Changes in liver lobe volume
Cirrhosis causes profound remodeling of the organ's angioarchitecture. A classic sign is atrophy of the right hepatic lobe, which is often accompanied by compensatory hypertrophy of the left lobe.
Anatomical landmarks for evaluation on CT and MRI include:
- Falciform ligament — divides the left lobe into medial (IV) and lateral (II, III) segments.
- Gallbladder — separates the right and left lobes. Due to lobular shrinkage, its topography may change, and the gallbladder itself often appears contracted.
Isolated atrophy of the left lobe is also possible, defined relative to the main plane of the liver (principal plane).
Signs of fibrosis and cirrhosis
Early stages of fibrosis are subtle on CT and MRI. In advanced stages, the imaging pattern becomes specific:
- Contours: a nodular margin forms (nodular hepatic margin).
- Parenchyma: becomes heterogeneous due to a combination of regenerative areas (normal attenuation), fibrosis (decreased attenuation), and iron deposition (increased attenuation).
- MRI: confluent fibrosis (confluent hepatic fibrosis) yields high signal intensity on T2-WI (often near the falciform ligament). On contrast-enhanced CT, fibrotic areas show delayed contrast enhancement.
- Vascular changes: splenomegaly, recanalization of the paraumbilical vein. Angiography may reveal tortuosity of intrahepatic arteries — the "corkscrew vessels" sign (corkscrew vessels).
Liver nodules in cirrhosis
Nodular parenchymal remodeling (nodularity) is a key feature of cirrhosis. Several types of nodules are distinguished:
- Regenerative nodules (regenerative nodules):
- Isointense (similar to normal parenchyma) on T2-WI and T1-WI.
- Lack hypervascularity in the arterial phase.
- Can mimic hepatocellular carcinoma (HCC) if surrounded by contrast-enhancing fibrous tissue (creating a false "washout" effect).
- Atypical (dominant) regenerative nodules:
- Large, may appear as exophytic masses on ultrasound.
- On MRI, only the fibrous septa within them enhance with contrast, rather than the solid hepatocellular components.
Hepatocellular carcinoma (HCC) is a formidable complication of cirrhosis. It actively enhances in the arterial phase and demonstrates true washout (washout) in the equilibrium phase.
Metabolic disorders: hemochromatosis and Wilson's disease
Cirrhosis can develop in the setting of heavy metal accumulation:
- Hemochromatosis: excess iron accumulates in hepatocytes. On unenhanced CT, liver attenuation exceeds 75 HU. On MRI, iron decreases signal intensity on T2 and T2* (susceptibility effect). Pathognomonic triad: nodular liver with low MRI signal + iron deposition in the pancreas.
- Wilson's disease (Wilson Disease): copper accumulation. Causes generalized cirrhotic changes, but copper accumulation itself is difficult to detect on imaging due to concomitant steatosis.
Briefly: answers to topical questions
What classic changes in liver lobe volume are observed in cirrhosis?
Classic changes in liver lobe volume in cirrhosis include atrophy of certain segments and compensatory hypertrophy of others.
- Atrophy of the right lobe — most commonly affects the posterior segments (VI, VII).
- Hypertrophy of the left lobe — lateral segments (II, III) are frequently enlarged.
- Hypertrophy of the caudate lobe — characteristic of advanced cirrhosis.
In some cases, marked atrophy of the left hepatic lobe may also be visualized.
What vascular changes are characteristic of portal hypertension in cirrhosis?
Portal hypertension in cirrhosis is characterized by hemodynamic alterations and the formation of portosystemic collaterals.
- Portal vein changes — diameter greater than 15 mm, reduction in mean peak flow velocity to less than 10 cm/s, continuous or oscillating flow; flow reversal is possible in severe cases.
- Portosystemic collaterals — splenogastric, gastroesophageal, splenorenal, and recanalized paraumbilical veins.
- Vascular manifestations — dilation of mesenteric veins and varices, particularly esophageal varices; edema of the gallbladder, gastric, and small bowel walls may also be observed.
What types of nodules form in the liver parenchyma in cirrhosis?
Nodules reflecting processes of regeneration, substance deposition, and dysplasia form in the liver parenchyma in cirrhosis.
- Regenerative nodules (regenerative nodule) — have a signal intensity matching that of unaltered parenchyma.
- Atypical regenerative nodules (atypical regenerative nodules) — large dominant nodules, often isointense on T2-WI.
- Steatotic nodules — contain fat, yielding high signal on T1- and T2-WI.
- Siderotic nodules — contain iron, exhibiting low signal on all sequences.
- Dysplastic nodules — premalignant lesions with high signal on T2-WI.
Which complications of liver cirrhosis are identified on diagnostic imaging?
Diagnostic imaging of liver cirrhosis can identify:
- Portovenous hypertension with the formation of portosystemic collaterals.
- Ascites.
- Splenomegaly.
- Portal vein thrombosis, including tumor thrombosis.
- Hepatocellular carcinoma (HCC) as a complication of cirrhosis, the development of which is monitored using imaging methods.
Class and exam questions
Why can MRI falsely mimic cancer (HCC) in cirrhosis?
Regenerative nodules may be surrounded by fibrosis. In the equilibrium phase, fibrosis enhances with contrast while the nodule does not, mimicking the washout sign characteristic of a malignant tumor.
How to distinguish confluent fibrosis from other masses on MRI?
Confluent fibrosis is frequently localized near the falciform ligament, has a "geographic" shape, exhibits high signal on T2-WI, and demonstrates delayed contrast enhancement.
Which method is best suited for early diagnosis of fibrosis?
Conventional CT and MRI are insensitive to early fibrosis. The most accurate method for assessing liver stiffness is MR elastography (MR elastography).
What else to study on this topic
- Assessment of portal hypertension on CT and MRI
- Differential diagnosis of HCC and regenerative nodules
- Spontaneous rupture of hepatocellular carcinoma (hemoperitoneum)
- Multiple biliary hamartomas on ultrasound and MRI
- Diffuse steatosis: chemical shift on MRI
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