2.53. Axial contrast‐enhanced fat saturated T1 MRI demonstrating heterogenous enhancement consistent with abscess of the left accessory parotid gland.
Figure 2.54. Reformatted coronal CT demonstrating enlargement and enhancement of the submandibular glands consistent with viral sialadenitis.
HIV‐ASSOCIATED LYMPHOEPITHELIAL LESIONS
These lesions are comprised of mixed cystic and solid masses within the parotid (much less in the SMG and SLG). CT shows multiple cystic and solid masses with associated parotid enlargement. IV contrast shows mild peripheral enhancement in the cysts and more heterogenous enhancement in the solid lesions (Figure 2.55). MRI images of the cysts are typical with low signal on T1 and high on T2. The more solid lesions are of heterogenous soft‐tissue signal on T1 and increase on T2. Contrast MRI images follow the same pattern as CT (Holliday 1998). The US images show heterogenous cystic lesions with internal architecture of septation and vascularity and slightly hypoechoic signal of the solid masses. Mural nodules may be seen in predominantly cystic lesion. Associated cervical lymphadenopathy is commonly seen as well as hypertrophy of tonsillar tissues. Differential diagnosis of these findings includes Sjögren syndrome, lymphoma, sarcoidosis, other granulomatous diseases, metastases, and Warthin tumor (Kirshenbaum et al. 1991; Som et al. 1995; Martinoli et al. 1995; Shah 2002; Madani and Beale 2006a).
Figure 2.55. Axial CT demonstrating a large cystic lesion in the right parotid gland and multiple small lesions in the left parotid diagnosed as lymphoepithelial cysts.
MUCOUS ESCAPE PHENOMENA
The mucous escape phenomenon most commonly results from obstruction in the sublingual gland, resulting in a backup of salivary secretions (see Chapter 4). Ductal obstruction may be caused by calculi, stricture from prior infection or trauma. The chronic dilatation of the duct and accumulation of fluid produces a cystic mass by CT, MRI, and US. The simple ranula remains in the sublingual space and typically presents with a unilocular, well‐demarcated and homogenous structure unless complicated by hemorrhage or infection. The walls may enhance slightly if a ranula remains contained above the mylohyoid muscle. It may rupture into the surrounding tissues and extravasate along a path of least resistance and extend inferiorly into the submandibular space or posteriorly into the parapharyngeal space under which circumstances it is termed a plunging ranula (see Chapter 4). The non‐plunging ranula has a dilated ovoid configuration on axial images, but when it herniates into the submandibular space the dilated space shrinks into a tail‐like configuration in the sublingual space. The tail sign is pathognomonic for ranulae and may be seen in both simple and plunging types. The ranula can usually be differentiated from a hemangioma and lymphangioma by its lack of internal architecture (unless complicated). The ranulas are typically homogenous internally with well‐defined margins, unless infected or hemorrhagic, follow fluid density on CT (isodense to simple fluid) and intensity on MRI (low on T1 and high on T2). Both simple and plunging ranulae have these characteristics. The plunging component may be in the parapharyngeal space if the lesion plunges posterior to the mylohyoid muscle or in the anterior submandibular space if it plunges through the anterior and posterior portions of the mylohyoid muscle or through a defect in the muscle. Involvement of the parapharyngeal space and the submandibular space results in a large cystic mass termed “giant ranula” and may mimic a cystic hygroma (Cholankeril and Scioscia 1993; Kurabayashi et al. 2000; Macdonald et al. 2003; Makariou et al. 2003).
SIALADENOSIS (SIALOSIS)
Sialadenosis, also known as sialosis, is a painless bilateral enlargement of the parotid glands and less commonly the submandibular and sublingual glands (see Chapter 6). It is typically bilateral and without inflammatory changes. No underlying mass is present. It has been associated with malnutrition, alcoholism, medications, and a variety of endocrine abnormalities, the most common of which is diabetes mellitus. In the early stages, there is gland enlargement but may progress to fatty replacement and reduction in size by late stages. By CT, there is slight increase in density of the entire gland in the early setting but the density decreases in the late stage when the gland is predominantly fatty. On T1 weighted MRI images in the early stage, the gland demonstrates a slight decrease in signal corresponding to the lower fat content and increased cellular component. T2 images show a slight increase in signal (Som and Curtin 1996; Bialek et al. 2006; Madani and Beale 2006a).
SIALOLITHIASIS
Approximately 80–90% of salivary calculi form in the submandibular gland due to the chemistry of the secretions as well as the orientation and size of the duct in the floor of mouth. Eighty percent of submandibular calculi are radio‐opaque while approximately 40% of parotid sialoliths are radio‐opaque (see Chapter 5). CT without contrast is the imaging modality of choice as it easily depicts the dense calculi (Figures 2.56 through 2.58 ). MRI is less sensitive and may miss calculi. Vascular flow voids can be false positives on MRI. MR sialography as previously discussed may become more important in the assessment of calculi not readily visible by CT or for evaluation of strictures and is more important as part of therapeutic maneuvers. US can demonstrate stones over two millimeters with distal shadowing (Shah 2002; Bialek et al. 2006; Madani and Beale 2006a).
SJÖGREN SYNDROME
This autoimmune disease affects the salivary glands and lacrimal glands and is designated primary Sjogren if no systemic connective tissue disease is present but designated secondary Sjogren if the salivary disease is associated with systemic connective tissue disease (Madani and Beale 2006a). The presentations vary radiographically according to stage. Typically, early in the disease the gland may appear normal on CT and MRI. Early during the disease, there may be premature fat deposition, which may be demonstrated radiographically and may be correlated with abnormal salivary flow (Izumi et al. 1997). Also, in the early course of disease, tiny cysts may form consistent with dilated acinar ducts and either enlarge or coalesce as the disease progresses. These can give a mixed density appearance of the gland with focal areas of increased and decreased density by CT and areas of increased and decreased signal on T1 and T2 MRI, giving a “salt and pepper” appearance (Takashima et al. 1991, 1992). There may be either diffuse glandular swelling from the inflammatory reaction or this may present as a focal area of swelling. The diffuse swelling may mimic viral or bacterial sialadenitis. The focal swelling may mimic a tumor, benign or malignant, including lymphoma. Pseudotumors may be cystic lesions from coalescence or formation of cysts or dilatation of ducts, or they may be solid from lymphocytic infiltrates (Takashima et al. 1991, 1992). As glandular enlargement and cellular infiltration replaces the fatty elements, the gland appears denser on CT and lower in signal on T1 and T2 MRI. But when chronic inflammatory changes have progressed, tiny or course calcifications may develop. The cysts are variable in size, and the larger cysts may represent confluent small cysts or abscesses.