Sclerosing angiomatoid nodular transformation of the spleen: CT, MR, PET, and ⁹⁹(m)Tc-sulfur colloid SPECT CT findings with gross and histopathological correlation

Abstract

Sclerosing angiomatoid nodular transformation (SANT) is a benign, proliferative vascular lesion affecting the spleen. Few reports detailing the cross sectional and PET appearance of this lesion are available, and the lesion's behavior with ⁹⁹(m)Tc-sulfur colloid scintigraphy is previously unreported. Sclerosing nodular transformation of the spleen shows increased tracer accumulation on positron emission tomography, and a central scar-like appearance with an enhancing capsule and radiating septae on CT and MR studies that reflects the gross and histopathological features of the lesion may be visible. An understanding of this pathological finding may allow prospective recognition of the sclerosing nodular transformation of the spleen on cross sectional imaging studies.

Fig. 1

SANT of the spleen: 2-[¹⁸F]-Fluoro-2-Deoxy-D-Glucose (FDG-PET) findings. Axial fused image shows intense tracer activity (standard uptake value = 4.5) within the splenic lesion.

Fig. 2

SANT of the spleen: CT findings. Axial unenhanced (A), arterial phase (B), portal venous phase (C), and delayed (D) enhanced imaging of the abdomen show that the splenic lesion is initially isodense or mildly hypodense to normal spleen (A). Arterial phase imaging (B) shows marked nodular enhancement of the periphery of the lesion (arrows) with a few faintly visible septae (arrowheads) penetrating the center of the lesion from the periphery. The portal venous phase image (C) again shows the hypervascular rim of the lesion (arrows). Vague areas of decreased attenuation centrally represent the fibrosclerotic center of the lesion (when correlated with gross appearance in Fig. 5). Delayed enhanced imaging (D) shows that the lesion progressively enhances toward its center, becoming nearly isodense to the normal spleen. Note, however, that the central “scar” remains visible (when compared with gross pathological appearance in Fig. 5).

Fig. 3

SANT of the spleen: MR findings. Axial T1-weighted [TR = 690 ms, TE = 40 ms] (A) and T2-weighted fat saturation [TR = 16000 ms, TE = 91 ms] (B) images show the lesion to be predominantly low signal on both sequences, with a few foci of relatively hyperintense T1- and T2-weighted signal (arrows) representing foci of hemorrhage. Unenhanced (C) and arterial (D), venous (E) and delayed (F) enhanced axial 3D T1-weighted gradient echo images with fat saturation [LAVA, TR = 4.5 ms, TE = 2.2 ms] images show initial intense enhancement of the periphery of the lesion (double arrow) with progressive appearance of thin enhancing septae (arrowheads) penetrating the center of the lesion from the periphery. Areas of nodular enhancement (arrows) correlate with the presence of angiomatoid nodules (compare with gross pathological appearance in Fig. 5). Axial in-phase [TR = 180 ms, TE = 2.4 ms] (G) and out-of-phase [TR = 180 ms, TE = 2.4 ms] (H) images show a progressive signal increase on the shorter TE sequence (H), consistent with the presence of iron within the lesion. Pathological analysis shows that iron within SANT of the spleen is likely due to the presence of blood products.

Fig. 4

SANT of the spleen: ^99mTc-sulfur colloid scan findings. SPECT CT shows normal tracer activity within the liver and spleen with essentially no activity within the splenic lesion, confirming the absence of reticuloendothelial elements within this abnormality.

Fig. 5

SANT of the spleen: gross pathological findings. Cut specimen shows a central fibrosclerotic scar (*) with septae (arrowheads) and hemorrhagic angiomatoid nodules (arrow). The spleen is visible at the left of the image.

Fig. 6

SANT of the spleen: histopathological findings. Low-power (A, 20×) photomicrograph (hematoxylin and eosin) shows the formation of fibrous nodules in a background of splenic red pulp. High-power (B, 400×) photomicrograph (hematoxylin and eosin) of the central portion of one of the nodules shows proliferation of irregular vascular spaces lined by plump endothelial cells, circumscribed by bands of concentric fibrosis, and abundant hemosiderin.