PMC9908034_01
Computed tomography four months after admission.. The images show (a) atrophic liver (arrow 1), a treated hepatocellular carcinoma nest (arrow 2), collateral veins (arrow 3), ascites (arrow 4); and (b) splenomegaly (arrow 5), which remained unchanged during hospitalization.
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FIG1
Both computed tomography (CT) and ultrasound revealed atrophic liver with a treated nodule, collateral vessels, ascites, and splenomegaly, but no gastric wall thickening (Figures 1a, 1b).
Microscopic view of the stomach.. Endotoxin (+) Gram-negative diplococci (Moraxella {Branhamella} catarrhalis) had penetrated and eroded the stomach wall (arrow), (a) H&E stain, (b) Giemsa stain, and (c) Gram stain. (a) x40, (b, c) x400.
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FIG2
The bacteria were considered as probably being endotoxin-producing Moraxella (Branhamella) catarrhalis (Figures 2a-2c).
Microscopic view of the liver.. The images show (a) nonalcoholic steatohepatitis-related liver cirrhosis (LC). Small nodular LC showing macrovesicular steatosis and injured, ballooned hepatic cells. (b) Histological analysis of cholangitis lenta showed proliferation and dilatation of the canals of Hering at the border of the portal vein, presence of bile thrombi, and infiltration of neutrophils and lymphocytes. Changes in the interlobular bile duct were scarce. (a) x40, (b) x200.
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FIG3
Further, numerous bile thrombi were seen congesting and proliferating the canals of Hering, with scattered neutrophils and lymphocytes, corresponding to sepsis- or endotoxin-related cholangitis lenta (Figures 3a, 3b).