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Objective. To review the CT and MRI features of hypervascular pancreatic metastases (HPM) and to discuss the main differential diagnosis of HPM.

Disseminations pathways. The pancreatic metastases are divided depending on the patterns of spread: direct invasion by a primary tumor arising from adjacent organ, and hematogenous spread of metastases^(1-16). The hematogenous spread of metastases to the pancreas tissue is uncommon and represents only 2% of the pancreatic malignancies. There may be a significantly long latency period between the initial diagnosis of the primary tumor and the subsequent detection of pancreatic metastases^(1,2). The most common primary tumors that colonize the pancreas in studies based on surgical specimens are renal cell carcinoma, breast cancer, lung cancer, colorectal cancer and melanoma⁽³⁾. Another analysis of a surgical and autopsy database showed that, in the autopsy series, the most frequent primary tumors with pancreatic metastases were represented by lung carcinoma (42%), gastrointestinal tract (24.7%) and kidney carcinomas (5%), whereas in the surgical database, there were lymphomas (29%), carcinomas of the stomach (18.4%), kidney (15.7%), malignant gastrointestinal stromal tumor (7.9%), and lung carcinoma (5.3%)^(2,4).

Clinical aspects. Pancreatic metastases (PM) are asymptomatic in more than 50% of cases; these lesions are typically an incidental finding on CT performed for follow-up in oncological patients⁽⁵⁾. The clinical symptoms produced by PM are variable and nonspecific, including abdominal pain, back pain, weight loss, nausea, melena, jaundice, gastrointestinal obstruction and upper gastrointestinal bleeding⁽²⁾.

Lesion distribution and morphology. Three pat­terns of pancreatic metastases have been de­scribed⁽²⁾: 1) mul­tiple small nodules, which can coalesce occasionally into larger masses (5-10% of cases); 2) diffuse infiltration of the pancreas, given a global enlarged organ (15-44% of cases); 3) a solitary mass (50-75% of cases).

Materials and method. We retrospectively ana­lyzed the imaging exams of six patients (three men and three women) who were diagnosed with HPM by mor­pho­patho­lo­gical examination during a 10-year period.

CT technique. Non-enhanced CT (NECT) and con­trast-en­hanced CT (CECT), using currently tree pha­ses: early ar­terial phase at 25-30 s after contrast ma­te­rial (CM) i.v.injection, pancreatic phase obtained 40-45 s after CM i.v. injection, and portal venous phase obtained 70 s after CM i.v. injection, after the injection of 1.5 ml/kg b.w. of non-ionic iodine-based CM with a power in­jec­tor, flow rate 3 ml/s, and a bolus trigger/ROI into the abdominal aorta (threshold 120 UH). After the CT examination, we performed multiplanar reconstructions (MPR), maximum intensity projection reconstructions (MIP), or volumetric rendering technique (VRT).

MRI technique. We used breath hold acquisitions at a 1.5 T MR system and a body phased array abdominal coils. The protocol included three plane localizer, axial and coronal T2 ,T1 Fat Sat weighted sequences, MRCP, long and short TE SS FSE acquisition, diffusion weighted image (DWI) with multiple b values (0; 500; 800 mm/s²) correlated with ADC (apparent diffusion coefficient) map analysis, and non-enhanced and enhanced 3D FSPGR T1 Fat Sat sequence, using a dynamic multiphase acquisition, with gadolinium-based CM i.v. injection (0.1 ml/kg b.w.).

Imaging findings. In our study, hypervascular PM corresponded to: renal cell carcinoma (three ca­­ses), breast carcinoma (one case) and uterine leio­myo­­sar­co­ma (one case).

1. Renal cell carcinoma (RCC). Pancreatic meta­sta­ses can be synchronous with the RCC or can ap­pear many years after surgical procedures. The longest interval for PM appearance after RCC in our study was 22 years old. We found two patterns of PM distribution: solitary mass (one case), and multiple small nodules (two cases).

CT aspects (Figure 1). In NECT, pancreatic meta­sta­ses from RCC appear as an isodense/slightly hypo­dense nodule (s); in CECT, pancreatic metastases showed early arterial phase enhancement, followed by rapid washout in the portal and late phase. A large mass may present heterogeneous enhancement caused by areas of necrosis.

MRI aspects (Figure 2). HPM are hypointense in T1 FS wi, with moderate hyperintense pattern in T2wi compared to the normal pancreatic parenchyma; after Gd-based CM i.v. injection HPM are hyperenhancing lesion(s), and present in DWI restricted diffusion. 

2. Uterine leiomyosarcoma (LMS). Uterine leio­myo­sarcoma is a rare and aggressive malignant neo­plasm of the myometrial smooth muscle cells. The most com­mon sites of distant metastases from LMS are the lung, kidney and liver⁽¹¹⁾. Metastases to the pancreas are rare^(12-16).

CT aspect (Figure 3). In our case, the pancreatic metastasis corresponded to a hypodense nodule localised in the pancreatic body with a gradual enhancement in CECT.

MRI aspect. The pancreatic metastasis appears as a hypointense nodule on T1wi, with moderate hypersignal on T2wi and restricted diffusion. After Gd-based CM i.v. injection, small nodule of PM shows gradual enhancement.
 

3. Breast carcinoma. Breast cancer most commonly spreads to the liver, brain, adrenals, lung, ovary and bone. Metastases to the pancreas from breast cancer usually occur in the setting of diffusely metastatic mul­ti­organ disease⁽¹⁴⁾. Pancreatic metastases from breast cancer are rare, with a reported rate of 13% in an autopsy series⁽¹⁵⁾.

CT aspects. In NECT, pancreatic metastases are isodense lesions with hyperattenuation in CECT compared to the normal enhanced pancreatic pa­ren­chyma.

MRI aspects. T1wi: hypointense lesion; T2wi: mo­de­rate hyperintense lesion with restricted diffusion; after Gd injection, the small metastases present a ho­mo­genous hyperenhancement, while the large lesions pre­sent a heterogeneous enhancing.

Differential diagnosis

1. Pancreatic neuroendocrine tumors (PNET). Neuroendocrine tumors of the pancreas represent 3% of all pancreatic neoplasms. The insulinoma is the most common, followed by gastrinoma, VIPoma and glucagonoma. Somatostatinoma is very rare^(16-23).

Imaging findings. In general, PNETs are iso­dense with pancreatic parenchyma in NECT images and demonstrate avid arterial enhancement. They can be localized within the gland or have an exo­phy­tic growth. Rarely, they may cause pancreatic duct di­la­tation or obstruction and local vascular en­case­ment or invasion⁽¹⁵⁾.

2. Invasive Duodenal GIST – CT findings. Many of these tumors arise from the muscularis pro­pria and have an exophytic growth (Figure 4). NECT:  isodense mass; homogenous early arterial en­hance­ment for small lesions, and heterogeneous en­han­cing for large lesions due to necrotic areas.

3. Vascular entities: aneurysms of the splenic artery. Peripancreatic arterial aneurysm may mimic pancreatic hypervascular lesions. The most common visceral aneurysms involve the splenic artery (60%) and the hepatic artery (20%), while mesenteric and pancreaticoduodenal arterial aneurysms are less frequent⁽²⁴⁾.

Imaging findings – CECT: an aneurysm appears as an oval or round lesion with similar enhancement with the abdominal aorta (Figure 5).
 

4. Intrapancreatic accessory spleen. Accessory spleen represents a congenital ectopic splenic tissue. The prevalence of intrapancreatic accessory spleen is 9.3%⁽²⁴⁾.

What should the clinician know? The description of the pancreatic lesion: localization, number, dimensions; the involvement of adjacent vessels and other anatomical struc­ture (duodenum, extrahepatic biliary ducts). Is it a pri­ma­ry or a secondary pancreatic tumor? The pancreatic me­ta­stases are isolated metastases or a generalized dis­se­mi­na­tion? Is there a primary tumor recurrence associated?

Conclusions

The imaging findings in HPM may create a diagnostic challenge. The morphopathological examination is essential and represents the gold standard for the final diagnosis.