13.2 Diffuse Liver Disease

Diffuse liver diseases alter the entire parenchyma rather than forming discrete masses, so the exam tests pattern recognition against the normal mid-level, homogeneous baseline.

Fatty Infiltration (Hepatic Steatosis)

Hepatic steatosis is the most common diffuse liver abnormality, seen with obesity, diabetes, alcohol use, and hyperlipidemia. Sonographic features:

• Diffuse increase in echogenicity — the liver appears abnormally bright compared with the right renal cortex (hepatorenal contrast).
• Increased attenuation — the sound beam is absorbed, so the deep liver and the diaphragm become hard to visualize; you may need to lower the frequency.
• Poorly visualized vessel walls as parenchymal echogenicity approaches that of the portal triads.

Focal fatty sparing is the classic mimic: a hypoechoic, geographic region of normal tissue surrounded by bright fatty liver, typically adjacent to the gallbladder fossa and the porta hepatis (segment IV). Unlike a true mass, it has geographic rather than rounded margins, causes no contour bulge, and vessels course through it undisturbed. The reverse pattern, focal fatty infiltration, is a hyperechoic patch in the same typical locations.

Hepatitis

Acute hepatitis often looks sonographically normal. When abnormal, the parenchyma becomes hypoechoic from edema while the portal triad walls remain bright — the 'starry sky' liver. The gallbladder wall may be thickened. Chronic hepatitis produces a coarsened, increasingly echogenic texture that overlaps with early cirrhosis. Laboratory correlation is essential: acute hepatitis elevates alanine aminotransferase (ALT) and aspartate aminotransferase (AST) disproportionately, often with hyperbilirubinemia.

Practical Points on Steatosis and Hepatitis

Steatosis can be loosely graded: mild disease brightens the liver slightly with the diaphragm and vessels still seen; moderate disease blurs vessel walls and the deep diaphragm; severe disease renders the posterior liver nearly invisible at standard settings. Because fatty change is reversible, the finding is reported with the clinical context (obesity, diabetes, alcohol, steroids, chemotherapy). Viral hepatitis is caused most often by hepatitis A (fecal-oral, self-limited), hepatitis B, and hepatitis C (both blood-borne; both can become chronic and progress through fibrosis to cirrhosis and hepatocellular carcinoma — alcohol-associated liver disease is now the leading indication for liver transplantation in the United States, having overtaken hepatitis C after direct-acting antivirals came into use). Remember that ultrasound's role in acute hepatitis is largely to exclude biliary obstruction as the cause of jaundice, because the parenchyma may look entirely normal.

Cirrhosis

Cirrhosis is end-stage fibrosis with regenerative nodules, most often from chronic viral hepatitis or alcohol. Sonographic signs:

• Coarse, heterogeneous echotexture and increased attenuation.
• Surface nodularity, best appreciated along the liver edge when ascites provides an acoustic window, or with a high-frequency linear transducer.
• Lobar redistribution: right lobe atrophy with hypertrophy of the caudate and left lobes. A caudate-to-right-lobe width ratio greater than 0.65 is a classic indicator of cirrhosis.

Signs of Portal Hypertension

• Portal vein diameter exceeding about 13 mm, with loss of normal respiratory variation.
• Splenomegaly (spleen longer than roughly 12-13 cm) and ascites.
• Portosystemic collaterals, including a recanalized paraumbilical vein within the ligamentum teres and coronary (left gastric) varices.
• Advanced disease: slowed portal venous velocity, bidirectional flow, or frankly hepatofugal flow (away from the liver).

Doppler in Cirrhosis

The normal hepatic vein waveform is triphasic, reflecting cardiac cycle pressure changes transmitted from the right atrium. In cirrhosis the stiff, fibrotic parenchyma buffers these pulsations, so the tracing becomes dampened or monophasic — an early, sensitive clue. Portal venous flow normally is continuous, mildly undulating, and hepatopetal (toward the liver) at roughly 15-30 cm/s; velocity falls as portal hypertension worsens.

Storage and Deposition Disorders

• Glycogen storage disease (von Gierke, type I): marked hepatomegaly with diffusely increased echogenicity resembling fatty liver; patients have an increased incidence of hepatic adenomas.
• Hemochromatosis: iron deposition produces increased echogenicity and can progress to cirrhosis with an elevated hepatocellular carcinoma risk; serum ferritin and transferrin saturation are elevated.

Putting the Differential Together

A few extra patterns round out this section. Regenerative nodules in cirrhosis are usually isoechoic and invisible; dysplastic nodules are premalignant and warrant shorter-interval surveillance. Wilson disease (copper deposition) and alpha-1 antitrypsin deficiency are less common metabolic causes of a cirrhotic-looking liver in younger patients. When the liver is enlarged and hyperechoic with normal labs, think fatty infiltration or glycogen storage disease; when it is shrunken, coarse, and nodular with splenomegaly and ascites, think cirrhosis with portal hypertension. Ultrasound is also the first-line tool for grading the complications: it detects ascites, measures spleen size, maps collateral vessels, and screens the parenchyma for the development of hepatocellular carcinoma, which is why cirrhotic patients enter surveillance programs rather than one-time imaging.