The authors present imaging anatomy of the parotid space and discuss non-neoplastic lesions, autoimmune disorders, cysts, neoplastic lesions, epithelial tumors, and nonepithelial lesions. They describe the diseases and their appearance on imaging, describing how the differential diagnoses appear, along with presenting examples of the images, primarily computed tomography and magnetic resonance imaging.
Key Points
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Most of the pathologies related to parotid space arise from the parotid gland, which may be involved by various neoplastic or non-neoplastic pathologies.
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Cross-sectional examinations are very helpful in localizing the mass, characterizing the parotid tumor, differentiating neoplastic from non-neoplastic lesions, and evaluating the contralateral gland for nonpalpablemass.
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Ultrasonography can be helpful in differentiating cystic lesions from solid lesions, localizing intraglandular from extraglandular masses and providing image guidance for fine needle aspiration biopsy.
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From the surgeon’s point of view, the most vital information received from imaging is the evaluation of the extent of the mass as well as invasion of adjacent facial nerve.
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To improve diagnostic accuracy, dynamic contrast-enhanced computed tomography/magnetic resonance imaging (MRI), diffusion weighted MRI, positron emission tomography, proton magnetic resonance spectroscopy imaging, and Tc-99 m pertechnetate scintigraphy may be used.
| 1H-MRS | Proton magnetic resonance spectroscopy imaging |
| ACC | Acinic cell carcinoma |
| AdCC | Adenoid cystic carcinoma |
| BCC | Branchial cleft cyst |
| BLEL | Benign lymphoepithelial lesion |
| MALT | Mucosa-associated lymphoid tissue |
| MALTOMA | MALT-type lymphoma |
| MEC | Mucoepidermoid carcinoma |
| PA | Pleomorphic adenoma |
| PNI | Perineural invasion |
| SCC | Squamous cell carcinoma |
| SS | Sjögren syndrome |
| WT | Warthin tumor |
Introduction
The parotid space extends from the external auditory canal and mastoid tip superiorly to the angle of mandible inferiorly and is confined within the superficial layers of the deep cervical facia. In addition to the parotid gland, this space also contains intraparotid and extraparotid lymph nodes, the retromandibular vein, the external carotid artery, and extracranial branches of facial nerve. The late encapsulation of the gland and close intimacy of the developing lymphatic system explain the presence of intraparotid lymph nodes and epithelial salivary gland inclusions within periparotid and intraparotid lymph nodes.
Most of the pathologies related to parotid space arise from the parotid gland, which may be involved by various neoplastic or non-neoplastic pathologies. Physical examination of these pathologies is often nonspecific, and therefore imaging plays a vital role in the evaluation of parotid space pathologies. Cross-sectional examinations such as computed tomography (CT) and magnetic resonance imaging (MRI) are very helpful in differentiating neoplastic from non-neoplastic lesions, localizing the mass (intraglandular vs extraglandular), evaluating the contralateral gland for nonpalpable mass, and characterizing the parotid tumor. From the surgeon’s point of view, the most important information these modalities provide is the evaluation of the extent of the mass, such as superficial or deep lobe involvement, as well as invasion of adjacent facial nerve. Another imaging modality commonly used in evaluation of parotid pathologies is ultrasonography (US). US is noninvasive and cost-effective and can be helpful in differentiating cystic lesions from solid lesions, localizing intraglandular from extra-glandular masses, and providing image guidance for fine needle aspiration biopsy. Limitations of US include operator dependence and poor evaluation of the deep parotid lobe, parapharyngeal region, and pedunculated parotid tumors.
The conventional imaging characteristics of parotid tumors are nonspecific. Margins, bilateral occurrence or multiplicity, signal intensity or density, intratumoral calcifications, and internal hemorrhage do not definitively distinguish malignant tumors from benign tumors. To improve diagnostic accuracy, alternative methods, such as dynamic contrast-enhanced CT/MRI, diffusion weighted MRI (DWMRI), positron emission tomography (PET), proton magnetic resonance spectroscopy imaging (1H-MRS), and Tc-99 m pertechnetate scintigraphy are used.
Non-neoplastic parotid lesions
Inflammatory and non-neoplastic conditions of the parotid gland far outnumber the neoplastic lesions ( Algorithm 1 ). Etiologies include developmental anomalies, sialoadenitis, sialolithiasis, autoimmune, cystic lesions (developmental or acquired) and sialoadenosis.
Developmental Anomalies
Developmental disorders of the parotid gland are rare. Anomalies like aplasia, atresia, or agenesis may be either unilateral or bilateral and are mostly associated with other facial anomalies. Clinically, they present with xerostomia, sialoadenitis, and dental caries. Parotid gland agenesis has been reported with hemifacial microstomia, mandibulofacial dysostosis, cleft palate, and anophthalmia. CT or MRI will show absence of normal gland. Glandular absence needs to be confirmed with the clinicians and/or patient for any prior surgery of parotidectomy. In cases of unilateral agenesis of the parotid gland, the existing unilateral gland may be palpated as a mass and referred for imaging. Ectopic gland tissue may be seen in soft tissues or the skin of the anterior neck. This finding is most commonly seen along the anterior border of the sternocleidomastoid muscle. Other rare sites include the middle ear, posterior triangle of the neck, mandible, and maxilla. Non-neoplastic ectopic (choristomatous) masses can be treated with simple excision, while neoplastic lesions should be treated as per their histology.
Sialadenitis
Infection of the salivary gland is called silitis. Primary infection of the gland is termed sialadenitis, while infection of the ducts is known as sialoditis. Infectious sialadenitis may be caused by a variety of microbial agents such as bacteria, viruses, mycobacteria, fungi, parasites, and protozoa. Acute parotitis is most commonly due to bacterial or viral infections.
Most of the bacterial infections are retrograde via the oral cavity. One of the most common precipitating factors is decrease in the salivary flow. Ascending infections are common in the parotid gland because of the wider orifice of the Stensen duct and serous secretions of the parotid gland, which lack antibacterial elements such as lysosomes and immunoglobulin (Ig)A antibodies. Bacterial infections present with acute painful enlargement of gland. Purulent exudates may be seen at the orifice of Stensen duct. Sialadenitis in adults is associated in approximately 50% of cases with sialolithiasis. The most common offending agents are Staphylococcus aureus, Streptococcus viridans, Streptococcus pneumoniae, and Haemophilus influenza.
US reveals diffusely enlarged hypoechoic gland with duct dilatation. There may be enlarged intraglandular lymph nodes. CT scan is rarely indicated and if performed shows diffuse enlargement and enhancement of the gland ( Fig. 1 ). There may be dilatation of the central ducts with wall enhancement. A stone may be seen within the parotid gland duct with resultant either partial or complete blockage of flow of secretions. Hydration and antibiotic therapy are the treatments of choice. Delayed treatment may result in intraglandular abscess formation ( Fig. 2 ). These cases require surgical drainage with adequate antibiotic therapy.
Mumps, caused by paramyxovirus, is the most common viral infection affecting the salivary gland. The parotid gland is the salivary gland most commonly affected by mumps. Clinically, patients present with prodromal symptoms followed by an acute, painful swelling of the bilateral glands that may persist for 1 week or more. Unilateral involvement is seen in about 20% to 33.3% of the cases. Clinical presentation is sufficient for definitive diagnosis, and imaging findings are nonspecific. Imaging is therefore rarely obtained. Several other viruses including coxsackie virus, lymphocytic choriomeningitis virus, herpes virus, influenza A, parainfluenza, cytomegalovirus, and adenovirus have been associated with sialadenitis. Treatment is predominantly symptomatic.
Chronic sialadenitis of the parotid gland may be either due to obstructive or nonobstructive diseases. Imaging is most commonly performed to differentiate between these 2 etiologies. Chronic sialadenitis may be due to infection (eg, bacteria, mycobacteria, syphilis, toxoplasmosis, and actinomycosis) or noninfectious processes like sarcoidosis, prior irradiation, or autoimmune disease. Chronic inflammation results in shrinkage of the gland, which is inhomogeneous on US. Ductal ectasia may occasionally be seen. Sialadenitis is a common complication of radiotherapy, a common treatment modality for head and neck cancers as well as neck lymphoma. The serous acini of the glands are particularly sensitive to radiation injury, leading to atrophy with xerostomia.
Sarcoidosis, a noncaseating granulomatous infection, involves the parotid glands in 10% to 30% of the cases. Clinically it presents as nontender, nonpainful, chronic enlargement of the gland. On palpation, the gland is often multinodular and may mimic a malignancy. Parotid gland enlargement with sarcoid uveitis and facial nerve paralysis (Heerfordt syndrome ) should not be confused with a parotid gland malignancy. On CT or MRI, sarcoid may either present as a solitary parotid mass (indistinguishable from malignancy) or multiple, benign-appearing, noncavitating masses ( Fig. 3 ). There may be associated cervical lymphadenopathy and/or associated pulmonary and mediastinal findings.
Sialolithiasis
Sialolithiasis is more common in the submandibular gland/duct (80% and 90%) due to the increased viscosity of submandibular saliva and the upward curved path of the submandibular duct. The parotid gland is involved in 20% of cases. Stones are rarely encountered in the sublingual gland. Symptoms are mainly due to ductal obstruction, leading to episodic swelling and postprandial pain. CT is very sensitive in detection of parotid stones. Sialolithiasis may cause mechanical obstruction, resulting in acute or chronic sialoadenitis. They may lead to focal stricture or central dilatation (sialectasia) of the ducts.
Autoimmune
Sjögren syndrome
Sjögren’s syndrome (SS) is a systemic autoimmune disorder of the exocrine glands that occurs either as a solitary finding (primary SS) or as a conglomerate of connective tissue diseases (secondary SS ) . SS is characterized by periductal lymphocytic and plasma cell infiltration, leading to destruction of exocrine glands, which causes decreased secretions and dryness. When SS involves the parotid gland, the lymphoid infiltrate produces a localized parenchymal mass referred to as a benign lymphoepithelial lesion (BLEL) or Godwin tumor. SS is most commonly seen between 40 to 60 years of age, with a striking female predominance (90% to 95%). Clinically, SS presents with exocrinopathy involving the lacrimal and salivary glands, leading to keratoconjunctivitis sicca and xerostomia. There may be associated extrasalivary involvement with articular, neurologic, pulmonary, and hepatic manifestations. Although the gland is usually diffusely affected, in some patients a localized area may be more involved, clinically simulating a solitary mass. This finding needs to be further evaluated with biopsy to exclude lymphoma, especially since the risk of developing non-Hodgkin lymphoma in the setting of SS is estimated to be about 44 times greater than in the general population.
The primary site of disease in SS is the most peripheral intraglandular ducts and acini. Therefore in the early stages of SS, a sialogram may be more sensitive to early changes than cross-sectional imaging. During this early stage, the sialogram shows a normal central ductal system and numerous peripheral punctate collections of contrast throughout the gland. On CT and MRI, the gland appears normal in early stages. As the disease progresses to acinar destruction, sialogram may show dilatation of the central ducts and changes of sialoadenitis. In the later stages, CT demonstrates glandular enlargement with diffuse high attenuation value. As the stages progress, a honeycomb glandular appearance develops on CT, and MRI shows globular enlargement of the parotid ducts with speckled high T2-weighted collections reflecting saliva collections within the dilated ducts ( Fig. 4 ). In the advanced stages, the parotid gland shows low signal on T2 WI (weighted image) due to focal accumulation of lymphocytes and fibrous tissue.
Premature deposition of fat associated with SS is easily diagnosed on CT or MRI. Some authors have concluded that monitoring of fat deposition might be useful in diagnosing SS and assessing its progression. MRI sialogram (heavily T2-weighted, fast spin echo sequence with spectral fat suppression) has been shown to be useful in the diagnosis of SS, which shows punctate, globular, cavitary, or destructive appearance within the parotid glands.
Cystic lesions
Primary cystic disease of the parotid gland accounts for 2% to 5% of all the parotid lesions. These cystic lesions can be classified into: developmental (lymphoepithelial cyst, branchial cleft cyst, polycystic dysgenetic disease, epidermoid inclusion cyst, cystic hygroma and congenital sialectasis), or acquired cysts (eg, ductal sialocyst, acquired immunodeficiency syndrome [AIDS]-related parotid cysts, inflammatory cyst, or neoplastic lesions).
Developmental cyst
Lymphoepithelial Cyst
The probable origin of these lesions is from the intraparotid lymph nodal system. Cysts show predilection for men and present in adults (40–50 years) as painless masses. Most of these cysts are unilateral, and they may rarely present with facial nerve paralysis. The cysts are well circumscribed and predominantly unilocular, with contents ranging from fluid to mucoid to caseous appearance. On imaging they may be indistinguishable from cystic Warthin tumor (WT), low-grade mucoepidermoid carcinoma (MEC), and true branchial cleft cyst.
Branchial Cleft Cyst
Branchial cleft cyst (BCC) within the parotid glands is very rare. First, BCCs in the parotid space are classified into 1 subtypes (1 and 2). The most common subtype of first BCC is type 2, which is found in the preauricular region of the parotid gland with a fistulous tract extending up toward the membranous and cartilaginous external auditory canals ( Fig. 5 ). Type 1 first BCCs are intraparotid and rare. On CT or MRI, they are seen as single fluid-filled masses with thick enhancing walls. These cysts may get infected and clinically present as abscesses and may be difficult to differentiate both clinically and via imaging. Histologically, they are lined by squamous epithelium, ciliated columnar epithelium, or a mixture of both with admixture of skin appendages and cartilage.
Polycystic (dysgenetic) disease is a rare developmental abnormality of the salivary gland duct system that has histologic similarity to polycystic disease of the kidney. It is a benign process with female predominance. The entire glandular tissue is replaced by cysts, usually bilaterally. This condition needs to be differentiated from cystadenoma and cystadenocarcinoma, both of which are localized masses and, unlike polycystic disease, do not involve the entire gland.
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