PMC7234346_01
Enhanced CT imaging at the patient's first visit to our hospital. The results of CT showed a large hepatic tumor that occupied the liver, with left portal invasion (arrowhead) and metastasis of the left adrenal gland (arrow).
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Enhanced computed tomography (CT) showed that the hepatic tumors were enhanced in the arterial phase and washed out in the equilibrium phase, with Vp3 left portal vein tumor thrombosis (PVTT), metastasis to the left adrenal gland, splenomegaly, and no ascites were present (Figure 1).
Enhanced CT imaging and angiography at the time of HCC rupture. (a) The results of enhanced CT showed intraperitoneal ascites and high-density fluid pooled around the HCC within strange vessels in segment 3 (arrow). (b) The results of emergent angiography showed multiple hepatic tumor stains and irregular vessels in segment 3 (arrowhead).
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Enhanced CT showed intraperitoneal ascites, and high-density fluid pooled around the HCC within abnormal vessels in S3 (Figure 2(a)). S2, and a tumor with abnormal blood vessels was suspected to have ruptured on the caudal side of S3 (Figure 2(b)). Selective TAE was performed, using a microcatheter (Toray Medical Co., Ltd, Tokyo, Japan).
Macroscopic examination of the liver at autopsy. The liver was swollen and almost completely occupied by multiple tumors.
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At autopsy, the liver weight was approximately 5000 g, and there were countless multifocal tumors (Figure 3) with moderate ascites.
Histological examination of the liver tumor and non-cancerous lesions at autopsy. (a) Countless coated nodules occupied the liver (HE staining, 10-fold). (b) The moderately differentiated HCC showed a thick trabecular pattern, stratified appearance, and false duct structures of the cord-like type (HE staining, 100-fold). (c) Fibrosis around the central vein and developing bridging fibrosis were observed (Azan staining, 10-fold). (d) Sinusoidal dilation was apparent around the central vein. Interface hepatitis, hemorrhage, necrosis, and steatosis were not observed (HE staining, 40-fold).
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The hepatic tumors corresponded to moderately differentiated HCC because of their thick trabecular pattern, stratified appearance, and false duct structure of the cord-like type (Figure 4(a) and (b)). Non-cancerous liver lesions showed sinusoidal dilatation, significant fibrosis, and marked central-to-portal bridging fibrosis, which is equivalent to liver cirrhosis (Figure 4(c) and (d)).