ECR

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Management of the hypervascular pancreatic lesions andtheir mimics

Poster No.: C-1070

Congress: ECR 2012

Type: Educational Exhibit

Authors: J. C. Quintero1, F. Hermida1, P. PARDO2, R. Villaamil1, A. Abu-

Suboh Abadia1, M. Marey3; 1Ourense/ES, 2ourense/ES, 3Lugo/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, andhistopathological findings

Background

Hypervascular solid tumors of the pancreas may originate from primary pancreatic orfrom secondary involvement by nonpancreatic primary lesions (Figure 1).

Pancreatic hypervascular conditions are common and easily detected on multiphasiccontrast-enhanced MDCT and MR images. Unenhanced CT and, especially, fat-suppressed T1-weighted MRI, are valuable for detecting haemorrhage within pancreaticabnormalities.

Due to the differences in prognosis and treatment, it is critical to use to avaible tools indetection and classification of hypervascular lesions of the pancreas (Figure 2). Accuratediagnosis of hypervascular pancreatic abnormalities is contingent on optimized imagingtechnique (Figure 3).

Technique

Standard CT protocols vary by institution. Dual-phase pancreatic studies often includearterial phase images obtained at 20-25 seconds after injection of non-ionic intravenouscontrast material and portal venous phase images obtained at 55-70 seconds afterinjection. In patients with a known islet cell tumours (ICTs), the liver should be evaluatedfor hypervascular metastases. Pancreatic parenchymal phase images may be obtainedat 35-40 seconds after injection as part of a triphasic study or instead of the arterialphase images (Figure 4). Low-density oral contrast agents such as water may improvevisualization 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 T2-weighted sequences, either with or without fat suppression, as well as gadoliniumcontrast 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 themedial aspect of the second and third portions of the duodenum. When filled with fluidthey can mimic cystic lesions of the pancreatic head.

They also can simulate hypervascular pancreatic lesions and peripancreaticpseudoaneurysm if filled with oral contrast material.

Identifying gas within the diverticulum or persistent high density on delayed images canclarify the situation. MDCT may better delineate the thin, intraluminal diverticulum sacwall and the plane of separation between the duodenum and the pancreas. Gas causesa susceptibility blooming artefact on spoiled GRE MR images that can be identified in thesequence with the longer TE in dual-echo chemical shift imaging.

Spleen

Kidney

Lymphadenopathy

Certain nodal chains, when involved in neoplasm, inflammatory, or infectiousdisorders resulting in lymphadenopathy, may mimic lesions of the pancreas.These disorders include: lymphoma (usually non Hodgkin B-cell type), metastasisdisease, granulomatous disorders (sarcoidosis), angioproliferative disorders (Castlemandisease), 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 thepancreatic 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 enterochromaffincells (serotonin producing) and F cells (pancreatic polypeptide) are also present (Figure5).

All ICTs produce hormone to a variable degree, however, a dividing line exists betweenthose that result in a clinical syndrome and those that do not syndromic (85%) andnonsyndromic (15%) types on the basis of clinical and laboratory assessment. There is anassociation between syndromic ICTs and various medical syndromes including Zollinger-Ellison, multiple endocrine neoplasia type I, von Hippel-Lindau, neurofibromatosis typeI, tuberous sclerosis, and carcinoid syndrome

General imaging features

At ultrasonography (US), ICTs appear as well-circumscribed round or oval hypoechoicmasses with smooth margins. They may be heterogeneous or homogeneous, and whencontrast material is administered, they demonstrate a hypervascular pattern. Evidenceof malignancy includes enlarged peripancreatic lymph nodes and liver metastases. Liverlesions typically are hyperechoic, although they may be hypoechoic or have a targetlikeappearance.

At CT, ICTs appear as circumscribed solid masses that tend to displace surroundingstructures. They typically are hyperattenuating on arterial and venous phase images.Smaller lesions tend to be more homogeneous, and larger lesions are more likelyto demonstrate heterogeneous enhancement (due to areas of cystic degeneration,necrosis, fibrosis, and calcification). Lymph node and liver metastases also arehypervascular. Hepatic metastases often demonstrate ringlike enhancement.

MR imaging has sensitivity similar to that of MDCT for the detection of ICTs. Most ICTsdemonstrate signal intensity much higher than that of a normal pancreas on T2-weightedimages. They also may demonstrate intermediate or low signal intensity on T2-weightedimages, with lower signal intensity seen in lesions with substantial amounts of collagen.Typically, ICTs are hyperintense relative to a normal pancreas on contrast-enhancedarterial and venous phase images, and they may demonstrate homogeneous, ringlike,or heterogeneous enhancement; ringlike and heterogeneous enhancement typically areseen 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% ofall functioning ICTs. They have an incidence of two to four per million people eachyear. They tend to manifest earlier and have a smaller size than other functioning andnonfunctioning endocrine tumors, findings likely due to the dramatic clinical syndromecaused by insulin secretion. Insulinomas usually are sporadic, but they account for10%-30% of functioning ICTs in patients with MEN1 and they have been reported inpatients with neurofibromatosis type 1. They have a slight female predominance (female-to-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 withsymptoms of neuroglycopenia such as dizziness, diplopia, blurred vision, confusion,and personality changes. Symptoms resulting from catecholamine release such astachycardia, chest pain, palpitations, and diaphoresis are less common.

Insulinomas usually are small at diagnosis, with 90% of tumors being smaller than 2 cmindiameter and 40% smaller than 1 cm. Virtually all insulinomas are intrapancreatic, andthey have an even distribution throughout the pancreatic head, body, and tail (Figure6). 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 andusually is seen in lesions that are larger than2 cm. Large lesions (those >3 cm) maydemonstrate malignant behavior, with metastases most often seen in peripancreaticlymph nodes.

Gastrinoma

Gastrinomas are the second most common functioning ICTs (about one-half that ofinsulinomas). The peak incidence is in the 5th decade of life and there is a slightmale predominance (male-to-female ratio, 1.3:1). Although most gastrinomas arisesporadically, they are the most common functioning ICTs in patients with MEN1;20%-25% of all gastrinomas occur in these patients. Around 60% of gastrinomasdemonstrate malignant behavior.

Elevated gastrin levels cause hypersecretion of gastric acid, which leads to peptic ulcerdisease in nearly all patients with a gastrinoma. Zollinger-Ellison syndrome. Diarrhea iscommon. Other symptoms include epigastric pain, weight loss, and esophagitis.

Gastrinomas often arise in the gastrinoma triangle, an area bounded by the junctionsof the cystic duct and common bile duct superiorly, the second and third portions of theduodenum inferiorly, and the neck and body of the pancreas medially. They are morecommon 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 pancreaswas thought to be the most common location, but many of these masses may have beenperipancreatic nodal metastases from small duodenal tumors. Gastrinomas also mayarise from the stomach, jejunum, bile ducts, and lymph nodes around the head of thepancreas.

Pancreatic gastrinomas have an average diameter of 3-4 cm, and most are locatedin the pancreatic head. At CT and MR imaging, they commonly demonstrate solidhomogeneous or ring like enhancement, common findings of gastrinoma. Duodenalgastrinomas 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 alsomay lead to formation of multiple carcinoid tumors within the stomach. These tumors mayregress 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 aresporadic, and they are rarely associated with MEN1. Most glucagonomas demonstratemalignant and about 75% ultimately are fatal.

Glucagonoma syndrome is referred to as the 4D syndrome: dermatitis, diabetes, deepvein thrombosis, and depression. The form of dermatitis seen in glucagonoma syndromeis necrolytic migratory erythema, which occurs in over two-thirds of patients. Diabetesmellitus is present in most patients, and it may be mild or severe. Glucagonoma also isassociated with an increased frequency of thromboembolism, most commonly deep veinthrombosis and pulmonary embolism.

Most glucagonomas originate from the pancreas, usually the body or tail (Figure 8). Thediagnosis often is delayed, and most primary tumors have a diameter larger than 5-6cm. At CT and MR imaging, they may demonstrate homogeneous or heterogeneousenhancement with areas of hypoattenuation or hypointensity.

VIPoma

Similar to other ICTs, vipomas usually manifest in the 5th-6th decades, although theyhave 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-Morrisonsyndrome, 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 theremainders were extrapancreatic and nonneurogenic. Extrapancreatic vipomas typicallyarise from the sympathetic ganglia of the retroperitoneum or mediastinum.

Pancreatic vipomas most frequently occur in the pancreatic tail (Figure 8). Their meansize at diagnosis is just over5 cm. Smaller lesions may demonstrate homogeneousenhancement, and cystic change and calcification may be seen in larger masses.Most vipomas demonstrate malignant behavior, with metastases present in 60%-80% ofpatients at the time of presentation.

Somatostatinoma

Somatostatinomas account for less than 2% of all well-differentiated ICTs. The mean ageat presentation is 50 years, and there is an equal sex distribution. Somatostatinomas mostfrequently occur in the pancreas or periampullary region of the duodenum. Duodenalsomatostatinomas are more likely to be associated with neurofibromatosis type 1 thanare pancreatic tumors.

The clinical symptoms of somatostatinoma syndrome are nonspecific and occur in lessthan 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, andrectum. In the pancreas, most occur in the head, and the average size is 5-6 cm. Theimaging characteristics of the primary tumor are similar to those of other ICTs. Metastasesare 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 offunctioning tumors. Many of these nonfunctioning tumors secrete pancreatic polypeptideor 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 inpatients 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, especiallyinsulinomas and gastrinomas. They have an average size of 5-6 cm, and they are solitaryexcept when they are associated with familial syndromes. Because of their large size,most nonfunctioning ICTs demonstrate heterogeneity with areas of cystic degenerationand necrosis at imaging (Figure 10). They have an even distribution throughout thepancreas, and diffuse involvement of the entire pancreas is rare. The frequency ofmetastatic 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 ofmetastasis to the pancreas is low.

The appearance of metastases on US is usually as a single or multiple hypoechoicmasses. However, the sensibility of CT is much greater than US for detection andcharacterization of small intrapancreatic tumors (Figure 11). Hypervascular metastasesare commonly seen with renal cell carcinoma and melanoma.

On MRI, most pancreatic metastases are hypointense on T1-weighted images andhyperintense on T2-weighted images. The use of intravenous contrast in MR maybe useful in establishing hypervacularity in the metastasic lesion in the setting of ahypervascular primary tumor, such as renal cell or melanoma.

LYMPHOMA

Pancreatic lymphoma is predominantly of the non-Hodgkin's B-cell subtype andcan present as a solid pancreatic mass. Primary pancreatic lymphoma is lesscommon than secondary disease. Extranodal lymphoma is more frequently seen inimmunocompromised patients and can be very aggressive in these cases. Secondarydisease is the more common form of pancreatic lymphoma and represents tumor invasionof the pancreas usually from adjacent structures such as duodenum or peripancreaticlymph 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. Mostfocal lesions enhance homogeneously to a lesser degree than the surrounding normalpancreatic parenchyma.

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On MRI, the focal form of pancreatic lymphoma usually demonstrates homogeneoushypointense signal on T1- weighted images relative to normal pancreatic parenchyma.On T2-weighted images, focal pancreatic lymphoma demonstrates low to intermediatesignal, which is slightly higher than normal pancreatic parenchyma, but less than fluidsignal. In the diffuse form of pancreatic lymphoma, MRI will show diffuse enlargement ofthe 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 pancreaticparenchyma 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 in2-5% of patients with acute pancreatitis. High-attenuation material within the pancreaticbed on unenhanced CT scans and high signal intensity on fat-suppressed T1-weightedimages correlate with the presence of blood products. Pseudocysts also may exhibithemorrhage.

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. Earlydetection and management are paramount given the high mortality associated withrupture. Rupture can occur into the peritoneum, adjacent hollow organs, pseudocyst, orpancreatic duct.

Dedicated MDCT or MR angiography can elegantly depict the pseudoaneurysm asa well-delineated rounded structure originating from the donor artery (Figure 12).High-attenuation or high-signalintensity/ thrombus may be seen within the sac onunenhanced CT scans and fat-suppressed T1-weighted MR images. After contrastadministration, 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 capabilityof endovascular management.

Peripancreatic veins

There are multiple causes of portal hypertension. Regardless of the cause, multiple sitesof portosystemic collateralization can decompress the increased portal pressure. In theregion of the pancreatic head, pancreaticoduodenal varices can develop and simulatea pancreatic hypervascular lesion. Findings at MDCT or MRI performed with meticuloustechnique can lead to accurate diagnosis.

Rendu-Osler-Weber syndrome

Hereditary hemorrhagic telangiectasia (HHT) is diagnosed on the basis of the Curaçaocriteria. 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 withHHT.

Three criteria indicate a definitive diagnosis of the disorder in adults, and two criteriaindicate 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 easilydiagnosed 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 toautotransplantation of splenic tissue, and this usually happens after splenectomy; andaccessory spleens that are congenital foci of healthy splenic tissue that are separate fromthe main body of the spleen.

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Accessory spleens are structurally identical to the spleen and they arise from the failureof fusion of the splenic anlage located in the dorsal mesogastrium during the fifthweek of fetal life. The locations of accessory spleens vary, i.e., the splenic hilum, thetail of the pancreas, the greater omentum, the splenic ligament, the small and largeintestinal mesentery, the wall of the small intestine, the female adnexa and the scrotumin descending order of prevalence.

Although intrapancreatic accessory spleen (IPAS) has rarely been noted radiologicallybecause the spatial resolution of conventional images was too low to detect them, it isnot uncommon.

Typically, IPAS appears as a solid enhancing mass with a smooth, round, ovoid orminimally lobulated shape within the tail of the pancreas. The reported size of IPAS of aseries 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 asleukemia/lymphoma, passive congestion, hemosiderosis or thrombopenia, accessoryspleens are usually also involved, and IPAS may change its size according to the mainspleen.

IPAS usually located at the tip of the tail of the pancreas, or close to the tip of the tailof the pancreas.

Ultrasonography

On gray-scale baselineUS, an accessory spleen is usually seen as a round or oval masswith a mildly echogenic and homogeneous texture and shows posterior enhancementbehind the lesion. Accessory spleens are usually surrounded by a high-amplitudeinterface 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 avascular hilum entering the lesion.,

CT attenuation and enhancement pattern

The blood supply to an accessory spleen is usually derived from the splenic artery, withdrainage occurring into the splenic vein. Accessory splenic tissue tends to exhibit thesimilar attenuation both on noncontrast and postcontrast scans, and same pattern ofcontrast enhancement as does the spleen itself on all phases.

Arterial phase CT imaging may be particularly helpful, especially when the characteristicheterogeneous, serpiginous enhancement pattern of normal spleen is also observedwithin IPAS. On venous phase CT imaging, IPAS also shows same pattern of contrastenhancement as does the spleen. Typically, IPAS enhances homogeneously and to thesame degree as the spleen (Figure 14).

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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 splenictissue 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 imagingfindings can occur that include pancreatic hematoma, laceration, transection, anddiffuse 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 MRcholangiopancreatography or ERCP.

Pancreatic paraganglioma

Paragangliomas or extraadrenal pheochromocytomas are rare, affecting about onein 2,000,000 people. Although most paragangliomas are solitary and they arisesporadically, they can be multicentric or hereditary.

Paragangliomas of the abdomen predominantly arise from paraganglia that aresymmetrically distributed along the abdominal aorta in the retroperitoneum. The mostprominent collection is near the origin of the inferior mesenteric artery (the organ ofZuckerkandl), which is where the majority of abdominal paragangliomas originate. Otherless 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 agewas 67 years (range: 42 to 85 years) with a male to female ratio of 1/7. Six of these eighttumors were located in the pancreatic head, whereas the remaining two originated fromthe body of the pancreas.

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The imaging findings were generally characterized as a well-defined mass with frequentareas of hypoechogenicity on US, a well-marginated, hypervascular tumor with cysticareas of low-attenuation on contrast enhanced CT, and tumor displacement of the mainpancreatic 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 ofconditions. 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 differentialdiagnosis and facilitates an accurate presumptive diagnosis, resulting in optimalpatient care.

Several entities can mimic pancreatic hypervascular and hemorrhagic lesions, andan appreciation of these conditions is crucial to prevent unnecessary intervention.

Familiarity with the spectrum of possible underlying causes and the imagingfeatures and conditions that can act as mimics assists radiologist in making anaccurate 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 authorsReferences: J. C. Quintero; Radiology, Ourense, SPAIN

[email protected]

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