Abdominal Radiology

, Volume 43, Issue 4, pp 1013–1028 | Cite as

Hypervascular pancreatic “lesions”: a pattern-based approach to differentiation

  • Prasad R. Shankar
  • Ashish P. Wasnik
  • Mahmoud M. Al-Hawary
  • Isaac R. Francis
  • Ravi K. Kaza
Pictorial essay


Hypervascular pancreatic lesions/masses can arise due to a variety of causes, both benign and malignant, leading to a wide differential diagnosis. Accurate differentiation of these lesions into appropriate diagnoses can be challenging; however, this is important for directing clinical management. This manuscript provides a multimodality imaging review of hypervascular pancreatic lesion, with emphasis on an imaging-based algorithmic approach for differentiation of these lesions, which may serve as a decision support tool when encountering these uncommon lesions. Additionally, we stratify these lesions into three categories based on malignant potential, to help guide clinical management.


Pancreas Hypervascular masses Decision support Neuroendocrine tumor Pancreatic neoplasm 

A broad variety of conditions can manifest as hypervascular pancreatic masses on contrast-enhanced cross-sectional imaging, and differentiation into specific diagnoses can be challenging due to overlapping morphologies and appearances. These lesions include primary pancreatic tumors, metastatic tumors to the pancreas, as well as lesions arising from structures which can mimic intrinsic pancreatic processes.

In this article we present a flowchart-based algorithmic approach for differentiation of these lesions (Fig. 1), which provides a top-down hierarchy to assist in the differentiation of these lesions from the perspective of the interpreting radiologist. This flowchart-based approach incorporates imaging findings of these lesions on CT, MR, and nuclear medicine exams and provides a diagnostic algorithm for yet-to-be determined hypervascular lesions. In addition to imaging features, clinically relevant history is incorporated into this algorithm to help with lesion characterization.
Fig. 1

Flowchart-based approach to differentiation of hypervascular pancreatic lesions

Pancreatic hypervascular lesions can be broadly classified into three categories based on malignant potential, which is beneficial in guiding clinical management of these lesions. Lesions with no-risk for malignancy include intra-/peripancreatic vascular anomalies, and intrapancreatic accessory spleen. Lesions with low risk for malignancy include solid pseudopapillary tumors and solid-appearing serous cystadenomas. Lesions with high risk for malignancy include pancreatic neuroendocrine tumors (pancreatic NETs), acinar pancreatic carcinomas, and hypervascular pancreatic metastases. Pancreatic NETs are further discussed based on the presence or absence of clinically significant manifestation of hormone secretion, and on the basis of associated syndromic states.

“No-risk for malignancy” lesions

Vascular structures

Based on the flowchart-based approach, a hypervascular pancreatic lesion should first be assessed for its relationship with any adjacent vascular structures (Fig. 1). If a lesion is directly arising from a vascular structure, this is consistent with a vascular process adjacent to the pancreas, rather than a true pancreatic lesion. This initial identification is crucial, so as to prevent inadvertent biopsy or workup of a non-malignant vascular entity. The use of multiphasic reformatted CT or MR imaging can be helpful in determining relationships between these “lesions” and adjacent vessels. Vascular structures appearing as pancreatic vascular masses can be further divided based on arterial or venous origin (Fig. 1).

Arterial origin

Arterial anomalies abutting the pancreas can appear as hypervascular masses arising from the pancreas itself. True aneurysms, maintaining all three vascular wall layers (lined by intima, media, and adventitia), of the gastroduodenal artery account for 1.5% of visceral aneurysms [1]. These appear on CT as well-circumscribed structures with luminal communication with the adjacent vessels and enhancement pattern identical to the aorta, often with peripheral atherosclerotic calcifications (Fig. 2). Pancreaticoduodenal and gastroduodenal artery aneurysms can be seen in the setting of atherosclerosis and vasculitis [2, 3]. Association between these aneurysms and celiac artery occlusive disease has been described, and is more likely to involve the pancreaticoduodenal artery than the gastroduodenal artery [4]. The primary concern when encountering these lesions is the risk of life-threatening rupture, related to weakening of the arterial wall and the appropriate referral to interventional radiology or vascular surgery for treatment should be undertaken [5].
Fig. 2

Gastroduodenal artery aneurysm in a 76-year-old male. Arterial contrast-enhanced axial CT image shows a round vascular lesion abutting the pancreatic head (arrow), the same density of the adjacent aorta. Sequential images revealed this to contiguous with the gastroduodenal artery, compatible with a gastroduodenal artery aneurysm. A saccular abdominal aortic aneurysm (arrowhead) is also present

Pseudoaneurysms differ from true aneurysms by lacking one or more of the normal three vascular wall layers. While differentiation between pseudoaneurysms and true aneurysms can be challenging, the former arise secondary to erosion of the arterial adventitia, and typically should be considered in the setting of pancreatitis or trauma [6]. Pseudoaneurysms can appear as peripancreatic or intrapancreatic. Pseudoaneurysms occur in up to 10% of patients with pancreatitis and most commonly involve the splenic artery (40%), gastroduodenal artery (30%), and pancreaticoduodenal arteries (10%) [7].

On contrast-enhanced CT, pseudoaneurysms appear as hypervascular peripancreatic foci, closely adjacent to the pancreas and often surrounded by inflammatory fluid (pseudocysts) or extravasation of injected contrast material (Fig. 3). Peripancreatic pseudoaneurysms are at an increased risk of rupture and prompt endoscopic or surgical intervention is necessary [7, 8].
Fig. 3

Short gastric artery pseudoaneurysm in a 61-year-old male with epigastric pain. Axial (A) and coronal (B, C) post-contrast CT images show a small round hypervascular focus (white arrows) in the region of the pancreatic tail, compatible with a short gastric artery pseudoaneurysm, surrounded by low attenuation fluid/pseudocyst. Calcifications within the pancreatic head (arrowhead) are consistent with chronic pancreatitis

Venous origin

Venous aneurysms involving the portal (Fig. 4) and splenic veins (Fig. 5) are rare, but can mimic pancreatic masses. Portal venous phase-enhanced CT images reveal enhancement pattern similar to adjacent venous structures and multiplanar reformatted images can confirm luminal communication of these structures. Portal venous aneurysms are most commonly seen in the setting of cirrhosis and portal hypertension [9]. Splenic vein aneurysms are extremely rare and can occur secondary to congenital, post-traumatic, or infectious etiologies [10]. Management of splenic vein aneurysms is variable and can range from conservative treatment to splenectomy [9, 10].
Fig. 4

Portal vein aneurysm in a 65-year-old female. Axial post-contrast arterial phase (A), portal venous phase (B), and coronal reformatted maximum intensity projection portal venous phase (C) images show a portal vein aneurysm (arrow) at the level of the portal confluence; mimicking a mass posterior to the pancreatic neck

Fig. 5

Splenic vein aneurysm in an asymptomatic 63-year-old female. Axial arterial phase (A) and portal venous phase (B) CT images and a venous digital subtraction angiography image (C) are presented. A round hypervascular lesion adjacent to the pancreatic tail is confirmed by angiography to represent a splenic venous aneurysm

Intrapancreatic accessory spleen

Based on the flowchart-based algorithm, intrapancreatic accessory spleen should be considered in cases where there is no direct vascular connection involving the lesion, the patient does not present with clinical features of neuroendocrine tumors, and in which the lesion specifically involves the pancreatic tail (Fig. 1). Accessory splenic tissue, in all locations, is common and occurs in 10–30% of the population [11, 12]. Intrapancreatic accessory spleens are relatively less frequent with an autopsy series reporting a prevalence of 17% [13].

Intrapancreatic accessory spleens follow the enhancement pattern of the spleen on all phases of post-contrast imaging and follow the signal intensity of the spleen on all MR pulse sequences (Fig. 6) [14]. Arterial phase imaging may be of particular benefit, given the serpiginous enhancement pattern of an intrapancreatic accessory spleen, similar to the remainder of splenic tissue [15].
Fig. 6

Intrapancreatic accessory spleen in an asymptomatic 45-year-old male. A small round mass is incidentally detected within the pancreatic tail (arrows). MR in-phase (A), out-of-phase (B), T2 fat-saturated (C), T1 post-contrast arterial phase (D), and T1 delayed post-contrast (E) images all show identical signal intensity between this lesion and the adjacent spleen, consistent with an intrapancreatic accessory spleen

In equivocal cases, the use of Tc-99m heat-damaged red blood cell (HDRBC) and Tc-99m sulfur colloid nuclear medicine scanning can be helpful in confirming the nature of these lesions, based on preferential uptake within the lesion and adjacent spleen (Fig. 7) [15, 16]. Though both agents show uptake within splenic tissue, the use of Tc-99m HDRBC is preferable to Tc-99m sulfur colloid, when clinically feasible, due to the increased specificity of uptake in splenic tissue, with 90% of HDRBCs localized within splenic tissue [17, 18]. However, Tc-99m HDRBC scanning is more time consuming and requires handling of blood products [18].
Fig. 7

Intrapancreatic accessory spleen in a 63-year-old female initially evaluated for abdominal pain. An ovoid lesion (arrows) within the pancreatic tail follows splenic parenchymal enhancement on arterial (A) and venous (B) axial CT images. Technetium-99m-fused SPECT-CT sulfur colloid scan (C) shows uptake similar to splenic tissue confirming the diagnosis of an intrapancreatic accessory spleen

Intrapancreatic accessory spleens are benign, and no further invasive workup or treatment is needed, if the diagnosis can be confidently made on the basis of imaging alone. Lesions which remain indeterminate on imaging may require further evaluation with endoscopic ultrasound and fine needle aspiration [19].

“Low-risk for malignancy” lesions

Solid pseudopapillary tumors (SPT)

When following the proposed flowchart-based algorithm, solid pseudopapillary tumors should be considered in cases where there is no vascular connection with the lesion, the patient does not present with clinical features of neuroendocrine tumors, and in which there is no known history of primary hypervascular malignancy (Fig. 1). Solid pseudopapillary tumors are benign or low-grade malignant tumors that occur almost exclusively in young females [3, 20]. These are well-circumscribed masses which can occur anywhere in the pancreas with variable solid and cystic components.

CT imaging of SPT shows a homogenous or slightly heterogeneous enhancing pancreatic parenchymal mass. MRI evaluation of these lesions should be considered, due to superior soft tissue and fluid resolution compared with CT. Solid pseudopapillary tumors should be suggested when there is heterogeneous enhancement and intrinsic MRI T1 hyperintensity, suggestive of intralesional blood (Fig. 8) [20]. In some cases endoscopic ultrasound and biopsy may be beneficial in confirming the diagnosis [21].
Fig. 8

Solid pseudopapillary tumor in a 29-year-old female with epigastric pain. Axial (A) and coronal (B) contrast-enhanced CT images reveal a complex cystic pancreatic head mass with peripheral mural enhancement (arrows). T1 pre-contrast MRI (C) shows areas of hyperintensity compatible with hemorrhage. Subtraction post-contrast MR images (D) again show mural enhancement. Surgical histology revealed a solid pseudopapillary tumor

These lesions can be detected incidentally or present with abdominal pain. Management is typically with surgical resection [22].

Solid-appearing serous cystadenomas

Following the flowchart-based algorithm, solid-appearing serous cystadenomas should be considered in cases where there is no vascular connection with the lesion, the patient does not have with clinical features of neuroendocrine tumors, and in whom there is no history of primary hypervascular malignancy (Fig. 1). Solid-appearing serous cystadenomas are rarely malignant and typically occur in asymptomatic elderly women [3, 21]. While the most common subtype of these lesions is the microcystic variant, which appears cystic on CT, these lesions can also rarely appear solid, due to enhancement of closely opposed walls and septa of cystic spaces, and can be mistaken for an alternative solid-enhancing pancreatic mass such as a neuroendocrine tumor [20].

CT imaging of solid-appearing serous cystadenomas shows a solid heterogeneously enhancing mass with possible central calcification/scar (Fig. 9) [23]. MRI is beneficial in showing small closely clustered cystic spaces within these lesions (Fig. 10) [20, 21].
Fig. 9

Solid-appearing serous cystadenoma in a 73-year-old female with left upper quadrant pain. A contrast-enhanced CT shows a lobular hypervascular pancreatic tail mass (arrow) with central calcification (arrow head). This was shown on surgical pathology to represent a serous cystadenoma

Fig. 10

Solid-appearing serous cystadenoma in a 68-year-old female with early satiety and weight loss. Contrast-enhanced arterial phase (A) and portal venous phase (B) CT images show a lobular hypervascular pancreatic head mass (arrow). Subsequent T2-weighted MR images (C), show that this mass actually comprised closely opposed cystic spaces with a stellate central scar, consistent with a serous cystadenoma, confirmed by surgical histology

Management of these lesions is typically conservative and with periodic surveillance [22].

“High risk for malignancy” lesions

Pancreatic acinar cell carcinoma

Pancreatic acinar cell carcinomas should be considered in cases where there is no vascular communication with the lesion, the patient does not have clinical features of neuroendocrine tumors, and where there is no history of a primary hypervascular malignancy (Fig. 1). Acinar cell carcinoma of the pancreas is a rare primary pancreatic malignancy, most commonly seen in elderly males [24]. These tumors typically present as larger (> 4 cm) hypervascular pancreatic masses, arising from the exocrine pancreas [3]. A characteristic paraneoplastic syndrome associated with these lesions is polyarthritis, eosinophilia, fat necrosis, and subcutaneous nodules, due to systemic secretion of pancreatic enzymes by these tumors.

Pancreatic acinar cell carcinoma most commonly appear on CT as exophytic well-defined masses with homogeneous enhancement and variable cystic components [3, 25]. MRI is beneficial in showing that these are solid-enhancing intrapancreatic masses. Tissue sampling, is necessary to distinguish these lesions from other similarly appearing entities, such as non-functioning neuroendocrine tumors.

Management of these lesions is with surgical resection, in the absence of metastatic disease [24].

Hypervascular pancreatic metastases

Based on the flowchart-based algorithm, hypervascular pancreatic metastases should be considered in cases where there is no vascular communication with the lesion, the patient does not have clinical features of neuroendocrine tumor, and the patient has a history of a primary hypervascular malignancy (Fig. 1). Additionally, multiplicity of lesions should also prompt inclusion of this entity (Fig. 11). Hypervascular pancreatic metastases can occur in any portion of the gland.
Fig. 11

Pancreatic metastases from renal cell carcinoma in a 63-year-old male. Axial contrast-enhanced CT images (AC) of the abdomen in a patient status post right nephrectomy for renal cell carcinoma. Hypervascular small masses within the pancreatic head (arrow, A) and neck (arrow, B) are compatible with metastases. A contralateral renal malignancy (arrowhead, C) is also present

Metastases to the pancreas are relatively rare and account for 2–5% of pancreatic malignancies [26, 27]. The prevalence of metastatic disease to the pancreas ranges between 1.6 and 11% based on autopsy data [26, 28]. The most common primary malignancies to metastasize to the pancreas are renal cell carcinomas, followed by breast, lung, colorectal, and melanoma [29, 30].

Pancreatic metastases are most often incidentally detected, as a part of routine follow-up imaging [26]. Though the time to metastasis is variable, long periods of latency have been shown between the initial treatment of renal cell carcinoma and the development of pancreatic metastases [31]. In the setting of isolated “pauci-metastatic” pancreatic metastases from renal cell carcinoma, studies have shown a survival benefit to the resection of these lesions [29, 32].

Neuroendocrine tumors

Pancreatic neuroendocrine tumors (pancreatic NETs) are pancreatic tumors arising from the endocrine pancreas with variable behavior, ranging from slow-growing indolent lesions to aggressively metastasizing lesions [33, 34]. These have previously been called islet cell tumors, although these tumors arise from the pluripotent pancreatic ductal epithelium rather than pancreatic islet cells [3, 35]. These tumors all secrete hormones, but are subdivided as functional and non-functional tumors based on the presence or absence of a clinically significant syndromic state related to hormone secretion [3, 35, 36]. Classically, neuroendocrine tumors are described as solid hypervascular masses without associated ductal obstruction [36, 37]. While previously size was thought to be the primary indicator of tumor aggressiveness, tumors are now subdivided into low-, intermediate-, and high-grade lesions based on mitotic activity and percentage of nuclear antigen Ki-67 [34, 35, 38].

Functional neuroendocrine tumors

Following the flowchart-based algorithm, functional neuroendocrine tumors should be considered in cases where the patient has clinical symptoms suggestive of a neuroendocrine tumor (Fig. 1). Subsequently, these entities can be confirmed with either tissue sampling or confirmatory nuclear medicine imaging using somatostatin receptor agents [36, 39].

On contrast-enhanced CT, pancreatic neuroendocrine tumors appear as hypervascular pancreatic masses. Increased vascularity of these structures is secondary to a rich capillary network [40]. Smaller lesions tend to enhance more homogeneously, whereas larger lesions may show more heterogeneity in enhancement, due to internal necrosis or calcification [40]. Both arterial and portal venous phase images are complimentary in the detection of these lesions [41, 42].

MRI has been reported as having a sensitivity of 74–94% and specificity of 78–100% for the detection of neuroendocrine tumors [43]. Neuroendocrine tumors on MRI, classically show intrinsic T1-hypointensity, T2-hyperintensity, and restricted diffusion on MRI, relative to normal pancreatic parenchyma [3]. These lesions are typically vascular on both arterial and venous phase imaging with heterogeneity of enhancement increasing with lesion size [40]. Conspicuity of lesions between arterial and venous phase is variable, with both phases serving in a complimentary capacity to optimize lesion detection [40, 42, 44].

Pancreatic neuroendocrine tumors and associated metastases can be localized by nuclear medicine imaging due to the presence of somatostatin receptors on these tumors. The most widely used test for this purpose is the planar In-111 octreotide scan, with single photon emission computed tomography [40]. The sensitivity of this method, while dependent on tumor size and histology, is 80% [40]. Newer somatostatin analogues bound to positron-emitting isotopes, such as Ga-68 DOTATATE, in conjunction with PET/CT have yielded greater diagnostic accuracy with sensitivity of 93% and specificity of 96% and are now being used more frequently [45, 46, 47].

Neuroendocrine tumor-associated syndromic states are named based on the hormone of excess secretion, such as: insulinoma, VIPoma, glucagonoma, somatostatinoma, etc. The most common of these is the insulinoma (Fig. 12) which presents with hypoglycemia, secondary to excess insulin secretion [3, 48]. Though approximately 10% of insulinomas are malignant, the majority are benign and treated with surgical enucleation [48, 49]. The second most common functioning neuroendocrine tumor is the gastrinoma (Fig. 13), which account for approximately 16–30% of functional neuroendocrine tumors [34]. Due to excess gastrin secretions, patients can develop Zollinger–Ellison syndrome, manifested by gastritis and peptic ulcer disease [34, 50, 51]. Unlike insulinomas, the majority of gastrinomas are malignant and are managed with surgical resection, in the absence of metastasis [3, 34].
Fig. 12

Insulinoma in a 55-year-old female with hypoglycemia. Fat-saturated T2-weighted (A), T1-weighted (B), and T1 post-contrast (C) MR images reveal a lobular mass within the pancreatic tail (arrows). This lesion shows intrinsic T2 hyperintensity, T1 hypointensity, and nearly homogeneous enhancement. Pathology from distal pancreatectomy revealed an insulinoma

Fig. 13

Gastrinoma in a 62-year-old male with history of peptic ulcer disease. An axial post-contrast CT of the abdomen (A) reveals a hypervascular pancreatic tail mass and circumferential gastric wall thickening (arrowhead). The pancreatic lesion showed uptake of In-111 pentetreoctide (B, arrow), compatible with a gastrinoma

Non-functional neuroendocrine tumors

Based on the flowchart-based algorithm, non-functional pancreatic NETs should be considered in cases where there is no vascular communication with the lesion, the patient does not have clinical features of neuroendocrine tumors, and where there is no history of a primary hypervascular malignancy (Fig. 1). The majority (approximately 90%) of pancreatic NETs are clinically classified as non-functional [34]. Non-functional pancreatic NETs are often larger than their functional counterparts on presentation and can present with ductal obstruction (Fig. 14) [35, 36].
Fig. 14

Non-functioning neuroendocrine tumor in a 57-year-old female with left upper quadrant pain. Arterial (A) and portal venous phase (B) CT images show a heterogeneous lobular pancreatic tail mass (arrows). This was shown to represent a neuroendocrine tumor following surgical resection

The CT and MRI appearance of these tumors is similar to that of functional neuroendocrine tumors, described above. MRI is helpful to confirm the solid nature of these tumors. However, due to the absence of suggestive clinical features, these lesions can be difficult to definitively diagnose on the basis of imaging alone, and tissue sampling is often required.

Syndromic states associated with neuroendocrine tumors

Neuroendocrine tumors can arise both spontaneously and in association with predisposing syndromic conditions such as von Hippel–Lindau (Fig. 15), multiple endocrine neoplasia type I (MEN I) (Fig. 16), tuberous sclerosis, and neurofibromatosis [3, 34, 35]. Approximately 10% of pancreatic NETs are associated with these inherited syndromic conditions, and the presence of other characteristic imaging findings can help in classifying pancreatic lesions as pancreatic NETs in these patients [11, 33].
Fig. 15

Neuroendocrine tumor in a 38-year-old male with von Hippel–Lindau syndrome. Arterial (A) and portal venous phase (B) axial CT images in a patient with von Hippel–Lindau syndrome. An enhancing pancreatic head neuroendocrine tumor (white arrow) and right hepatic lobe metastasis (curved arrow) are present. Bilateral renal cell carcinomas (arrow heads) and right adrenal pheochromocytoma (A, black arrow) are also present

Fig. 16

Neuroendocrine tumor in a 41-year-old male with multiple endocrine neoplasms, type I. Portal venous phase axial CT images of the abdomen (A, B) and sagittal T2-weighted MRI of the brain (C) in a patient with multiple endocrine neoplasms (MEN) type I. Lobular-enhancing pancreatic body/tail masses (arrows) are consistent with neuroendocrine tumors. Also shown is a pituitary adenoma (arrowhead)


There are a spectrum of diagnoses associated with hypervascular pancreatic lesions and it is important for the radiologist to lead clinicians towards the correct diagnosis, in order to appropriately guide management and direct patient care. While there are additional less common hypervascular pancreatic lesions, not presented in this review, (i.e., pancreatoblastomas, solitary fibrous tumors of the pancreas, and pancreatic hamartomas) these diagnoses are often reached by histology. The flowchart-based approach presented in this manuscript is a helpful decision support tool for both trainees and practicing radiologists who may not encounter hypervascular pancreatic lesions on a regular basis.


Compliance with ethical standards


No funding was received for this study.

Conflict of interest

All authors declare that they have no conflict of interest.

Ethical approval

This article does not contain any studies with human participants or animals performed by any of the authors.

Informed consent

Statement of informed consent was not applicable since the manuscript does not contain any patient data.


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Copyright information

© Springer Science+Business Media, LLC 2017

Authors and Affiliations

  • Prasad R. Shankar
    • 1
  • Ashish P. Wasnik
    • 1
  • Mahmoud M. Al-Hawary
    • 1
  • Isaac R. Francis
    • 1
  • Ravi K. Kaza
    • 1
  1. 1.Department of RadiologyMichigan MedicineAnn ArborUSA

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