Management of the hypervascular pancreatic lesions and

their mimics
Poster No.:

C-1070

Congress:

ECR 2012

Type:

Educational Exhibit

Authors:

J. C. Quintero , F. Hermida , P. PARDO , R. Villaamil , A. Abu-

3 1

Suboh Abadia , M. Marey ; Ourense/ES, ourense/ES, Lugo/ES

Keywords:

Normal variants, Computer Applications-Detection, diagnosis, MR,

CT, Pancreas, Abdomen, Neoplasia, Pathology

DOI:

10.1594/ecr2012/C-1070

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Learning objectives
To analyze enhancement characteristics of hypervascular pancreatic lesions
To determine the ability of multiphase CT to localize these lesions
To discuss the importance of differentiating clinical, radiological, and
histopathological findings

Background
Hypervascular solid tumors of the pancreas may originate from primary pancreatic or
from secondary involvement by nonpancreatic primary lesions (Figure 1).
Pancreatic hypervascular conditions are common and easily detected on multiphasic
contrast-enhanced MDCT and MR images. Unenhanced CT and, especially, fatsuppressed T1-weighted MRI, are valuable for detecting haemorrhage within pancreatic
abnormalities.
Due to the differences in prognosis and treatment, it is critical to use to avaible tools in
detection and classification of hypervascular lesions of the pancreas (Figure 2). Accurate
diagnosis of hypervascular pancreatic abnormalities is contingent on optimized imaging
technique (Figure 3).
Technique
Standard CT protocols vary by institution. Dual-phase pancreatic studies often include
arterial phase images obtained at 20-25 seconds after injection of non-ionic intravenous
contrast material and portal venous phase images obtained at 55-70 seconds after
injection. In patients with a known islet cell tumours (ICTs), the liver should be evaluated
for hypervascular metastases. Pancreatic parenchymal phase images may be obtained
at 35-40 seconds after injection as part of a triphasic study or instead of the arterial
phase images (Figure 4). Low-density oral contrast agents such as water may improve
visualization of intraluminal tumors or pancreatic tumors that are close to the bowel
A typical pancreatic MR imaging protocol to evaluate for ICTs includes T1- and T2weighted sequences, either with or without fat suppression, as well as gadolinium
contrast enhanced T1-weighted fat-suppressed dynamic imaging.

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Images for this section:

Fig. 1: Hypervascular and hyperenhancing pancreatic lesions

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Fig. 2: Hypervascular and hyperenhancing pancreatic lesions

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Fig. 3: Differential diagnosis and eventual pitfalls

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Fig. 4: MDCT technique from adequeate study of pancreas

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Imaging findings OR Procedure details

YUXTAPANCREATIC LESIONS
Stomach/duodenum (diverticles)
Duodenal diverticula are located most frequently in the periampullary region along the
medial aspect of the second and third portions of the duodenum. When filled with fluid
they can mimic cystic lesions of the pancreatic head.
They also can simulate hypervascular pancreatic lesions and peripancreatic
pseudoaneurysm if filled with oral contrast material.
Identifying gas within the diverticulum or persistent high density on delayed images can
clarify the situation. MDCT may better delineate the thin, intraluminal diverticulum sac
wall and the plane of separation between the duodenum and the pancreas. Gas causes
a susceptibility blooming artefact on spoiled GRE MR images that can be identified in the
sequence with the longer TE in dual-echo chemical shift imaging.
Spleen
Kidney
Lymphadenopathy
Certain nodal chains, when involved in neoplasm, inflammatory, or infectious
disorders resulting in lymphadenopathy, may mimic lesions of the pancreas.
These disorders include: lymphoma (usually non Hodgkin B-cell type), metastasis
disease, granulomatous disorders (sarcoidosis), angioproliferative disorders (Castleman
disease), and tuberculosis

ENDOCRINE PANCREATIC TUMORS

Epidemiology and clinical

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Islet cell tumors (ICTs) are rare neoplasm arising from the cells of the endocrine pancreas.
They account for 1% to 5% of all pancreatic tumors. The ICTs are scattered in the
pancreatic tail, body, and head.
Te cell types that are found in the islets include: alpha cells (glucagon), beta cells (insulin),
delta cells (somatostatin), D cells (gastrin), and A-D cells (VIP). A few enterochromaffin
cells (serotonin producing) and F cells (pancreatic polypeptide) are also present (Figure
5).
All ICTs produce hormone to a variable degree, however, a dividing line exists between
those that result in a clinical syndrome and those that do not syndromic (85%) and
nonsyndromic (15%) types on the basis of clinical and laboratory assessment. There is an
association between syndromic ICTs and various medical syndromes including ZollingerEllison, multiple endocrine neoplasia type I, von Hippel-Lindau, neurofibromatosis type
I, tuberous sclerosis, and carcinoid syndrome
General imaging features
At ultrasonography (US), ICTs appear as well-circumscribed round or oval hypoechoic
masses with smooth margins. They may be heterogeneous or homogeneous, and when
contrast material is administered, they demonstrate a hypervascular pattern. Evidence
of malignancy includes enlarged peripancreatic lymph nodes and liver metastases. Liver
lesions typically are hyperechoic, although they may be hypoechoic or have a targetlike
appearance.
At CT, ICTs appear as circumscribed solid masses that tend to displace surrounding
structures. They typically are hyperattenuating on arterial and venous phase images.
Smaller lesions tend to be more homogeneous, and larger lesions are more likely
to demonstrate heterogeneous enhancement (due to areas of cystic degeneration,
necrosis, fibrosis, and calcification). Lymph node and liver metastases also are
hypervascular. Hepatic metastases often demonstrate ringlike enhancement.
MR imaging has sensitivity similar to that of MDCT for the detection of ICTs. Most ICTs
demonstrate signal intensity much higher than that of a normal pancreas on T2-weighted
images. They also may demonstrate intermediate or low signal intensity on T2-weighted
images, with lower signal intensity seen in lesions with substantial amounts of collagen.
Typically, ICTs are hyperintense relative to a normal pancreas on contrast-enhanced
arterial and venous phase images, and they may demonstrate homogeneous, ringlike,
or heterogeneous enhancement; ringlike and heterogeneous enhancement typically are
seen in larger lesions with cystic or necrotic areas
Insulinoma

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Insulinomas are the most common functioning ICTs, accounting for just over 40% of
all functioning ICTs. They have an incidence of two to four per million people each
year. They tend to manifest earlier and have a smaller size than other functioning and
nonfunctioning endocrine tumors, findings likely due to the dramatic clinical syndrome
caused by insulin secretion. Insulinomas usually are sporadic, but they account for
10%-30% of functioning ICTs in patients with MEN1 and they have been reported in
patients with neurofibromatosis type 1. They have a slight female predominance (femaleto-male ratio, 1.4:1), and the mean age at presentation is 47 years.
Classic clinical triad of insulinomas: symptoms of hypoglycemia, low blood glucose,
and relief of symptoms with administration of glucose. Almost all patients present with
symptoms of neuroglycopenia such as dizziness, diplopia, blurred vision, confusion,
and personality changes. Symptoms resulting from catecholamine release such as
tachycardia, chest pain, palpitations, and diaphoresis are less common.
Insulinomas usually are small at diagnosis, with 90% of tumors being smaller than 2 cmin
diameter and 40% smaller than 1 cm. Virtually all insulinomas are intrapancreatic, and
they have an even distribution throughout the pancreatic head, body, and tail (Figure
6). They usually occur singly; however, multiple tumors are seen in 2%-10% of patients,
frequently those with MEN1.
At CT and MR imaging, insulinomas typically are homogeneous and hyperenhancing
(Figure 7). Heterogeneous enhancement from cystic change or necrosis is rare and
usually is seen in lesions that are larger than2 cm. Large lesions (those >3 cm) may
demonstrate malignant behavior, with metastases most often seen in peripancreatic
lymph nodes.
Gastrinoma
Gastrinomas are the second most common functioning ICTs (about one-half that of
insulinomas). The peak incidence is in the 5th decade of life and there is a slight
male predominance (male-to-female ratio, 1.3:1). Although most gastrinomas arise
sporadically, they are the most common functioning ICTs in patients with MEN1;
20%-25% of all gastrinomas occur in these patients. Around 60% of gastrinomas
demonstrate malignant behavior.
Elevated gastrin levels cause hypersecretion of gastric acid, which leads to peptic ulcer
disease in nearly all patients with a gastrinoma. Zollinger-Ellison syndrome. Diarrhea is
common. Other symptoms include epigastric pain, weight loss, and esophagitis.
Gastrinomas often arise in the gastrinoma triangle, an area bounded by the junctions
of the cystic duct and common bile duct superiorly, the second and third portions of the
duodenum inferiorly, and the neck and body of the pancreas medially. They are more
common in the duodenum than in the pancreas; around 80% of sporadic lesions and 90%

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of lesions associated with MEN1 originate from the duodenum. Previously, the pancreas
was thought to be the most common location, but many of these masses may have been
peripancreatic nodal metastases from small duodenal tumors. Gastrinomas also may
arise from the stomach, jejunum, bile ducts, and lymph nodes around the head of the
pancreas.
Pancreatic gastrinomas have an average diameter of 3-4 cm, and most are located
in the pancreatic head. At CT and MR imaging, they commonly demonstrate solid
homogeneous or ring like enhancement, common findings of gastrinoma. Duodenal
gastrinomas usually are less than1 cmin diameter, and they often are multicentric,
especially in patients with MEN1.
Imaging findings that result from high levels of gastric acid include thickened gastric folds,
ulcers, and those related to complications of ulcer disease. Elevated gastrin levels also
may lead to formation of multiple carcinoid tumors within the stomach. These tumors may
regress after surgical resection of the gastrinoma.
Glucagonoma.
Glucagonoma usually occurs in those who are between 40 and 60 years of age (range,
19-84 years), and it has an equal sex distribution. Glucagonomas almost always are
sporadic, and they are rarely associated with MEN1. Most glucagonomas demonstrate
malignant and about 75% ultimately are fatal.
Glucagonoma syndrome is referred to as the 4D syndrome: dermatitis, diabetes, deep
vein thrombosis, and depression. The form of dermatitis seen in glucagonoma syndrome
is necrolytic migratory erythema, which occurs in over two-thirds of patients. Diabetes
mellitus is present in most patients, and it may be mild or severe. Glucagonoma also is
associated with an increased frequency of thromboembolism, most commonly deep vein
thrombosis and pulmonary embolism.
Most glucagonomas originate from the pancreas, usually the body or tail (Figure 8). The
diagnosis often is delayed, and most primary tumors have a diameter larger than 5-6
cm. At CT and MR imaging, they may demonstrate homogeneous or heterogeneous
enhancement with areas of hypoattenuation or hypointensity.
VIPoma
Similar to other ICTs, vipomas usually manifest in the 5th-6th decades, although they
have been reported in patients 2-83 years old. There is an almost-equal sex distribution,
and they rarely are associated with MEN1.

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The clinical syndrome associated with vipomas has been referred to as Verner-Morrison
syndrome, pancreatic cholera, and WDHA syndrome (watery diarrhea, hypokalemia,
achlorhydria). The amount of diarrhea often is more than 6-8 L per day, even with fasting,
and it leads to hypokalemia, hypochlorhydria, and profound dehydration. Weight loss,
facial flushing, and abdominal pain also may be present.
74% were intrapancreatic, 20% were extrapancreatic and neurogenic, and the
remainders were extrapancreatic and nonneurogenic. Extrapancreatic vipomas typically
arise from the sympathetic ganglia of the retroperitoneum or mediastinum.
Pancreatic vipomas most frequently occur in the pancreatic tail (Figure 8). Their mean
size at diagnosis is just over5 cm. Smaller lesions may demonstrate homogeneous
enhancement, and cystic change and calcification may be seen in larger masses.
Most vipomas demonstrate malignant behavior, with metastases present in 60%-80% of
patients at the time of presentation.
Somatostatinoma
Somatostatinomas account for less than 2% of all well-differentiated ICTs. The mean age
at presentation is 50 years, and there is an equal sex distribution. Somatostatinomas most
frequently occur in the pancreas or periampullary region of the duodenum. Duodenal
somatostatinomas are more likely to be associated with neurofibromatosis type 1 than
are pancreatic tumors.
The clinical symptoms of somatostatinoma syndrome are nonspecific and occur in less
than 20% of patients with a pancreatic somatostatinoma: diabetes mellitus, steatorrhea,
diarrhea, chole-lithiasis, hypochlorhydria, and weight loss.
Somatostatinomas also have been reported in the rest of the small bowel, colon, and
rectum. In the pancreas, most occur in the head, and the average size is 5-6 cm. The
imaging characteristics of the primary tumor are similar to those of other ICTs. Metastases
are present at diagnosis in 50%-75% of patients, usually in the lymph nodes or liver
Non syndromic endocrine tumors
The number of ICTs with no clinical evidence of hormone production is greater than that of
functioning tumors. Many of these nonfunctioning tumors secrete pancreatic polypeptide
or other hormones, without associated clinical symptoms.
The mean age at presentation was 55 years, and there was a slight female predominance.
Non-functioning ICTs usually are sporadic; however, they are the most common ICT in
patients with MEN1 and VHL syndrome.

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Symptoms such as abdominal pain, weight loss, an abdominal mass, and, rarely,
jaundice are a result of mass effect.
On average, non-functioning ICTs are larger than functioning ICTs, especially
insulinomas and gastrinomas. They have an average size of 5-6 cm, and they are solitary
except when they are associated with familial syndromes. Because of their large size,
most nonfunctioning ICTs demonstrate heterogeneity with areas of cystic degeneration
and necrosis at imaging (Figure 10). They have an even distribution throughout the
pancreas, and diffuse involvement of the entire pancreas is rare. The frequency of
metastatic disease at the time of diagnosis has been reported to be as high as 60%-80%

METASTASES
The most common primary cancers associated with pancreatic metastasis are lung,
renal cell, breast, colon, melanoma and soft tissue tumors. However the incidence of
metastasis to the pancreas is low.
The appearance of metastases on US is usually as a single or multiple hypoechoic
masses. However, the sensibility of CT is much greater than US for detection and
characterization of small intrapancreatic tumors (Figure 11). Hypervascular metastases
are commonly seen with renal cell carcinoma and melanoma.
On MRI, most pancreatic metastases are hypointense on T1-weighted images and
hyperintense on T2-weighted images. The use of intravenous contrast in MR may
be useful in establishing hypervacularity in the metastasic lesion in the setting of a
hypervascular primary tumor, such as renal cell or melanoma.

LYMPHOMA
Pancreatic lymphoma is predominantly of the non-Hodgkin's B-cell subtype and
can present as a solid pancreatic mass. Primary pancreatic lymphoma is less
common than secondary disease. Extranodal lymphoma is more frequently seen in
immunocompromised patients and can be very aggressive in these cases. Secondary
disease is the more common form of pancreatic lymphoma and represents tumor invasion
of the pancreas usually from adjacent structures such as duodenum or peripancreatic
lymph nodes.
There are two distinct morphologic patterns of pancreatic involvement by lymphoma,
which can be seen on CT: a focal mass or diffuse enlargement of the gland. Most
focal lesions enhance homogeneously to a lesser degree than the surrounding normal
pancreatic parenchyma.

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On MRI, the focal form of pancreatic lymphoma usually demonstrates homogeneous

hypointense signal on T1- weighted images relative to normal pancreatic parenchyma.
On T2-weighted images, focal pancreatic lymphoma demonstrates low to intermediate
signal, which is slightly higher than normal pancreatic parenchyma, but less than fluid
signal. In the diffuse form of pancreatic lymphoma, MRI will show diffuse enlargement of
the gland with isointense T1 and T2 signal relative to normal pancreatic parenchyma.
Focal pancreatic lymphoma appears as a well-defined hypoechoic mass on ultrasound.
The diffuse form is ill defined on ultrasound, largely following the shape of the pancreas.

INFLAMMATORY AND VASCULAR CONDITIONS

Hemorrhagic pancreatitis
Pancreatic necrosis occurs in approximately 20% of cases of acute pancreatitis.
This disorder can be associated with hemorrhagic changes affecting the pancreatic
parenchyma and the extrapancreatic fatty tissue.
Mortality in hemorrhagic pancreatitis is variable and reported to range from 33% to 100%.
The bleeding that ensues is usually self-limited, but marked hemorrhage can occur in
2-5% of patients with acute pancreatitis. High-attenuation material within the pancreatic
bed on unenhanced CT scans and high signal intensity on fat-suppressed T1-weighted
images correlate with the presence of blood products. Pseudocysts also may exhibit
hemorrhage.
Peripancreatic pseudoaneurysm
Pseudoaneurysm formation occurs in as many as 10% of cases of pancreatitis.
The time interval is variable, ranging from days to years after the acute episode.
The most common vessels affected are the splenic and gastroduodenal arteries. Early
detection and management are paramount given the high mortality associated with
rupture. Rupture can occur into the peritoneum, adjacent hollow organs, pseudocyst, or
pancreatic duct.
Dedicated MDCT or MR angiography can elegantly depict the pseudoaneurysm as
a well-delineated rounded structure originating from the donor artery (Figure 12).
High-attenuation or high-signalintensity/ thrombus may be seen within the sac on
unenhanced CT scans and fat-suppressed T1-weighted MR images. After contrast
administration, the sac may fill with contrast material if it is not completely thrombosed.

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Conventional angiography remains the standard of reference and provides the capability
of endovascular management.
Peripancreatic veins
There are multiple causes of portal hypertension. Regardless of the cause, multiple sites
of portosystemic collateralization can decompress the increased portal pressure. In the
region of the pancreatic head, pancreaticoduodenal varices can develop and simulate
a pancreatic hypervascular lesion. Findings at MDCT or MRI performed with meticulous
technique can lead to accurate diagnosis.
Rendu-Osler-Weber syndrome
Hereditary hemorrhagic telangiectasia (HHT) is diagnosed on the basis of the Curaao
criteria. Diagnosis is based on a combination of clinical and anamnesis findings: (a)
multiple mucocutaneous telangiectases at characteristic sites (lips, oral cavity, fingers,
nose); (b) epistaxis, defined as spontaneous and recurrent episodes of nosebleeds;
(c) visceral involvement, such as gastrointestinal telangiectases or pulmonary, hepatic,
cerebral, or spinal AVM; and (d) a family history, defined as a first degree relative with
HHT.
Three criteria indicate a definitive diagnosis of the disorder in adults, and two criteria
indicate a possible diagnosis. The most commonly affected visceral organs are the lung,
brain, spinal cord, and liver.
Pancreatic telangiectases are highly enhanced round or irregular lesions easily
diagnosed during the arterial phase after administration of iodinated contrast material.
During the portal phase, pancreatic telangiectases may no longer be visible in all cases
(Figure 13)

MISCELLANEOUS CONDITIONS
Accessory intrapancreatic spleen
Ectopic splenic tissue can be categorized as two entities: splenosis that is due to
autotransplantation of splenic tissue, and this usually happens after splenectomy; and
accessory spleens that are congenital foci of healthy splenic tissue that are separate from
the main body of the spleen.

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Accessory spleens are structurally identical to the spleen and they arise from the failure
of fusion of the splenic anlage located in the dorsal mesogastrium during the fifth
week of fetal life. The locations of accessory spleens vary, i.e., the splenic hilum, the
tail of the pancreas, the greater omentum, the splenic ligament, the small and large
intestinal mesentery, the wall of the small intestine, the female adnexa and the scrotum
in descending order of prevalence.
Although intrapancreatic accessory spleen (IPAS) has rarely been noted radiologically
because the spatial resolution of conventional images was too low to detect them, it is
not uncommon.
Typically, IPAS appears as a solid enhancing mass with a smooth, round, ovoid or
minimally lobulated shape within the tail of the pancreas. The reported size of IPAS of a
series of seven cases was from 1.1 to2.5 cm(average 1.5 0.5 cm).
When the spleen is involved with hematologic or other systemic disorder such as
leukemia/lymphoma, passive congestion, hemosiderosis or thrombopenia, accessory
spleens are usually also involved, and IPAS may change its size according to the main
spleen.
IPAS usually located at the tip of the tail of the pancreas, or close to the tip of the tail
of the pancreas.
Ultrasonography
On gray-scale baselineUS, an accessory spleen is usually seen as a round or oval mass
with a mildly echogenic and homogeneous texture and shows posterior enhancement
behind the lesion. Accessory spleens are usually surrounded by a high-amplitude
interface that is observed to be a fibrotic capsule on histologic examination.
On color or power Doppler US, a characteristic blood supply, that is, the presence of a
vascular hilum entering the lesion.,
CT attenuation and enhancement pattern
The blood supply to an accessory spleen is usually derived from the splenic artery, with
drainage occurring into the splenic vein. Accessory splenic tissue tends to exhibit the
similar attenuation both on noncontrast and postcontrast scans, and same pattern of
contrast enhancement as does the spleen itself on all phases.
Arterial phase CT imaging may be particularly helpful, especially when the characteristic
heterogeneous, serpiginous enhancement pattern of normal spleen is also observed
within IPAS. On venous phase CT imaging, IPAS also shows same pattern of contrast
enhancement as does the spleen. Typically, IPAS enhances homogeneously and to the
same degree as the spleen (Figure 14).
Page 15 of 30

MR findings
The MR findings of IPAS have rarely been reported.
Tc-99m Heat-damaged Red Blood Cell Scintigraphy
Technetium-99m HDRBC scintigraphy is a highly specific method for detecting splenic
tissue as up to 90% of the injected HDRBCs are trapped by splenic tissue.

Trauma
Pancreatic injury can result from blunt (27%) and penetrating (73%) trauma In addition,
iatrogenic causes such as biopsy and surgery can result in injury.
The primary method of evaluation is contrast-enhanced MDCT. A spectrum of imaging
findings can occur that include pancreatic hematoma, laceration, transection, and
diffuse gland enlargement. Extrapancreatic findings such as peripancreatic fat stranding,
hematoma, and fluid also can be identified.
The integrity of the pancreatic duct can be assessed with secretin-enhanced MR
cholangiopancreatography or ERCP.

Pancreatic paraganglioma
Paragangliomas or extraadrenal pheochromocytomas are rare, affecting about one
in 2,000,000 people. Although most paragangliomas are solitary and they arise
sporadically, they can be multicentric or hereditary.
Paragangliomas of the abdomen predominantly arise from paraganglia that are
symmetrically distributed along the abdominal aorta in the retroperitoneum. The most
prominent collection is near the origin of the inferior mesenteric artery (the organ of
Zuckerkandl), which is where the majority of abdominal paragangliomas originate. Other
less common locations include the gallbladder, urinary bladder, prostate, spermatic cord,
uterus and duodenum.
Paragangliomas of the pancreas are very rare (eight cases published). The mean age
was 67 years (range: 42 to 85 years) with a male to female ratio of 1/7. Six of these eight
tumors were located in the pancreatic head, whereas the remaining two originated from
the body of the pancreas.

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The imaging findings were generally characterized as a well-defined mass with frequent
areas of hypoechogenicity on US, a well-marginated, hypervascular tumor with cystic
areas of low-attenuation on contrast enhanced CT, and tumor displacement of the main
pancreatic duct on ERCP.

Images for this section:

Fig. 5: Summary of clinical manifestation, size, and location of ICTs

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Fig. 6: Small insulinoma in the tail of pancreas. MDCT, ultrasonography and MR findings

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Fig. 7: Small insulinoma in the tail of pancreas. MDCT findings

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Fig. 8: Glucagonoma and VIPoma

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Fig. 9: Somatostatinoma. MDCT and MR findings

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Fig. 10: Large tumoral mass in the pancreas. Gross specimen, MDCT and MR features.
Non-functioning endocrine tumor of pancreas

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Fig. 11: Metastases

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Fig. 12: Vascular conditions

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Fig. 13: Pancreatic manifestations in hereditary hemorrhagic telangiectasia

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Fig. 14: Accesory intrapancreatic spleen

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Conclusion
Hypervascular and hemorrhagic pancreatic abnormalities are a diverse group of
conditions. They have a wide spectrum of causes that include neoplastic, vascular,
inflammatory, traumatic, and congenital conditions.
Knowledge of the range of pathologic findings is helpful in limiting the differential
diagnosis and facilitates an accurate presumptive diagnosis, resulting in optimal
patient care.
Several entities can mimic pancreatic hypervascular and hemorrhagic lesions, and
an appreciation of these conditions is crucial to prevent unnecessary intervention.
Familiarity with the spectrum of possible underlying causes and the imaging
features and conditions that can act as mimics assists radiologist in making an
accurate presumptive diagnosis (Figure 15).
Images for this section:

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Fig. 15: Conclusions

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Personal Information

Fig. 16: Title and authors

References: J. C. Quintero; Radiology, Ourense, SPAIN
juan.carlos.quintero.rivera@sergas.es

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