Liver cirrhosis

Clinical History

Episode of acute abdominal pain, jaundice, tachycardia in the patient who has suffered from viral hepatitis B five years ago and has the history of alcohol abuse.

Imaging Findings

Patient was referred to our Medical Centre to undergo CT and MRI studies of abdomen. Recent complaints about abominal pain, jaundice, tachycardia. Five years ago he had viral hepatitis B. History of alcohol abuse. The patient has been considered as Child’s class B according to clinical and laboratory findings. Computed tomography was performed in a single-slice mode, 10/10mm, without contrast enhancement. MRI was performed with 1 Tesla MR imager. The following pulse sequences were used: SE, FLASH and TSE T1- and T2-weighted sequences, 2D FLASH MR phlebography (8mm slices, without contrast enhancement).

Discussion

Cirrhosis is the destruction of normal liver tissue which is replaced with nonfunctioning scar tissue surrounding areas of functioning liver tissue and nodules of pathologic regeneration. The scar tissue and regenerative nodules compress portal tracts and cause portal hypertension with dilatation of varicose veins at the lower part of the esophagus, enlargement of the spleen and fluid accumulation in the abdomen (ascites). Spectrum of imaging findings of the cirrotic liver includes: 1. Changes of the liver’s margin; 2. Liver atrophy and hypertrophy; 3. Diffuse heterogeneity. The process of cirrhosis distorts the hepatic parenchyma. Although present in all patients with end-stage cirrhosis, this distortion has a variable effect on the configuration of the liver’s margin which may be smooth, nodular (fine to coarse “cobble stone” margin with nodules < 3 cm), or grossly lobular (deformed by more than one nodule > 3 cm). Margins that are smooth or deformed by multiple small nodules are typical for micronodular cirrhosis, whereas a coarse nodularity of the margin is the result of macronodular cirrhosis. However, lobular livers are usually the resullt of marked subsegmental atrophy and hypertrophy rather than of large regenerative nodules (1). Approximately 25% of end-stage cirrhotic livers are normal in size and configuration; 36% are diffusely atrophic. Most of the remaining end-stage cirrhotic livers exhibit a combination of segmental atrophy and hypertrophy (1). Main cause of heterogeneity of the liver in CT and MR images is diffuse fibrosis. In our case the liver’s margin is nodular with nodules < 3 cm that are typical for macronodular cirrhosis, the liver’s size is normal. Diffuse fibrosis is clearly depicted in unenhanced CT and T1-weighted MR images as patchy, poorly defined region of low attenuation. In T2-weighted MR images fibrosis looks like some regions of high signal intensity of similar configuration as seen in unenhanced CT. Enlarged abdominal lymph nodes can be detected with CT in approximately 50% of patients. They are more common in the portacaval space and porta hepatis (2). Liver cirrhosis is the prime risk factor for hepatocarcinogenesis. Kubicka et al. showed that among patients with hepatocellular carcinoma 74.6% had liver cirrhosis (3). Moreover, Rodriguez et al. showed that the risk of hepatocellular carcinoma increased to 17% after 5 years of follow-up in patients with Child stage A or B cirrhosis (4).

Differential Diagnosis List

Final Diagnosis

Macronodular liver chirrosis

URL:	https://www.eurorad.org/case/835
DOI:	10.1594/EURORAD/CASE.835
ISSN:	1563-4086