Pathology
What to know
Focal liver lesions: hemangioma is well defined and hyperechoic with posterior enhancement and no internal Doppler flow; focal nodular hyperplasia is near-isoechoic with a central scar and spoke-wheel vascularity; hepatocellular carcinoma in a cirrhotic liver shows arterial hyperenhancement with portal-venous or late washout on contrast-enhanced ultrasound; metastases are often multiple and target-like.
Diffuse disease: cirrhosis produces a coarse nodular surface, caudate hypertrophy, right-lobe atrophy, and signs of portal hypertension; steatosis brightens the liver, degrades deep penetration, and blurs vessel walls.
Biliary disease: stones are mobile and shadow; sludge is low-level and does not shadow; polyps are fixed, do not shadow, and may have a vascular stalk; wall thickening above 3 mm is abnormal.
Pancreatitis shows an enlarged hypoechoic gland with peripancreatic fluid; pseudocysts are encapsulated fluid collections. Renal simple cysts are anechoic with thin walls and posterior enhancement; hydronephrosis shows dilated calyces communicating with the pelvis. Appendicitis is a blind-ending, non-compressible tubular structure over 6 mm.
Traps
Sludge versus tumor, hemangioma versus metastasis, and stone versus gas all hinge on shadowing and mobility. Shadowing alone does not prove a stone.
Rule of thumb
Simple cyst: anechoic, smooth thin wall, posterior enhancement, no internal flow.
Worked example
A 3 cm lesion in a cirrhotic liver that enhances arterially and washes out by 60 seconds is HCC until proven otherwise.