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Parotid Tumors: An overview of the classification, presentation and management of tumors of the parotid. Introduction.

The salivary glands in humans are a group exocrine glands. They are divided into major glands (consisting of paired parotid, submandibular, and sublingual glands) and up to 1000 minor glands located in the oral mucosa, floor of mouth, palate, uvula, pharynx and larynx.. Salivary glands are responsible for secreting saliva with lubricating, immunologic and digestive functions. The largest of the salivary glands is the parotid gland and can be involved into a variety of disease processes that can be classified into cystic, obstructive, inflammatory and neoplastic. This paper will focus on the clinical presentation and management of parotid tumors. Anatomy(GRAYs anatomy) . The parotid glands are the largest of the salivary glands located in the preauricular region along the posterior mandibular surface . They extend superiorly up to the zygomatic arch and inferiorly via the parotid tail to the lower border of the mandible. The parotid tail abutshthe anteromedialimargin of the sternocleidomastoid and extends posteriorly towards the mastoid process. The gland is further subdivided by the facial nerve into a superficial lobe, overlying the masseter muscle and the deep lobe extending deep between the mastoid process and the posterior ramus of the mandible. These lobes are not anatomically discrete but are of significance in surgical interventions of the parotid (discussed later). In approximately 21 % of humans (book), an accessory parotid gland is located anterior to the main parotid gland and is connected to it by its own duct. The parotid duct exits from the anterior edge of the parotid halfway between the zygomatic arch and the angle of the mouth to run along the masseter muscle and course deeply through the buccal fat and the buccinator muscle to open into the oral cavity near the second upper molar tooth. Several important neurovascular structures pass through or just deep to the parotid glands including: 1) Facial nerve (CN VII): exits skull through stylomastoid foramen and enters the parotid gland, where it divides into the lower cervicofacial (supplying muscles of mouth and neck) and upper temporofacial branches (supplying forehead and eye muscles). The two trunks undergo further branching and anastomosis to terminate as the temporal, zygomatic, buccal, marginal, and cervical branches. The coarse of the facial nerve through the parotid gland and its subsequent terminal branching will be of significance in surgical interventions of the parotid gland. The plane through which the facial nerve courses divides the parotid into a superficial and a deep lobe 2) Vascular: The external carotid artery and retromandibular vein pass through the deep lobe of the parotid gland. These structures are also at risk of compromise in surgical intervention of the parotid gland.

Adapted from: Grays Anatomy for Students, 2nd edition, Drake . Tumours Salivary gland tumors are a group of neoplasms that can pose significant diagnostic and management challenges due to their diverse morpohological and clinical presentation. Tumours of the salivary glands are relatively rare with a yearly incidence of 1-3 cases per 100,000 {{13 Speight, PM 2002;}} (Improving outcomes in head and neck cancers, NICE (2004)) in the western world and account for 3% to 5% of head and neck cancers {{13 Speight, PM 2002;}}. Of all salivary gland tumours, approximately 70-80% arise in the parotid gland {{13 Speight, PM 2002;}}, of which 80% are benign {{12 Eneroth, CM 1971;}}.

Classification:
The World Health Organization (WHO) classification of salivary gland tumours provides a useful general scheme of categorizing salivary neoplasia according to their morphological and behavioral characteristics (Appendix 1). In fact, up to 40 epithelial tumours {{13 Speight, PM 2002;}} have been indicated in salivary glands with some subtypes only being rarely reported in as little as few cases in the literature. Thus, this article will focus on parotid tumours that are more frequently encountered in clinical practice. Parotid gland tumours can be broadly classified as follows 1) Malignant epithelial tumours Malignant tumors can be further classified according to their clinical behavior and prognosis into high grade or low-intermediate grade High Grade: Mucoepidermoid {{17 Boahene, Derek Kofi O 2004;}}: Most common malignancy accounting for 30% of parotid maliganacies {{15 Laforga,J.B. 1999;}}. Can be further subdivided into: High grade malignancy: High mitotic frequency with focal necrosis. Clinically associated with rapid growth, pain, ulceration, bleeding and facial nerve involvement. 5 year survival is only 5 % if lymph node metastasis. {{16 Suzuki, Masashi 1998;}} Low grade malignancy: well differentiated cystic tumour with low metastatic potential. 5 year survival is 75% to 95% without nodal metastasis. {{16 Suzuki, Masashi 1998;}}

Adenoid cystic carcinoma: Highly aggressive malignancy with a high recurrence rate and prolonged clinical course and tendency to infiltrate and spread along perineural planes. It makes up 7.5% of malignant epithelial tumours of the parotid. Distant metastasis is common and carries a worse prognosis. Is further sub classified into Grade I, II, III with respective 15 year survival rates of 39%, 26% and 5%. {{18 Szanto, Philip A 1984;}} Adenocarcinoma (MEDSCAPE malignant tumours): Relatively rare but aggressive patortid malignancy. High potential for local lymph node and distant metastasis. In fact, a third of patient have local or distant metastasis at presentation. 5 year survival ranges from 19-75% depending on grade and stage at presentation.

Low grade: Acinic cell carcinoma: Third most common parotid malignancy. Characterized by low distant metastatic potential but can invade perineural planes. Usually presents as bilateral or multicentric solid lesions with associated pain in more than 33% of patients. (MEDSCAPE MALIGNANT TUMOURS)(CANCER.gov). 5 years survival is 82%. Prognosis predictors include features of pain, fixation and gross invasion. {{19 Lewis, Jean E 1991;}}. 2)Benign epithelial tumours: Pleomorphic adenoma: The most common of all parotid tumors accounting for 80% of benign parotid tumours. Its characterized by various histological characteristics, hence the term pleomorphic. Presents as a slow growing circumbscribed surrounded by an incomplete capsule. Compromise of the capsule during surgical intervention can leave behind neoplastic tissue that form the bases of high recurrence rates of this tumour. Can progress to its malignanct counterpart (carcinoma ex-pleomorphic adenoma) in 2-10 % of long-standing adenomas (MEDSCAPE BENIGN PAROTID TUMOURS) Warthins tumor: Second most common benign tumour accounting for 5 % of benign parotid tumours.. More common in men than women with a ratio approaching 2:1. They are bilateral in 12 % of cases and are associated with an 8-fold increased incidence in smokers compared to nonsmokers {{20 Kotwall, Cyrus A 1992;}}. Usually asymptomatic and presents most often in the 6th and 7th decades in men and women, respectively {{21 Hatch, Robert L 2005;}}

3)Soft tissue tumours: Haemangiomas: Most common childhood salivary tumour {{23 Callender, David L 1992;}}. 4) Haematolymphoid. Lymphoma: A non-epithelial malignant tumour that accounts for approximately 16% of parotid malignancies. Increased incidence in patients with a background of chronic autoimmune disease, such as Sjogrens syndrome, leading to marginal zone lymphomas of MALT (nonHodgkins) and display an indolent coarse. {{22 Harris,N.L. 1999;}}. Primary lymphomas can also present in the parotid glands. Clinically, the parotid gland is enlarged with a

ruberry consistency; regional lymph nodes may also be palpated and biopsied to confirm diagnosis, thus avoiding unnecessary parotid surgery as primary treatment is chemotherapy and/or radiation.. (MEDSCAPE MALIGNANT PAROTID TUMOUR) 5)Secondary tumours. Approximately 16% of malignancies of the parotid can be attributed to secondary metastasis from distant malignancies along the following three routes: Direct invasion by cancers lying adjacent to parotid. Haematogenous metastasis Lymphatic metastasis. Approximately 80% of secondary parotid tumours arise from primary tumors of the head and neck; the remaining 20% arise from infraclavicular sites including skin, renal, lung, breast and gastrointestinal. (CELLULAR CLASSIFICATION OF SALIVARY TUMOURS)

Etiology and Risk factors:


Etiology: The etiology of primary parotid tumors remains unknown; however, a bicellular theory (MEDSCAPE SALIVARY TUMOURS)of origin has been proposed to account for the various histological subtypes . This theory describes tumors as arising from one of two undifferentiated stem cells: excretory or intercalated duct reserve cells. Excretory stem cells account for mucoepidermoid, while pleomorphic adenomas, adenoid cystic carcinomas, adenocarcinomas and acinic cell carcinomas originate from intercalated duct stem cells. (MEDSCAPE SALIVARY TUMOURS). Several genes (WHO 2005-end of paper) (EGFR, TP53, c-Kit, HER2/neu) have also been implicated and targeting them could advance treatments of parotid tumors {{29 Milano, Amalia 2007;}}. Risk factors: Radiation exposure has been associated with both benign and malignant parotid tumors. This is reflected in various studies where it has been observed that long-term cancer survivors who received radiotherapy to the head and neck where at an increased risk of developing neoplasia with an average latency of 15-20 years. (MEDSCAPE salivary gland neoplasm). Smoking and alcohol, well known risk factors for various head and neck cancers, do not appear to play a role in development of neoplasm; however, smoking has been shown to be related to the development of Warthins tumor, with a smoking history present in about 96% of patients {{30 Yu, GY 1998;}}.

Epidemiology
Salivary gland neoplasms have an incidence of 1-2/100,000 in England and Wales, with approximately 470 new yearly diagnosis (Improving outcomes in head and neck cancers, NICE (2004)). Approximately 80% of all salivary tumours arise in the parotid glands {{13 Speight, PM 2002;}}. Benign tumours typically present after 5th decade, while malignant tumors typically present after the 7th decade. Benign tumours, apart from warthins tumor, are more common in women, but malignant tumors have equal incidence in both sexes. (salivary gland neoplasms MEDSCAPE)

CLINICAL PRESENTATION
In England and Wales, Patients with parotid malignancy present in about 13% of cases with early disease, 17% with locally advanced, 7% with lymph node spread and 28% with metastatis. (PATIENT UK REFERENCE 5). A patient presenting with a parotid mass needs to be fully examinated and investigated as a variety of pathological causes including neoplastic, infectious, autoimmune, and inflammatory (TABLE). In fact, up to 25% of parotid masses could be attributed to non-neoplastic (MEDSCAPE) causes and these have to ruled out before proceeding with unnecessary surgical interventions. Therefore, it is important to approach a consulatation with an initial focused history of the mass and its onset, duration, growth rate, size or symptom change with meals, facial weakness, and pain. This should be followed by a thorough general history to rule out infectious, inflammatory or autoimmune causes. Other aspects of the history to enquire about include prior squamous cell carcinoma, malignant melanoma or previous parotid lesion excision to rule out possible metastatic or recurrent tumor lesions. The most common presentation (80%) is a painless, asymptomatic mass in the posterior check; this is followed by less common presentations including pain(12%) and facial dysfunction(7%) ({{26 Byrne, Maria N 1988;}} . Pain is present in 5.6% of benign presentations and 6.5% of malignanies; thus, pain is not a good indicator in differentiating the bengin from malignant {{31 Lee, YYP 2008;}}Facial paralysis in the presence of a parotid mass indicates perineural invasion and is highly suggestive of malignancy and may indicate nodal metastasis at time of presentation in up to 80% of patients. It should be appreciated that only 12-15% of patients with malignant lesions present with facial dysfunction {{27 O'Brien, Christopher J 2001;}} . Dysphagia or foreign-body sensation in the oropharynx may indicate a tumor of the deep lobe. Ear pain may suggest extension of the tumor into the ear canal. Clinical examination of a parotid mass is simple in itself; however, it should be accompanied by a thorough head and neck assessment of the local lymph nodes for signs of metastasis, an examination of the oral , oropharyngeal and nasopharyngeal cavity as well as inspection for skin lesions to rule out sites of primary tumors. Cervical node metastasis can be detected in about 20% of patients with malignancy at time of presentation. Physical examination of the parotid should aim to assess the clinical features of the mass including its degree of firmness (a rock hard mass signifies malignancy); skin fixation, ulceration, fixation to adjacent structures, and blood or pus from the parotid duct also

indicate malignancy. (patient uk ). Moreover, bimanual lateral pharyngeal wall palpation is valuable in assessing for parapharyngeal wall extension of a deep lobe tumour. (Medscape salivary tumours). The facial nerve should be carefully assessed for any indication of dysfunction or weakness signifying paraneural infiltration and malignancy.

Investigations:
In addition to obtaining a thorough history and examination, imaging can be utilized by the clinician to differentiate benign versus malignant lesions, intra versusllextra-glandular location, local extension9and invasion, and nodal or distant metastasis. Various imaging modalities can be employed in the investigation of parotid tumors. These include ultrasound, MRI and CT imaging. For superficial parotid lesions, high resolution ultrasound is a cheap and safe imaging tool providing A useful tool in the assessment of suspected parotid tumors is the high-resolution ultrasound (US); US can characterize the tissue and assess for cervical node involvement (___) without the risk of radiation exposure and can be combined with fine needle aspiration cytology (FNAC). In fact, a recent study concluded that the combination of US and FNAC is highly sensitive and specific for detecting benign superficial lobe tumors and that no other additional information would be gained from MR or CT imaging. {{32 Brennan, PA 2011;}}. Ultrasound, however, is not useful in detecting deep lobe pathologies and depends on specialist expertise (___). Thus, MR and CT imaging are the modalities of choice when suspecting a parotid malignancy or a deep lobe tumor. MR and CT imaging are optimal in assessing tumour extent and regional lymph node metastasis. In particular, MRI is better at soft tissue differentiation, detection of deep tissue/marrow infiltration, facial nerve invasion as well as demonstrating tumor margins {{4 Lee, YYP 2008;}}. MRI can help differentiate benign from malignant masses: benign and low grade tumors appear white on T2 weighted images whereas high grade malignancies tend to have low intensity on T1 and T2 images. The disadvantages of MRI is the relatively higher cost, long scan times and claustrophobic environment and poorer bony structure evaluation when compared to CT (pogril book) {{33 Koyuncu, Mehmet 2003;}}. CT scan provides better visualization of the surrounding tissues whereas MRI will enable visualization of mass in greater contrast. The reported sensitivity of MRI and CT is 88% and 100% respectively, and the specificity is 77% and 42% respectively. {{4 Lee, YYP 2008;}} Ultra sound or CT guided final needle aspiration cytology is valuable tool in determining a histological diagnosis and grading of malignancy thus assisting in pretreatment planning and patient counseling. {{4 Lee, YYP 2008;}} However, the effectiveness of FNAC is highly diependant on cytologist expertise with a reported sensitivity and specificity ranging from 88%-93% and 75%-99%, respectively, depending on level of expertise {{4 Lee, YYP 2008;}}. The positive predictive value and negative predictive value of malignancy in FNAC is 84.6% and 96.4% , respectively (SALIVARY NEOPLASN MEDSCAPE). FNA is useful in establishing wether a lesion is neoplastic or inflammatory, epithelial or nonepithelial in origin and metastatic or primary. (END OF PAGE REFERECNE)

If the aspirate is unable to determine a diagnosis, an ultrasound guided core biopsy can be performed but this carries a risk of facial nerve damage and should be kept as a last resort (malignant parotid tumor Medscape).

Treatment
Treatment of parotid tumor depends on whether it is benign or malignant, its location, size,8invasiveness andirelationship to facial nerve. The parotid gland is divided into a superficial and deep lobe by the facial nerve. The chief treatment is adequate surgical resection with the objective of preserving the facial nerve; this is followed by postoperative radiotherapy when necessary. BENIGN TUMOURS Superficial paridoctomy with facial nerve preservation is recommended for benign tumors restricted to the superficial lobe. However, a recent study has shown partial superficial paridoctomy to be as effective as superficial paridoctomy in resection of localized benign neoplasia. {{34 O'Brien, Christopher J 2003;}}. Moreover, in a series conducted at Christies Hospital in Manchester, extracapsular dissection of pleomorphic adenomas was as effective as superficial paridectomy with similar recurrence rates of 2% but with significantly reduced morbidity {{36 McGurk, M 1996;}}. In benign tumors occurring in the deep lobe, total paridectomy is indicated with effort to preserve the facial nerve {{35 Roh, JongLyel 2008;}}. It has been noted that, after simple enucleation, pleomorphic adenomas are associated with a recurrence rate of 20%-45% versus <5% in superficial parotidectomy; this phenomenon may be due to the increased possibility of capsule rupture and tumour spillage in enucleation resulting in seeding of tumor cells into parotid tissue. In the case of suspected tumor recurrence, an MRI combined with FNAC will confirm the recurrence. (BOOK).

Superficial parotidectomy is the treatment of choice for pleomorphic adenomas arising in the parotid gland. The recurrence rate after simple enucleation is 20 to 45 percent; with superficial parotidectomy, recurrence rates are reduced to less than five percent [74,75]. For most pleomorphic adenomas, a more extensive procedure (total parotidectomy) does not reduce the risk of recurrence further and is associated with higher rates of facial nerve dysfunction and other complications [74,76,77]. Positive margins, capsule rupture, and tumor spillage have been implicated as a potential causes for high recurrence rates, and these should be avoided when possible. However, positive margins are common after resection of this tumor; these occur because of an incomplete tumor capsule, a tendency of the tumor to form perforating pseudopodia, and close proximity of the tumor to the facial nerve [3,74,78].

Malignant tumours For malignant lesions, the degree of resection is determined by the histological subtype, location and size of tumour. Typically, malignant tumors require a total parotidectomy with every effort made to preserve the facial nerve. Tumors confined to the superficial lobe can be effectively excised using superficial parotidectomy. Aggressive tumors with invasion to the perineural plane and/or surrounding structures require a radical parotidectomy with

excision of involved strcutures. (BOOK); Resection should be along a tumor free margin, and this may be not be possible with large masses; for this reason, adjuvant radiotherapy is associated with better outcomes {{37 Mendenhall, William M 2005;}}. Resection of the facial nerve should ideally be reconstructed in the same operation using a nerve graft to aid in its functional recovery {{38 Kimata, Yoshihiro 2005;}}. The use of intraoperative facial nerve monitoring may be of good aid, but data is inconclusive as to its effectiveness in reducing postoperative facial nerve dysfunction. {{39 Meier, Jason D 2006;}} Complications: Temporary facial nerve paralysis could be expected in up to 46% of patients with less than 4% progressing to permenant dysfunction {{40 Mehle, Mark E 1993;}}. Another possible complication occurring in upto 10% of patients is Gustatory sweating. This is characterized by sweating and flushing of the facial skin overlying the parotid gland during mastication and is thought to be due to regeneration of parasympathetic fibers resulting in abnormaloinnervation of sweat glands and subcutaneous vessels {{41 de Bree, Remco 2007;}}; a long-lasting, effective treatment is the use of botulism toxin injection. Radiotherapy Isolated radiotherapy is the treatment of choice for lymphoma and is reserved for medically inoperable or unresectable tumors; the extent of invasion or location of the tumor may be such that surgical resection would result in significant functional or cosmetic dysfunction. This may cure up to 20% of patients with advanced disease {{37 Mendenhall, William M 2005;}}. Adjuvant radiation therapy Surgery in combination with radiotherapy is indicated in tumors with high risk features such as tumors with a large diameter (>4cm), high-grade or advanced stage, skin or neural infiltration, a positive surgical margin, deep lobe rumors, recurrent following resection and lymph node metastasis. Thus, radiotherapy is indicated in all malignancies excluding small low-grade malignancies with no evidence of local invasion or metastasis. {{37 Mendenhall, William M 2005;}}
Consequently, adjuvant RT is suggested after surgical resection for patients who have T2 or greater high-grade tumors, locally advanced T3 and T4 tumors or positive regional lymph nodes, positive resection margins in most high-grade and some low-grade tumors (instead of re-exploration), perineural, vascular, or lymphatic invasion, and extracapsular spread.

Prognosis. Various methods can be utilized to predict the prognosis of parotid tumours. These are discussed below: 1) Staging of parotid tumours can aid in predicting average survival times. The five year survival rates for stages 1-4 are 85%, 66%, 53%, and 32% in their respective orders.

2) Histological subtyping has correlation with the biological behavior and thus prognosis of parotid tumours. Low grade tumours (acinic cell carcinoma and low-grade mucoepidermoid carcinomas) correlate with an 80-90% 5 year survival. On the other hand, high grade tumours, (including high grade mucoepidermoid carcinoma, adenocarcinoma and carcinoma ex-plemorphic adenoma) the 5 year survival is 20-50%. http://www.cancerresearchuk.org/cancer-help/type/salivary-glandcancer/treatment/statistics-outlook-salivary-gland-cancer#stage 1) Clinical features of aggression, including rapid size change, metastisis and infiltratio of the tumor can determine its biological nature and is, in fact, the most important prognostic factor in determing treatment. (RED BOOK). A significant clinical prognostic indicator in malignancy is pain; studies report a 5 year survival rate of 35% in patients with carcinomas reporting pain versus 68 % of patient with carcinomas not reporting pain (MEDSCAPE SALIVARY GLANDS) . Moreover, facial nerve dysfunction can also be regarded as an independent risk factor for predicting survival rates {{24 Terhaard, Chris HJ 2004;}}.Carcinomas associated with normal nerve function had 69% 5 year survival compared with 37% in partial facial nerve dysfunction and 13 % with complete dysfunction. {{24 Terhaard, Chris HJ 2004;}}.. The role clinical features in determining the prognostic outcome can be appreciated in the prognostic index developed by the Dutch Head and Neck Cooperative Group for patients

with parotid cancer. This index uses a weighted combination of parameters including age, pain, skin invasion, facial nerve involvement, perinueral growth and involved surgical margin to quantify prognosis and aid in clinical management. {{25 Vander Poorten, Vincent LM 2003;}}

Conclusion:
Neoplasms of the parotid gland are relatively uncommon but account for approximately 85% of all salivary gland tumors and 6% of head and neck tumors. They are heterogenous in nature and vary in their anatomy , histology and biologic behavior. Patients presenting with a parotid mass will require a full workup consisting of a thorough history, examination and investigations to arrive at a definitive diagnosis. Staging and treatment options are based upon the clinical features of tumor and its histological subype. Although studies over the years have advanced our understanding of the diverse group of tumors, most evidence is based on reviews of clinical experience, hence the diagnosis and treatment remains challenging for the surgeon. Comprehensive randomized trials will help guide management with emphasis on providing the best quality of care and outcome for patients. uncommon, heterogeneous group of neoplasms that vary considerably in their anatomic site of origin, histology, and biologic behavior
NTRODUCTION Salivary gland tumors include a wide range of tumor types, which can be either benign or malignant (table 1). Approximately 85 percent arise in the parotid; the remainder originate in the submandibular,

sublingual, and minor salivary glands, which are located throughout the submucosa of the mouth and upper aerodigestive tract (figure 1) [1]. Approximately 25 percent of parotid tumors are malignant, compared with 40 to 45 percent of submandibular gland tumors, 70 to 90 percent of sublingual gland tumors, and 50 to 75 percent of minor salivary gland tumors. Treatment is based upon retrospective reviews of clinical experience, and there are almost no data from randomized trials to guide treatment decisions. The published literature predominately focuses on the parotid gland, reflecting the relative frequency of parotid gland tumors compared to tumors at other sites. The treatment of locoregional disease, which includes stages I through IVB, will be discussed here (table 2).

Neoplasms that arise in the salivary glands are relatively rare, yet they represent a wide variety of both benign and malignant histologic subtypes as seen in the image below. Although researchers have learned much from the study of this diverse group of tumors over the years, the diagnosis and treatment of salivary gland neoplasms remain complex and challenging problems for the head and neck surgeon. Some common salivary gland neoplasms are listed in the image below. Benign tumours of the parotid account for 80% of parotid gland tumour {{13 Speight, PM 2002;}}. The 2005 WHO classification of salivary gland tumours has

TABLE 1 The American Joint Committee on Cancer (AJCC) staging by TNM classification. Adapted from a) PRIMARY TUMOUR (T):

http://www.cancer.gov/cancertopics/pdq/treatment/salivarygland/HealthProfessional/page3 on 26-6-2013.

b) Regional Lymph Nodes (N)

c) Distant Metastasis (M)

d) Anatomic Staging/Prognostic groups.

Prognosis. Various methods can be utilized to predict the prognosis of parotid tumours. These are discussed below:

1) Staging of parotid tumours can aid in predicting average survival times. The five year survival rates for stages 1-4 are 85%, 66%, 53%, and 32% in their respective orders. 2) Histological subtyping has correlation with the biological behavior and thus prognosis of parotid tumours. Low grade tumours (acinic cell carcinoma and low-grade mucoepidermoid carcinomas) correlate with an 80-90% 5 year survival. On the other hand, high grade tumours, (including high grade mucoepidermoid carcinoma, adenocarcinoma and carcinoma ex-plemorphic adenoma) the 5 year survival is 20-50%. http://www.cancerresearchuk.org/cancer-help/type/salivary-glandcancer/treatment/statistics-outlook-salivary-gland-cancer#stage 2) Clinical features of aggression, including rapid size change, metastisis and infiltratio of the tumor can determine its biological nature and is, in fact, the most important prognostic factor in determing treatment. (RED BOOK). A significant clinical prognostic indicator in malignancy is pain; studies report a 5 year survival rate of 35% in patients with carcinomas reporting pain versus 68 % of patient with carcinomas not reporting pain (MEDSCAPE SALIVARY GLANDS) . Moreover, facial nerve dysfunction can also be regarded as an independent risk factor for predicting survival rates {{24 Terhaard, Chris HJ 2004;}}.Carcinomas associated with normal nerve function had 69% 5 year survival compared with 37% in partial facial nerve dysfunction and 13 % with complete dysfunction. {{24 Terhaard, Chris HJ 2004;}}.. The role clinical features in determining the prognostic outcome can be appreciated in the prognostic index developed by the Dutch Head and Neck Cooperative Group for patients

with parotid cancer. This index uses a weighted combination of parameters including age, pain, skin invasion, facial nerve involvement, perinueral growth and involved surgical margin to quantify prognosis and aid in clinical management. {{25 Vander Poorten, Vincent LM 2003;}}

Initial history taking should focus on the presentation of the mass, growth rate, changes in size or symptoms with meals, facial weakness or asymmetry, and associated pain. A thorough general history provides insight into possible inflammatory, infectious, or autoimmune etiologies.

Approach to parotid mass in clinical practice.

Masses of the parotid gland can be attributed to a variety of pathological or physiological causes. Approximately 75% of parotid masses are considered neoplastic , with the remaining 25% of parotid masses falling under the non-neoplastic category which includes cystic, obstructive and inflammatory causes. (Medscape) -History - Examination - Imaging and diagnostic tests. Treatment. Quality of life. The sensitivity, specificity, positive predictive value, negative predictive value and accuracy of ultrasound for the diagnosis of parotid gland masses were 38.9%, 90.1%, 29.2%, 93.3% and 85.2%, respectively, and accuracy for malignant masses was 20%. The sonographic characteristics of parotid masses between benign and malignant lesions had no significant differences. {{1 Wu, S 2012;}} Check ref id 4 for imaging.

Adapted from: www.uptodate.com ; Salivary gland tumors: Epidemiology, diagnosis, evaluation,


and staging on 26-6-2013

Tumours of the Salivary Glands. In: Pathology and Genetics of Head and Neck Tumours, Barnes L, Eveson JW, Reichart P, Sidransky D. (Eds), World Health Organization, Lyon 2005. p.215