2004).
Other rare vascular lesions within salivary glands, most commonly the parotid gland, include aneurysms, pseudoaneurysms, and arteriovenous fistulae (AVFs). The aneurysms or pseudoaneurysms are most commonly associated with trauma or infection (mycotic). MRI in high flow lesions demonstrates “flow voids” or an absence of signal but slow flow lesions or turbulent flow can demonstrate heterogenous signal mimicking a mass. Contrast enhancement and MRA can help delineate vascular lesions from masses. CT without contrast however demonstrates a mass or masses isodense to skeletal muscle or normal blood vessels. With contrast, large vascular channels become more obvious, although smaller lesions may still mimic a mass. US (especially Doppler US) can reveal characteristic flow patterns of arterial waveforms in the venous channels for AVFs. US can also delineate aneurysms with their turbulent flow patterns. Angiography is typically reserved for endovascular treatment. CTA or MRA is useful for noninvasive assessment of arterial feeders and venous anatomy in AVFs and in defining aneurysms (Wong et al. 2004).
Figure 2.49. Direct coronal CT displayed in bone window demonstrating smooth erosion of the hard palate on the right lateral aspect, along with a dense calcification consistent with a phlebolith (arrow). A hemangioma is presumed based on this CT scan.
Figure 2.50. Coronal fat suppressed contrast‐enhanced T1 MRI image corresponding to the same level as Figure 2.49, demonstrating a sharply marginated homogenously enhancing mass (arrow).
Figure 2.51. Coronal fat saturated T2 MRI image demonstrating a well‐demarcated hyperintense mass with a focal signal void centrally. A hemangioma containing a phlebolith (arrow) was presumed based on this MRI.
ACUTE SIALADENITIS
Acute sialadenitis may be bacterial or viral in nature and may be a result of obstruction from a calculus, stricture or mass (see Chapters 3 and 5). Viral parotitis or mumps may be caused by a variety of viruses but most commonly the paromyxovirus is the culprit. The patient presents with an enlarged, tender, and painful gland. Acute suppurative parotitis (sialadenitis) presents in a similar manner as viral parotitis with the additional sign of purulent exudate. Oral bacterial pathogens are the causative agents, with staphylococcal and streptococcal species being the most common. CT scan demonstrates an enlarged gland with ill‐defined margins and infiltration of the surrounding fat by edema fluid. The gland, especially the parotid, is increased in density because of the edema fluid, which is of higher density than fat. CT contrast demonstrates heterogenous enhancement and may show an abscess. On T1 MRI scan, the overall gland signal may be decreased slightly from the edema but does enhance heterogeneously with contrast. T2 MRI scan shows increased signal secondary to edema. Both CT and MRI may demonstrate enhancement and enlargement of the parotid (or sublingual) duct. US shows slight decrease in echogenicity relative to normal. These patterns are not unique to bacterial or viral infection or inflammation and may be seen with autoimmune diseases such as Sjögren syndrome or a diffusely infiltrating mass. The surrounding subcutaneous fat also demonstrates heterogenous increased density from edema, resulting in a “dirty fat” appearance. There is also thickening of fascia and the platysma muscle (Shah 2002; Bialek et al. 2006; Madani and Beale 2006a).
Figure 2.52. Axial CT with contrast at the level of the masseter muscles demonstrating a left accessory parotid gland abscess.
With acute submandibular sialadenitis, the gland becomes enlarged and may be associated with a dilated duct if a sialolith is present. By CT, the calculus may be readily identified but not as easily seen by MRI. There may be varying degrees of cellulitis or frank abscess formation. The inflamed gland undergoes greater contrast enhancement. MRI demonstrates an enlarged heterogenous gland with dilated fluid‐filled duct and gland which on T2 images is of high signal. On ultrasound, the acutely inflamed gland demonstrates enlargement with focal hypoechoic foci (Shah 2002; Bialek et al. 2006; Madani and Beale 2006a), (Figures 2.52 through 2.54 ).
CHRONIC SIALADENITIS
The etiology of chronic inflammatory states of the salivary glands varies by the specific gland in question. Chronic inflammatory changes in the parotid gland tend to be related to autoimmune disease (Sjögren syndrome), recurrent suppurative parotitis, or radiation injury. Other etiologies include granulomatous infections such as tuberculosis or sarcoidosis. Chronic inflammation of the submandibular gland and, to a lesser degree, the sublingual gland is more commonly due to obstructive disease, particularly sialolithiasis. In the chronically inflamed state, the glands are enlarged but over longer periods of time progressively reduced in size, and heterogenous density may be seen on CT with extensive fibrosis and small focal (punctate) calcification. The density on CT is often increased due to cellular infiltration and edema during acute phases of exacerbation. The surrounding subcutaneous fat may not show signs of edema as is seen with acute sialadenitis. MRI demonstrates similar changes with heterogenous signal on both T1 and T2. The duct or ducts may be dilated, strictured, or both. Both may be visible by contrast CT and MRI (Sumi et al. 1999b; Shah 2002; Bialek et al. 2006; Madani and Beale 2006a). Chronic sclerosing sialadenitis (aka Kuttner tumor, or IgG4‐related disease [see Chapter 6]) can mimic a mass of the salivary (most commonly submandibular) glands (Huang et al. 2002). It presents with a firm, enlarged gland mimicking a tumor. The most common etiology is sialolithiasis (50–83%) but other etiologies include chronic inflammation from autoimmune disease (Sjögren syndrome), congenital ductal dilatation and stasis, disorders of secretion (Huang et al. 2002). It is best diagnosed by gland removal and pathologic examination as fine needle aspiration biopsy may be misleading (Huang et al. 2002). Chronic sialadenitis can also be caused by chronic radiation injury. US studies have demonstrated a difference in imaging characteristics between submandibular sialadenitis caused by acalculus versus calculus disease. The acalculus sialadenitis submandibular gland US demonstrates multiple hypoechoic lesions, mimicking cysts, with diffuse distribution throughout a heterogenous hypoechoic gland. They did not, however, demonstrate increased thru transmission, which is typically seen with cysts and some soft‐tissue tumors. Sialadenitis caused by calculus disease demonstrates hyperechoic glands relative to the adjacent digastric muscle, but some are iso‐ or hypoechoic relative to the contralateral gland (Ching et al. 2001).
Figure