Sex: male
Age: 54 years
History
Liver cirrhosis CHILD A (due to alcohol abuse). Remitting abdominal pain in the right upper quadrant.
Laboratory data
Bilirubine 2.43mg/dl, gamma-GT 142 U/l, Ammoniak 109 mcg/dl, Platelets 43/nl, CEA 5.5 ng/ml (normal 0 - 2.5 ng/ml). Normal values for Alpha-Fetoproteine, CA 19/9, PSA.
Physical findings
Palpable slightly enlarged liver. No weight loss, no fever.
Case text
Sonography showed a focal lesion in the VIII hepatic segment. The patient was referred to CT examination for further work-up of this lesion.
Image 1-2
Helical CT of the liver.
Image 1: Arterial phase 30s after intravenous contrast injection; 5/1.5/5 collimation/pitch/reconstruction increment.
Image 2: Portal venous phase 80s after intravenous contrast injection; 5/1.5/5 collimation/pitch/reconstruction increment.
Image 3-4
MRI of the liver with intravenous injection of contrast with delayed scan.
Image 3: Axial T1-weighted sequence (TR 15, TE 6.8, FLIP 25°) immediately after Teslascan.
Image 4: Axial T1-weighted sequence (TR 15, TE 6.8, FLIP 25°) 23h after Teslascan.
Image 1-2
1. Is there an abnormality present in this examination?
In the arterial phase, a sudiaphragmal 3 cm focal lesion with little enhancement could be seen. However, the contrast to the surrounding liver tissue is very low. In the portal venous phase no lesion could be detected.
2. What is your next diagnostic step?
MRI of the liver with a liver specific contrast media.
Image 3-4
3. Is there an abnormality present in this examination?
The focal lesion could clearly be depicted, the contrast/noise ratio (C/N) was better than in CT. After delayed scanning, the C/N was found to be further increased.
4. Is there additional information due to the liver specific CM?
Two important pieces of functional information were required to make a precise diagnosis. The lesion contained hepatocytes, and the hepatobiliary secretion was delayed (late scan). So the lesion could not be a metastasis, cholangiocellular carcinoma or undifferentiated hepatocellular carcinoma.
5. What was your differential diagnosis?
Low grade hepatocellular carcinoma (minimal change hepatoma), adenoma, focal nodular hyperplasia (FNH).
Final diagnosis
Low-grade hepatocellular carcinoma (minimal change hepatoma).
Differential diagnosis
- Adenoma
- FNH
Discussion
Focal liver lesions in cirrhosis are commonly found during ultrasound examinations. Due to the high sensitivity but low specificity of the sonography further imaging information is needed in order to answer the most important differential diagnosis in cirrhosis: hepatocellular carcinoma or macroregenerative nodule. Appearance of HCC in CT after intravenous CM-administration depends strongly on the vascular supply of the lesion. In early stages or in a low-grade lesion, the malignant angiogenesis has not yet developed a different vascular bed than the surrounding tissue; these lesions are not seen in cirrhotic livers. Image guided biopsy (with CT or ultrasound) is limited due to impaired coagulation in liver cirrhosis. With MRI and liver specific CM additional information can be added. If the lesion contains no hepatocytes, it will appear hypointense compared with the surrounding liver tissue (malignant HCC, CCC, metastases). If it contains hepatocytes, the differential diagnosis is narrowed to minimal change hepatoma or adenoma (2 entities, which even using histology can not always be distinguished, and both require surgery), FNH or macroregenerative nodule. FNH and adenoma are both related to the female gender and contraceptives, and can therefore in our patient be ruled out. So the differential diagnosis is minimal change hepatoma (MCH) or macroregenerative nodule. After delayed scanning, in MCH the hepatobiliary excretion of the CM is delayed compared to the normal tissue, and the C/N is increasing substantially. The diagnosis was surgically proven after treatment of the cirrhosis with normalisation of the coagulation parameters.