Sialolithiasis

• Hyperechoic focus with acoustic shadowing on ultrasound, or low-signal void outlined by high-signal fluid on T2-weighted MRI
• Duct dilatation proximal to the obstructing stone with gland enlargement in acute cases
• Submandibular location (80-90% of cases) rather than parotid
• Radiopaque density on plain radiographs (visible in 80-90% of submandibular stones)

• On ultrasound: stone appears as strongly hyperechoic focus or line with distal acoustic shadowing; small stones (<2 mm) may not shadow; radiolucent stones are still visualized.
• On plain radiography: 80-90% of submandibular stones are radiopaque and visible; only 60% of parotid duct stones are radiopaque due to different secretion composition; oblique views help project stones away from overlying bone and teeth.
• On sialography: stone presents as a filling defect within the duct; contrast flow may be completely arrested distal to the obstruction, delineating exact size and location.
• On CT: stones are well-visualized both in duct and parenchyma; acute obstructive cases show gland enlargement, hyperdensity, stranding, and enhancement; chronic cases show fatty atrophy with reduced parenchymal volume.
• On MRI: stones appear as low-signal void on all sequences, outlined by high-signal saliva on T2-weighted images; acute obstruction shows gland enlargement with reduced T1 signal and increased T2 signal (best on fat-suppressed sequences).
• On MRI: chronic obstruction shows reduced gland size with fatty atrophy (increased T1 signal, reduced T2 signal); MRI can distinguish acute from chronic obstruction and identify incomplete obstruction.
• Submandibular location predominates (80-90% of sialoliths) due to increased viscosity of submandibular secretions compared to parotid gland.
• In chronic cases, gland undergoes irreversible fatty atrophy and becomes asymptomatic unless secondarily infected.

• Hemangioma or phlebolith: appear as calcific foci on plain radiography and CT but lack the characteristic ductal location and clinical presentation of recurrent gland swelling with eating.
• Atherosclerotic calcification: calcification is typically in vascular structures and soft tissues, not confined to salivary duct with associated filling defect and obstruction pattern.
• Air bubble on sialography: appears as filling defect but is immediately recognizable as distinct lucency without stone density and is not persistent.
• Tumor within duct: presents as filling defect on sialography but lacks the characteristic stone density on CT/plain radiographs and typically has soft-tissue signal on MRI.
• Blood clot: filling defect on sialography but occurs in acute post-procedural or traumatic setting; lacks density of calcified stone on CT and has blood signal characteristics on MRI.

Report the exact location of the stone (intra-ductal vs. intra-parenchymal), specify whether obstruction is complete or partial based on distal duct dilatation, assess for signs of acute inflammation or chronic fatty atrophy, and note the side of involvement for surgical planning; use modality-specific terminology (e.g., "hyperechoic focus with acoustic shadowing" for ultrasound, "low-signal void outlined by high T2 signal saliva" for MRI).

• Sialography is contraindicated in acute infection due to risk of exacerbating infection spread; ultrasound or non-contrast imaging should be preferred in clinically suspicious acute cases.
• Small stones (<2 mm) may not produce acoustic shadowing on ultrasound and can be missed; the absence of shadowing does not exclude sialolithiasis.
• Very small stones may not be evident on CT due to lower spatial resolution compared to plain radiography; multimodal imaging may be necessary.
• In chronic non-obstructive sialoliths, the gland may appear completely normal on all imaging sequences, potentially delaying diagnosis; clinical correlation is essential.