III T3 T1 T2 Stage IV T4 T3 T4 Any Any Any T T T N0 N0 N0 N1 N1 N0 N1 N1 N2 N3 Any M0 M0 M0 M0 M0 M0 M0 M0 M0 M0 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 Warthins 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. metastasis correlates strongly with a diminished overall survival. Regional

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 stensons 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

Warthins 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 warthins 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 childrens 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) (4) A metastasizing benign mixed tumour. 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. formation is common. Necrosis, haemorrhage and cyst

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. carcinoma of the parotid gland is a diagnosis of exclusion.16 Primarily squamous cell

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 Sjogrens 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. 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

It is seldom done because other studies yield more useful

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 Group I Treatment

T1 & T2, N0, Low grade (low Superficial or total parotidectomy with grade muco-epidermoid tumour, preservation of facial nerve. Nodal Acinic cell tumour) sampling sos neck dissection (N+ RND)

Group II

T1 & T2, N0, High grade Total parotidectomy with preservation of (Adenocarcinoma, Malignant the facial nerve Nodal sampling sos neck mixed tumour, Undifferentiated dissection (N+ RND) Post op radio carcinoma, Squamous carcinoma, therapy for primary and neck. Adenoid cystic carcinoma, High muco-epidermoid carcinoma)

Group III T3, N0/N+ and any recurrent Radical parotidectomy sacrificing the tumour not in group IV 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 surgeons 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 Stensens 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. 2. Infection: wound infection following parotidectomy is uncommon. 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. Freys 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 Freys Syndrome 1. Topical agents a. b. Antiperspirants Effective in milder cases Anti-cholinergic preparations Scopalamine, Glycopyrolate, Diphemanil, Methylsulfate, 2. Radiation therapy Dose of 50 gy is needed to control gustatory sweating. 3. Surgical procedures a. b. c. d. e. 7. Skin excision used for localised and relatively small areas Auricular nerve section Fascialata interposition Tympanic neurectomy Acellular human dermal (Allodelus) interposition

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. 2. Synergistic nerve crossover or substitution. Dynamic reanimation a. b. 3. 4. Alloplastic eyelid reanimation Muscle transposition

Static supportive procedures 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. 2. 3. An intact extra cranial facial nerve. Intact mimetic facial muscles. 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 longterm 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. 2. 3. 4. 5. 6. 7. 8. High grade tumours Recurrent lesions Tumour of the deep lobe Gross/microscopic residual disease Tumour adjacent to facial nerve Regional lymph node metastasis Extra-parotid extension/perineural invasion 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 patients 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 physicians 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, xray 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 Total % Group No. of Cases 11-20 21-30 31-40 41-50 51-60 61-70 71-80 Total 2 8 7 9 2 1 1 30 6.67 26.67 23.33 30.00 6.67 3.33 3.33 100 21 2 1 1 Onocytoma Malignant Acinic Pleomorphic Warthins Basal Cell Mixed Adenoma Tumour cell Carcino Tumour Adenoma ma 2 5 7 6 1 1 1 4 1 1 1 1 2 1 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 18 12 30 60 40 100 Pleomorphic Warthins Basalcell Oncocytoma Malignant Acinic Cell Adenoma Tumour Adenoma Mixed Carcinoma Tumour 11 10 21 2 1 1 2 1 1 2 2 4 1 1

Male Female Total

Sex Incidence

40%

60%

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

80 70 Percentage 60 50 40 30 20 10 0

no m

ou r

ou

yt om

no m

Tu

de

Tu

de

oc

M ix

ce

hi

th

or p

ar

al

B as

nt

eo

na

ig

Pl

Table 3 Incidence of benign and malignant parotid tumours Sl. No. 1 2 3 4 5 6 Individual Tumours Pleomorphic Adenoma Warthins Tumour Basal Cell Adenoma Oncocytoma Malignant Mixed Tumour Acinic cell carcinoma No. patients (n-30) 21 2 1 1 4 1 % 70 6.66 3.33 3.33 13.33 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

M al

Individual tumours

ci

ni

el

lC ar

in

ll

nc

ed

ci

no

Table 4 Distribution of benign tumours Benign Tumours Pleomorphic Adenoma Warthins Tumour Basal Cell Adenoma Oncocytoma No of cases (n=25) 21 2 1 1 % 84 8 4 4

Table 5 Distribution malignant tumours Malignant Tumours Malignant Mixed Tumour Acinic cell Carcinoma No of cases (n=5) 4 1 % 80 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 Left Side 69 12 18 % 40 60

Table 7 Clinical presentation of parotid tumours Signs and Symptoms Swelling Pain Fungating Mass Symptoms of facial palsy Cervical lymphadenopathy Deep Lobe Enlargement Fixity to Masseter/Mandible No. of Cases 30 14 0 2 2 Overall % 100 46.67 0 6.66 6.66

Clinical presentation of parotid tumours

35 30 25

No. of cases

20 15 10 5 0
Sy M m as pt s om so ff ac ia C lp er vi al ca sy ll ym ph ad en op D at ee hy p Lo be En la Fi rg xi em ty en to t M as se te r/ M an di bl e Sw el lin g Pa in Fu ng at in g

Signs and Symptoms

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 1 12 months 1 5 years 6 10 years 11 15 years

No. of Cases 5 15 9 1

Overall % 16.67 50.00 30.00 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 FNAC 28 Biopsy 25 Diagnosed as Malignant FNAC 2 Biopsy 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 Superficial Parotidectomy Conservative Total Parotidectomy No. of Cases 25 5 % 83.33 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 Warthins Basal cell Oncocytoma Malignant Acini Adenoma Tumour Adenoma Mixed cell Tumour ca Immediate post op facial nerve weakness Permanent facial nerve weakness Parotid fistula 5 1 0 1 Total (%)

7 (28.33)

5 (16.66)

2 (6.66) 2 4 (13.33) 1 (3.3)

Wound infection Freys syndrome

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 (%) 96 86 91 98 98 100 Exact overall Cytohistological Correlation (%) 57 79 74 92 88 89.2 Exact Cytohistological Correlation in malignancies (%) 56 83 60 92 79 40

Kline et al Koejan et al Sismanis et al Webb et al Qizilabash et al Present study

69 52 51 66 160 30

50 29 51 50 101 30

Overall Cytohistological Correlation (%)

100 Percentage 80 60 40 20 0 Kline et al Koejan et Sismanis et Webb et al Qizilabash al al et al Source Present study

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 JMH Debetes & JDK Munting et al Mehle et al and Laccourreye et al Present study
32

Permanent facial weakness 7% 4% 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 2 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 Warthins 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 Freys syndrome as a postoperative complication in our series.

83

BIBLIOGRAPHY
1. 2. Welton T.S. Biographical brevities Stensens duct Am. J. Surg. 1931; 14; 501. Mc. Evedy PG. Diseases of the salivary glands. Clinical Journal 1934; 63: 334338. 3. Patey DH. The treatment of mixed tumors of parotid gland Br J Surg 1940; 28; 29-38. 4. Bailey H. The treatment of the tumors of the parotid gland. Br J Surg 1941; 28: 337-346. 5. Patey DH. The present position of parotidectomy in the Surgery of the parotid gland. Arch Middx Hosp. 1954; 4: 91-105. 6. Hobsley M. In.: Kirk RM: Williamson RCN Surgery of Head and Neck. General Surgical Operations; Edinburgh; Churchill Livingstone 1987; 350-75. 7. S. E. Afify: Carcinoma of major salivary gland. Annals of Royal College of Surgeon of England 1992; 74: 186-191. 8. Richard L. Fabian, Salivary Glands Oxford Textbook of Surgery 1994; 2: 22202266. 9. Golden T. Deans, An audit of surgery of parotid Gland. Annals of Royal College of Surgeon of England 1995; 77; 188-192. 10. Mc. Gurk MK. Hussain. Role of fine needle aspiration cytology in parotid lump. . Annals of Royal College of Surgeon of England 1997; 79: 198-202. 11. Joseph Califano et al. Benign Salivary Gland neoplasms Otolaryngologic Clinics of North America 1999; 32 (5): 861-873.

84

12.

Petor L. Williams, Mary Dyson. Salivary Gland. Churchill Livingstone 1992 Grays Anatomy 37th ed, Avon The Bath Press, 1291-1292.

13.

Chummy S. Sinnatamby, Lasts Anatomy, Head Neck & Spine. 10th Edition, Churchill Livingstone (2000). Harcourt Publishers: 350-351.

14.

William F. Gannong. Review of Medical Physiology. 20th Edition. Mc Graw Hill 2001-473.

15.

Stephen S. Sternmberg. Diagnostic Surgical Pathology Vol 1, 3rd Edition. 1999; 853-875.

16.

Dale H. Rice. Malignant Salivary Glands Neoplasm. Salivary Gland disease. Otolaryngologic Clin N Am 1999; 32 (5): 875-885.

17.

K Harish. Management of Primary Malignant epithelial parotid tumors, Surgical Oncology 2004; 13: 7-16.

18.

Robert L. Witt, The significance of the margin in parotid surgery for pleomorphic adenoma, the laryngoscope 2002; 112: 2141 2153.

19.

Johns MM III, Westra W H, Califando JA et al: Alleotype of Salivary Gland tumors, Cancer Res 1996; 56: 1151.

20.

Joseph Califano, David W. Eisele Benign Salivary Gland neoplasms otolaryngologic Clin N Am 1999; 32: 861-873.

21.

Mark, May, Barry M. Schaitin, The facial Nerve, Rehabilitation Techniques for acute and long-standing facial paralysis. 2nd edition, Thieme 763-65.

22.

Garry R Warnock, Warthins tumor. Surgical pathology of salivary gland 1991. Chapter 11, Vol. 25: 187-199.

23.

Bataskis JG. Tumors of the major salivary gland: Clinical & Pathological consideration. Baltimore, Williams & Willkins 1979 1981.

85

24.

Michael Friedman et al.

Malignant Tumors of the Major Salivary Gland,

Otolaryngologic Clinics of North America 1986; 19: 625-636. 25. Charles W. Cummings et al, Otolaryngology. Head & Neck Surgery. Neoplasms of salivary Glands. 3rd edition, Mosby, 1283-1286. 26. Dale H. Rice, Non-inflammatory & non-neoplastic disorder of Salivary Glands Otolaryngologic Clin N Am 1999, 32 (5): 835-842. 27. RCG Russel, Norman S. Williams & Chistopher J.K. Bulstrode, Bailey & Loves Short Practice of Surgery. 24th edition, 2004. Arnold Publication, 732. 28. Uttam K. Sinha, Matthew Ng, Surgery of the Salivary Glands. Otolaryngologic Clin N Am 1999: 32 (5): 887-905. 29. Anderew U Lawrence G. Hutchins, Richard Berg, Preoperative Computed Tomograph. Scans for Parotid tumors evaluation. Laryngoscope 2001; 111: 19841988. 30. Peter Zbaren, Catherine Schar, Michel, Value of FNAC of parotid Gland masses, Laryngoscope 2001; 111: 1989-92. 31. Norman E Hugo, Peter Mc. Kinney, B Herold Griffth. Surg Clinic of North 1America 1973; (53): 105 111. 32. J. M. H. DEBETS & J D K Munting, Parotidectomy for parotid tumors. 19-year experience from Netherlands. Br J Surgery 1992 ; 79: 1159-1161.

86

CASE PROFORMA

Name: Age: Sex: Occupation: Address:

IP No: DOA: DOD: DOS:

CHIEF COMPLAINTS Duration: 1. 2. 3. 4. 5. 6. Swelling Pain Difficulty in chewing Difficulty in opening mouth Salivation: Normal/Increased/Decreased/Purulent/Otherwise 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 PERSONAL HISTORY a. b. c. d. e. f. Appetite Sleep Bowel/Bladder Smoking Alcohol intake Diet Marital status:

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. c. d. e. f. g. h. 2. Size Shape Extent Surface: Smooth / Lobulated Skin over the swelling: scar/ulcer/signs of inflammation Edge: well defined / diffuse Pulsation over the swelling: present/ absent Palpation a. b. c. d. e. f. g. h. Local temperature Tenderness Site, size, shape and extent Surface: Smooth / lobulated Edge: well defined / diffuse Consistency: soft /cystic/firm/hard Mobility: freely mobile/restricted/fixed 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. b. c. Oral hygiene Orifice of parotid duct 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. 2. 3. Per Abdominal examination CVS RS

Investigations
a. b. c. d. e. f. g. h. i. Hb, BT, CT ESR FBS, PPBS Blood Urea Serum Creatinine Chest x-Ray ECG FNAC of the swelling X ray of the part / Mandible

90

Treatment
1. Surgery : a. b. c. 2. 3. 3. Operative procedure: Postoperative complications Biopsy report

Radiotherapy Chemotherapy

Follow Up

91

KEYS TO MASTER CHART

DOA DOD DOO L L/N MS MD MMT PA R Rec. PA SP T TP WT

Date of admission Date of discharge Date of operation Left Lymph node Masseter muscle Mandible Malignant Mixed Tumour Pleomorphic Adenoma Right Recurrent Pleomorphic adenoma Superficial parotidectomy Temporary Total parotidectomy Warthins Tumour

MASTER CHART
Clinical features Associated Disease Fixity to MS & MD Clinical Diagnosis Complications

Facial nerve

Facial nerve

Occupation

Procedure

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30

Mehrunisa Puttalingamma Chandramma Mukesh Mahadeva Radha

46 30 48 35 50 14

F F F

749401 750262 753302

Housewife Coolie Teacher Coolie

Bangalore Kanakapura Madikeri Bangalore

3/9/2003 3/26/2006 6/12/2003 6/26/2003

3/13/2003 3/31/2003 6/15/2003 6/30/2003 7/17/2003 7/29/2003 8/11/2003 9/24/2003 9/15/2003 3/6/2004 3/14/2004 6/9/2004 7/18/2004 7/30/2004 8/16/2004 9/10/2004 9/23/2004 10/4/2004 11/4/2004 11/15/2004 12/15/2004 12/29/2004 1/20/2005 1/24/2005 2/24/2005 2/28/2005 3/4/2005 3/12/2005 3/20/2005 3/22/2005

3/21/2003 4/8/2003 6/26/2003 7/6/2003 7/23/2003 8/4/2003 8/19/2003 10/1/2003 9/22/2003 3/14/2004 3/20/2004 6/17/2004 7/25/2004 8/6/2004 8/22/2004 9/20/2004 9/30/2004 10/10/2004 10/11/2004 11/22/2004 1/20/2004 1/4/2005 1/27/2005 1/30/2005 3/2/2005 3/5/2005 3/10/2005 3/20/2005 3/26/2005 3/30/2005

5 years 8 years 10 years 7 years 2 years 1 year 6 years 9 months 7 years 4 years

R - 7x4 cm L - 3x3 cm L - 3x5 cm L - 4x3 cm R - 8x5 cm L - 3x2 cm L - 5x6 cm R - 3x7 cm L - 2x6 cm L - 3x4 cm

+ + + + + +

+ + -

+ + -

HTN TB TB DM -

PA PA/LN PA PA PA PA PA REC PA

PA PA PA PA PA PA PA ACINIC CELL CA PA PA PA PA PA PA PA PA MMT PA PA PA PA PA PA PA WT PA PA PA M MT PA

SP PA SP PA SP PA SP PA SP WT SP PA SP PA ACINIC CELL TP CA SP PA SP PA SP PA SP PA SP PA SP PA SP PA TP MMT TP MMT SP PA SP PA SP PA SP PA SP PA SP PA BASAL CELL SP ADENO CA SP WT TP MMT SP PA SP PA TP MMT SP Oncocytoma

-/0

+ + -

+ -

M 755228 M 755614 F 756706

-/T -/T -

Agriculturist Channarayapatna 7/7/2003 Student Coolie Bangalore Bangalore 7/25/2003 7/30/2003 9/15/2003 9/11/2003 3/2/2004 3/8/2004 6/6/2004 7/15/2004 7/26/2004 8/12/2004 9/7/2004 9/21/2004 9/28/2004 11/30/2004 11/11/2004 12/11/2004 12/27/2004 1/17/2005 1/20/2005 2/20/2005 2/25/2005 3/1/2005 3/10/2005 3/18/2005 3/20/2005

Shanmugamma 44 Muniraju Gulshan Manikantan Muniyappa Manjula Jamaluddin Padma Udayakumari Tersa Siddamma Satyanarayan Girija Shantamma Iqbal Ahmed Rajappa Shivanna Rajesh Nagaraj Gangappa Satyaveerappa K.B. Nanjappa Wazeer Ramanna 45 25 55 25 21 30 32 30 72 45 53 24 32 36 42 39 16 30 36 39 43 50 65

M 756450 M 759500 F 758860

+/T + -

Agriculturist Bangalore Housewife Bangalore

ASTHAMA PA HTN DM DM TB HTN DM PA PA PA PA PA PA PA PA PA PA PA PA PA PA PA PA PA PA PA MMT PA

+/P + +/P +/T + + + -

M 767347 M 716838 F 735892

Agriculturist Hosur Agriculturist Mysore Housewife Coolie Housewife Coolie Teacher Coolie Kolar Tumkur Bangalore Maddur Bangalore Kolar

1 1/2 years L - 3x2 cm 4 years 8 years 10 years 2 years 1 year 12 years 3 years 3 years 6 years 4 years 2 years 1year 8 months 5 years 9 years 3 years 2 years 7 years 2 years L - 4x4 cm

M 743188 F F F F 742253 750351 764321 774303

R - 12x5 cm L - 3x7 cm L - 4x5 cm R - 2x5 cm R - 4x3 cm L - 2x5 cm R - 3x1 cm L - 1x2 cm R - 2x3 cm L - 5x7 cm R - 3x4 cm L - 1x2 cm R - 2x3 cm L - 5x7 cm R - 3x4 cm R - 2x5 cm L - 6x7 cm L - 1x2 cm + + + + + + + + -

M 778890 F F 779425 790821

Agriculturist Bangalore Tailor Housewife Coolie Bidadi Bangalore Kolar

M 784281 M 789391 M 713814 M 718124 M 729139 M 734213 M 736413 M 739319 M 741214 M 742639

Agriculturist Bidadi Teacher Student Coolie Magadi Bangalore Bangalore

+/T -

+/T +/P -

Agriculturist Tumkur Agriculturist Anekal Coolie Coolie Bangalore Bangalore

+/T +/P -

Agriculturist Kanakapura

Frey's syn

Deep lobe

Duration

Address

Swelling

Fistula

Sl. No.

IP NO.

FNAC

Name

W. Inf

DOO

DOA

DOD

Pain

HPE

Age

Sex