PMC6159142_01
Abdominal CT showing multiple hepatic lesions ranging from a few to 5 cm, which do not significantly enhance and contain microcalcifications. (a) Simple phase: focal lesions are hypodense with microcalcifications (arrow); (b) arterial phase, without significant enhancement: no hypervascular lesions are identified. (c and d) Portal phase: discrete uptake; (e) late phase: persisting hypodense lesions without retention of contrast medium.
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MRI showing a similar pattern of enhancement. (a) Coronal sequence, T2 Half Fourier Single Shot Turbo-spin Echo, (HASTE): normal-sized liver with multiple, hyperintense lesions in all liver segments; (b and c) diffusion sequences: lesions show restriction predominantly in the periphery; (d) T1 fat suppression without contrast media: hypointense lesions in the liver; (e) T1 coronal sequence in portal phase: the lesions remain without significant uptake of contrast medium; (f) Axial T1 late phase, 5 min after administration of contrast medium: the lesions with some small zones of central uptake.
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The MRI findings (Figure 2) showed a liver of normal size and morphology, with multiple focal lesions distributed among all segments of the hepatic parenchyma, with variable sizes ranging from a few millimetres to several centimetres, the biggest lesion (in the right lobe) being 5 cm.
Cholangioresonance sequences.
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Cholangioresonance sequences were performed with results in normal ranges (Figure 3).
(a) MRI axial T1 late phase, 5 min after administration of contrast medium, showing low uptake of the contrast medium, which is heterogeneous; central sinus is seen in some lesions and peripheral in others. (b) MRI axial T1 late phase, 5 min. Lesions show little contrast medium uptake, simulating lesions of a cystic nature.
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This uptake is heterogeneous, being central in some lesions and peripheral in others (Figure 4).
(a, b) MRI axial, arterial phase: multiple low-intensity lesions are identified that do not show contrast medium uptake.
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Finally, in the MRI in the arterial phase, multiple low-intensity lesions are identified that do not show contrast media uptake (Figure 5).
(a and b) Phase and out-of-phase sequences were performed without identifying change in signal intensity, suggesting microscopic fat content in the lesions.
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Phase and out-of-phase sequences were performed without identifying change in intensity signal, suggesting microscopic fat content in the lesions (Figure 6).
Liver Ultrasound: (a and b) Multiple heterogeneous, predominantly echogenic hepatic lesions were identified, distributed among all liver segments. Some had target-like or annular appearance and others had calcifications. Some had a pattern similar to "hailstorm" described in echinococcosis.
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This study was complemented with ultrasound examination (Figure 7), which demonstrated solid, frank echogenic lesions with multiple punctate echogenic foci in their interiors explained by the presence of calcifications; some exhibited annular hyperechogic halo with less echogenic centres.
Liver biopsy. (a) Vascular channels lined by endothelial cells without dysplasia, separated by septa of fibrous enlargement (100x); (b) Vascular channels adjacent to a portal space that presents occasional lymphocytes and fibrosis (200x).
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A report was obtained within 3 days of the procedure; the pathology findings of the collected liver samples reported "fragments of liver tissue replaced by a benign lesion of vascular origin characterized by the presence of numerous anastomosing vascular channels within it, lined by endothelial cells without atypia, separated by fibrous connective tissue septa with ectatic and obliterated vessels; findings are consistent with sclerosing cavernous haemangioma" (Figure 8).