Ecb Ch04 Pancreas

7/31/2019 Ecb Ch04 Pancreas

1/22

Ultrasound of the pancreas 28.07.2010 18:06 1

EFSUMB European Course Book

Editor: Christoph F. Dietrich

PancreasDOnofrio Mirko1, Vullierme Marie-Pierre2, Vlek Vlastimil3, Principe Francesco1,

Canestrini Stefano1, Gallotti Anna

1, Pozzi Mucelli Roberto

1

1Department of Radiology, GB Rossi University Hospital, Verona, Italy;

2Department of

Radiology, Beaujon Hospital, Paris, France;3Department of Radiology, Brno University

Hospital, Czech Republic.


2/22


Content

Content ....................................................................................................................................... 2

Topographic Remarks ................................................................................................................2

Pancreas anatomy....................................................................................................................... 2

Pancreatic and peripancreatic veins .......................................................................................3Pancreatic and peripancreatic arteries ....................................................................................3

Pancreatic ductal system ........................................................................................................ 3

Pancreas development............................................................................................................4

US study of the pancreas and anatomy ......................................................................................4

Doppler study of the pancreas and vascular anatomy................................................................6

Pancreatic diffuse inflammatory disease.................................................................................... 8

Acute pancreatitis................................................................................................................... 8

Chronic pancreatitis................................................................................................................ 9

Autoimmune pancreatitis ..................................................................................................... 10

Pancreatic focal inflammatory disease .....................................................................................12

Mass-forming pancreatitis.................................................................................................... 12Pseudocyst............................................................................................................................ 12

Pancreatic solid neoplasm ........................................................................................................ 13

Ductal adenocarcinoma ........................................................................................................ 13

Endocrine tumors ................................................................................................................. 14

Lymphoma ........................................................................................................................... 16

Metastases ............................................................................................................................ 16

Pancreatic cystic neoplasm....................................................................................................... 16

Serous cystadenoma.............................................................................................................16

Mucin producing neoplasms ................................................................................................ 17

Mucinous cystoadenoma.................................................................................................. 17Mucinous cystoadenocarcinoma ......................................................................................18

IPMN....................................................................................................................................19

References ................................................................................................................................ 19

Topographic Remarks

The pancreas is a medium retroperitoneal organ, slightly flattened and tapered, located

transversally in front of the main vessels, at the level of the first or second lumbar vertebra. It

has to be considered a quite fixed posterior organ.

It presents a sligthly oblique shape extending left-upward, with the cephalic portion generallyin a lower position compared to the body and the tail. It lies against the vertebral column,

which determines a slight curvature of the organ, and is surrounded by soft retroperitoneal and

peritoneal tissue.

Pancreas anatomy

The pancreas is a compound racemose gland, which exocrine excretion of is represented by

the pancreatic juice, an important digestive fluid, while the endocrine secretion consists of

enzymes involved in sugar metabolism.

The pancreas is usually divided in four parts: head, with the uncinate process, neck, body andtail.


3/22


The head lies within the curve of the duodenum and appears completely leaned against the

posterior abdominal wall in contact with the inferior vena cava behind and the portal vein at

the top.

The uncinate process originates from the lower left portion of the head and lies posteriorly to

the superior mesenteric vessels.

The neck or isthmus generally appears as a slight constriction connecting the head to thebody. It is located in front of the superior mesenteric vein and completely overlaid on its

anterior surface by the posterior parietal peritoneum; its postero-inferior surface is related to

the origin of the portal vein, formed by the junction of the superior mesenteric and splenic

veins.

The body appears leaned against the posterior abdominal wall by the white line of Toldt. Here

the posterior parietal peritoneum, which overlays the front face of the pancreatic body, limits

the posterior face of the epiploon retrocavity. The pancreatic body is frontally covered by the

gastric cavity while posteriorly is in contact with the splenic vein; moreover it is related with

the superior mesenteric artery and the left renal vein, which courses between the superior

mesenteric artery and the aorta to merge into the inferior vena cava. The superior margin is

slightly anteriorly crossed by the splenic artery, which arises from the celiac artery, whereasthe inferior margin lies upon the duodenojejunal flexure.

The tail is quite posteriorly orientated, left-upward, getting in touch with the splenic hilum as

well as the left adrenal gland and upper kidney. It represents the mobile part of the gland and,

similarly to the body, is separated from the stomach by the epiploon retrocavity.

The anteroposterior dimension of the pancreas varies greatly among individuals and tends to

decrease with the age. The indicative measurements are: head 2 cm; neck 1 cm; body and

tail 1-2 cm, whereas the mean length is 13-15 cm [(1)].

Pancreatic and peripancreatic veins

The veins of the pancreas open into the splenic and superior mesenteric veins, from whichjunction the portal vein originates.

The superior mesenteric vein runs over the uncinate process, whereas the splenic vein, rising

from the splenic hilum, courses along the supero-posterior surface of the pancreas.

Pancreatic and peripancreatic arteries

The arteries of the pancreas derive from the splenic and the pancreaticoduodenal branches of

the hepatic and superior mesenteric arteries.

The splenic artery, arising from the celiac artery, runs along the superior margin of the gland.

From it, some arteries perpendicular to the splenic artery, enter the bodys and tails

parenchyma. In 92% of cases also the common hepatic artery, which courses along thesuperior margin of first portion of the duodenum and continues into the proper hepatic and

gastroduodenal arteries, arises from the celiac artery [(2)]. The gastroduodenal artery courses

along its ventral surface.

The superior mesenteric artery, arising from the aorta behind the lower portion of the

pancreatic body, courses anteriorly to the uncinate process and the third portion of the

duodenum.

Pancreatic ductal system

The pancreatic ductal system is represented by the main pancreatic duct (Wirsungs duct) and

the accessory, functional or not, pancreatic duct (Santorinis duct).


4/22


The main pancreatic duct takes origin from the junction of the small ducts of the tail lobules.

It ranges transversely from the left to the right through the substance of the pancreatic body to

flow into the major duodenal papilla (of Vater) jointly with the common bile duct. It appears

as a thin hypoechoic line bordered by two echogenic margins and its diameter varies from a

maximum of 3 mm in young adults to 5 mm in the erderly. The common bile duct, crossing

the anterior surface of the portal vein to the right of the proper hepatic artery, runs behind thefirst portion of the duodenum to arrive into the parenchyma of the pancreatic head, close to

the second portion of the duodenum.

The accessory pancreatic duct (Santorinis duct) originates from the duct of Wirsung and

crosses just the head of the pancreas, more superficially than to the main duct, to flow into the

minor duodenal papilla, 2 cm higher than the major one.

Pancreas development

The pancreas developes in two parts, the dorsal and the ventral. The dorsal part arises as a

diverticulum from the dorsal side of the duodenum, just above the hepatic digression and,

growing upward and backward into the dorsal mesogastrium, forms a part of the head and theuncinate process as well as body and tail as a whole.

The ventral portion appears as a diverticulum from the primitive bile-duct, forming the

remaining part of the head and the uncinate process. As a consequence the duct of the dorsal

part (accessory pancreatic duct) opens independently into the duodenum, while the duct of the

ventral part (main pancreatic duct) opens together with the common bile-duct. Around the

sixth week of gestation the two parts of the pancreas meet and fuse, establishing a

communication between their ducts. After that, the terminal part of the accessory duct

undergoes just a little enlargement and its opening into the duodenum is sometimes

obliterated, whereas the pancreatic duct increases in size and forms the main duct of the

gland.

At first the pancreas is directed upward and backward between the two layers of the dorsalmesogastrium, which give it a complete peritoneal sheath, its surfaces facing the right and the

left side. With the change in the position of the stomach, the dorsal mesogastrium is drawn

downward and to the left, so that the right side of the pancreas is directed backward and the

left forward. The right surface ends connected to the posterior abdominal wall and the

peritoneum covering it undergoes absorption; thus, in the adult, the gland appears to lie

behind the peritoneal cavity.

US study of the pancreas and anatomy

The study of the pancreas includes transverse, longitudinal and angled oblique scan planes[Figure 1].


5/22


Figure 1 Pancreas. Ultrasound oblique scan of the pancreatic gland with visualization of thepancreatic tail, the body, the isthmus and the upper part of the head of the pancreas.

The plane passing through the emergency of the celiac trunk should identify the body-tail, in

relation with the presence of gastric gas; the left portions of the gland result partially covered

by bowel gas.

The plane passing through the splenic vein demonstrates the typical comma morphology,

and by this scan is easily possible to evidence the body with the Wirsungs duct [Figure 2]

and the isthmus of the pancreas on the vein confluence of the splenic with the superior

mesenteric.

At the level of the lateral border of the head are often seen ventrally the gastroduodenal artery,represented by anechoic image, and dorsally the common bile duct.

Figure 2 Wirsungs duct. Ultrasound oblique scan of the pancreatic body with visualizationof the main pancreatic duct (arrow).


6/22


The scan passing through the mesenteric vessels visualizes the lower portion of the pancreatic

head and the uncinate process, anatomically located between the superior mesenteric vein and

the inferior vena cava. Moreover the superior mesenteric artery appears in front of the aorta,

to the left of the superior mesenteric vein.

The longitudinal scans are executed on the four anatomic parts of the pancreas. The head is

visualized in all its extension, as well as its relationship with the inferior vena cava. Itscephalic portion is cranially delimited by the portal vein and the first duodenal part; more

caudally it relates with the third duodenal portion.

By a longitudinal and slightly oblique scan is usually possible to visualize the intra-pancreatic

common bile duct [Figure 3].

Figure 3 Intrapancreatic common bile duct. Ultrasound longitudinal and slightly obliquescan of the pancreatic head with visualization of the Wirsungs duct and theintrapancreatic tract of the common bile duct (arrow).

The scans at the neck level need the superior mesenteric vein as reference point; it is

visualizable up to the junction with the splenic vein. Just more dorsally is possible to

recognize the uncinate process.

The Wirsungs duct can be visualized at the level of the pancreatic body [Figure 2].

The reference point on the body is represented by the splenic vessels, transversally orientated,

which course on the superior border.

The tail can be visualized by a longitudinal anterior scan, even if the demonstration of thisanatomic structure is often difficult, owing to the gastric gas covering.

The left intercostal scans are generally used to localize the caudal portion by using the splenic

acustic window.

Doppler study of the pancreas and vascular anatomy

Doppler studies are an integral part of ultrasound examination of the pancreas [(3)].

The peripancreatic vascular structures evaluated and well recognized are the portal vein, the

tripod trunk, the splenic artery and vein, the gastrodudenal artery, the superior mesenteric

artery and vein, the aorta and the inferior vena cava; whereas just a few parenchymal vessels

are usually appreciable in normal conditions. However the visualization of smaller


7/22


peripancreatic [Figure 4] and intrapancreatic [Figure 5] vessels is possible thanks to the

increased Doppler sensitivity.

Figure 4 Gastroduodenal artery. Color-Doppler ultrasound longitudinal scan of the

pancreatic head with the visualization of the gastroduodenal artery.

Figure 5 Pancreatic arterial arcades. Power-Doppler ultrasound transversal scan of thepancreatic head with the visualization of the pancreatic arterial arcades.

Clinical applications of the Doppler studies of peripancreatic vessels include the assessment

of patency and features of blood flow.

Doppler and pulsed-Doppler appearance of peripancreatic vessels has been well documented

[(1;2)]. In normal conditions, the mean speed of blood in peripancreatic arteries is about 103

18 cm/s in the celiac trunk, 78 16 cm/s in the hepatic artery, 85 18 cm/s in the splenic

artery and 100 22 cm/s in the superior mesenteric artery [(1)]. Mean portal flow velocity is


8/22


12-20 cm/s. The resistance index in the superior mesenteric artery is in general higher than in

the other arterial vessels [(1)].

Abnormal signals and physiological variations in Doppler waveform in peripancreatic vessels

are not quite understood, because of the influence of physiologic, pharmacologic and

pathological conditions [(1)]. However, Doppler examination allows recognizing the changes

produced by diseases in peripancreatic vessels.

Pancreatic diffuse inflammatory disease

Acute pancreatitis

Acute pancreatitis is an acute inflammatory process that may include suppuration, necrosis

and hemorrhage of pancreatic tissue, with variable involvement of other regional and remote

tissues. Diagnosis is usually based on the laboratory assay of serum amylase and lipase levels

[(3)]. Acute pancreatitis is classified as mild (interstitial edema) [Figure 6] or severe (necrosis,

fluid collections) [Figure 7]. Biliary stones can be detected at the time of the diagnosis.Peripancreatic collections [Figure 7] and then pseudocysts follow the different timing of the

disease.

Figure 6 Mild acute pancreatitis. Ultrasound oblique scan of the pancreatic gland showsenlargement of the gland with the body appearing slightly hypoechoic in respect tothe head.


9/22


Figure 7 Severe acute pancreatitis and pancreatic fluid collection. Ultrasound oblique scan ofthe pancreatic glad with visualization of huge inhomogeneous fluid collection at thepancreatic body-tail.

Normal US findings can be seen in patients with mild acute pancreatitis. Although the

pancreas can appear normal in acute pancreatitis, the most frequent findings are focal or

diffuse enlargement of the gland with a decrease of normal echogenicity [Figure 6].

The pancreas is seen as more hypoechoic than the liver and the pancreatic texture may also

appear heterogeneous. Acute pancreatitis can be focal or diffuse, depending on its distribution

[(4)].

At contrast-enhanced ultrasound (CEUS) the pancreatic segment involved by mild acute

pancreatitis shows an increased contrast enhancement due to hyperemia. Severe acute

pancreatitis is characterized by the presence of large confluent necrotic areas and CEUS may

improve the identification and delimitation of the these necrotic areas, which appear as

avascular at dynamic imaging [(5;6)].

Chronic pancreatitis

Chronic pancreatitis is an inflammatory disease characterized by the replacement of the

pancreatic glandular elements by fibrous tissue. It is clinically characterized by a progressive

pancreatic functional loss [(7)]. Although early morphologic changes of chronic pancreatitis

are difficult to recognize at imaging, the findings of advanced disease are readily detected.

Alterations in size of the pancreas may be seen in fewer than half of patients affected by

chronic pancreatitis [(8-10)]. Atrophy and focal alterations in pancreatic size are the mosteasily identified changes, expression of advanced stages. The glandular contours appear

irregular, sharp and sometimes lumpy.

Echogenicity of the pancreas is usually increased in chronic pancreatitis due to adipose

infiltration [(11)] and fibrosis [(12-14)]. However since the presence in elderly and obese

subjects, it is not a specific parameter. Parenchymal echo structure alteration, on the other

hand, is a more specific sign of chronic pancreatitis. The pancreatic echotexture is

inhomogeneous and coarse due to the coexistence of hyperechoic and hypoechoic foci,

fibrosis and inflammation signs respectively [(12;14)]. These findings are described in 50%-

70% of cases [(9;10)]. In patients affected by severe exocrine pancreatic insufficiency this

percentage increases to about 80% [(8)], therefore showing the fairly good sensitivity of this

finding. Apparent normality of the glandular echotexture in chronic pancreatitis is reported in

the literature in up to 40% of cases and expected especially in the early stages of the disease


10/22


[(9; 1517)]. However, state-of-the-art US imaging has good capabilities for identifying the

fine alterations of glandular texture present in the early stages of the disease, making the

evaluation of pancreatic echostructural alterations an important finding for diagnosis.

The most important diagnostic criterion for chronic pancreatitis is the presence of pancreatic

calcifications [(18)], whose identification is pathognomonic.

Caliber abnormalities in chronic pancreatitis are essentially represented by main pancreaticduct dilation.

Wirsungs duct can be considered dilated when its caliber is larger than 3 mm [(14)], with a

sensitivity of about 60%70% [(10;11)] and a specificity, of about 80%90% [(10;19;20)].

The limits of the reported sensitivity reflect the minor frequency of duct dilation in initial

and/or light cases of chronic pancreatitis. In the early phases of chronic pancreatitis the

Wirsung duct may have a normal diameter [(12)]. Moreover, compression of the main

pancreatic duct may lead to secondary obstructive chronic pancreatitis upstream of the

obstacle, with the same pathogenetic mechanism. Solid and cystic lesions may cause duct

compression (benign) or infiltration (malignant) if contiguous to the main pancreatic duct,

with progressive development of obstructive chronic pancreatitis upstream [(11)].

Therefore the most significant US findings in chronic pancreatitis are pancreatic duct dilationand intraductal calcifications [Figure 8].

Figure 8 Chronic pancreatitis. Ultrasound oblique scan of the pancreatic glad shows mainpancreatic duct dilation and calcifications.

Autoimmune pancreatitis

Autoimmune pancreatitis is a particular type of chronic pancreatitis, with a very recent

pathological definition. It is characterized by periductal inflammation, mainly substained by

lymphocytic infiltration, with evolution to fibrosis. As opposed to the other forms of chronic

pancreatitis, the pancreas is increased in volume, usually in a diffused way with the typical

sausage aspect and the Wirsung duct is compressed or string-like [(21)]. US features

include reduced echogenicity of the gland, diffuse or focal pancreatic enlargement, absence of

any fluid collection or calcification. US findings are typical in the diffuse form when the

entire gland is involved [Figure 9a]. The Wirsungs duct is compressed by glandular inflamed

parenchyma. The overall sensitivity of US in the diagnosis of chronic pancreatitis is variable,with an average range in most series of 60%70% [(7;8)].


11/22


Figure 9 Autoimmune pancreatitis. a) Ultrasound oblique scan of the pancreatic glad showsdiffuse enlargement of the gland with the typical sausage aspect in absence of anyfluid collection or calcification. b) at CEUS diffuse moderate enhancement is visible.

a

b

CEUS of autoimmune pancreatitis shows moderate diffuse enhancement in the early contrast-enhanced phase, though inhomogeneous [Figure 9b].

Contrast medium washout is usually slow but progressive. CEUS findings may be especially

useful in the study of focal forms of autoimmune chronic pancreatitis, in which differential

diagnosis with ductal adenocarcinoma is a priority [(22)]. Autoimmune chronic pancreatitis

shows a remarkable response to steroid therapy because of its autoimmune pathogenesis

[(23;24)].


12/22


Pancreatic focal inflammatory disease

Mass-forming pancreatitis

Mass-forming chronic pancreatitis usually occurs in patients with a history of chronic

pancreatitis [(25)] and must be differentiated from pancreatic ductal adenocarcinoma. AtCEUS, a mass-forming chronic pancreatitis shows a parenchymographic enhancement,

characterized by an enhancement pattern always comparable to that of the surrounding

pancreatic parenchyma. However, in long-standing chronic inflammatory processes,

inhomogeneous hypovascularization of the lesion may be observed, probably owing to the

presence of a large amount of fibrosis and the differential diagnosis becomes more difficult

[(5;26;27)].

Pseudocyst

Pseudocysts can be a complication of severe acute pancreatitis [Figure 10] or can occur in

chronic pancreatitis [(22)]. Characterized by a fibrous wall without an epithelial lining [(28)],pseudocysts must be differentiated from pancreatic cystic tumors, especially mucinous

cystadenomas (MCAs), as they require completely different therapeutic approaches [(28)].

CEUS has a crucial role in differential diagnosis of pseudocysts and pancreatic cystic tumors,

better evaluating the micro-vascularization of the intralesional inclusions.

Figure 10 Pseudocyst. Ultrasound oblique scan of the pancreatic body shows huge roundedcystic lesion after severe acute pancreatitis.

Even if characterized by an inhomogeneous content at conventional US, all the inclusions in

pseudocysts are always completely avascular, becoming homogeneously anechoic during

CEUS examination [(26)].


13/22


Pancreatic solid neoplasm

Ductal adenocarcinoma

About 90% of pancreatic tumors are ductal adenocarcinomas. Theyre composed of

infiltrating epithelium resuming ductal structures. In almost two thirds of patients withpancreatic adenocarcinoma, the tumor is located in the head of the pancreas; while involves

the body and/or the tail, or diffusely infiltrates the entire gland in the rest of them.

Macroscopically, ductal adenocarcinoma appears as schirrous infiltrating mass [(29-32)].

Masses in the head of the pancreas cause a ductal obstruction with secondary dilation of both

the common bile duct and the pancreatic duct, resulting in the so-called double-duct sign.

However this presentation can also be present in the case of chronic pancreatitis. In

particularly aggressive forms of adenocarcinoma the development of necrosis or colliquation

is common, resulting from the difference between the growth rate and the formation of

microvessels by angiogenesis. The necrotic/fluid part of the tumor is mainly located centrally.

A ductal adenocarcinoma is characterized by infiltrative margins with diffusion to the tumor

to the adjacent parenchyma and structures. This feature could explain the common lack of

clear-cut margins during examinations. More frequently, at US, the adenocarcinoma appears

hypoechoic to the adjacent pancreatic parenchyma [Figure 11].

Figure 11 Ductal adenocarcinoma. Ultrasound oblique scan of the pancreatic body showshypoechoic mass with ill-defined infiltrative margins and upstream main pancreaticduct dilation.

The main pancreatic duct is usually infiltrated and upstream dilated. Doppler studies show

poor or no vascularity inside the lesion. The vascular invasion is defined by a focal absence of

the echogenic interface of the vessel wall, or by a narrow lumen, with changes in blood flow

velocity [(33-35)]. Principal criteria of unresectable pancreatic cancer are liver or peritoneal

metastases and invasion of major peripancreatic vessels [(36)].

At CEUS, ductal adenocarcinoma enhancement is poor in all contrast-enhanced phases

[Figure 12].


14/22


Figure 12 Ductal adenocarcinoma. Contrast-enhanced ultrasound transversal scan of thepancreatic head showing a markedly hypovascularized mass with upstream mainpancreatic duct dilation.

The margins and size of the lesion are more clearly visible. The depiction of tumoral margins

at CEUS is more accurate at a low enhancement of pancreatic adenocarcinoma [(37)], because

in cases of well-differentiated lesions the mass tends to be isovascular compared to the

remaining parenchyma and the margins of the tumor are no longer visualized. Relationship

with peripancreatic arterial and venous vessels can also be evaluated for local staging

[(26;27;37:38)].

The degree of tumoral differentiation of the adenocarcinoma influences the microvascular

density [(26;27;37:38)]. Moreover, the pattern of enhancement of pancreatic adenocarcinoma

influences the depiction of tumoral margins at CEUS [(37)].

After studying a pancreatic lesion during the arterial, pancreatic and venous phases, the

presence of liver metastases have to be excluded during the late phase [(26)].

Since US often represents the first technique performed, the use of CEUS will improve the

diagnostic accuracy when a focal hypoechoic solid lesion has been detected.

Endocrine tumors

Pancreatic endocrine tumors or islet cell tumors arise from the neuroendocrine cells of the

pancreas. These tumors are classified as functioning or nonfunctioning, based on the presence

or not of symptoms related to hormone production. Insulinomas and gastrinomas are the most

common functioning islet cell tumors and they are usually small at the time of diagnosis. The

other functioning neuroendocrine tumors (vipoma, glucagonoma and somatostatinoma) are

rare, account for about 20% of functioning neuroendocrine tumors of the pancreas [(39;40)].

Nonfunctioning tumors are frequently large at diagnosis [Figure 13a] and often malignant

[(41)].

Figure 13 Endocrine tumor (nonfunctioning). a) Ultrasound transversal scan of the pancreatichead shows large hypoechoic mass with well-defined margins and upstream mainpancreatic duct dilation. b) the lesion is hypervascular at contrast-enhancedultrasound.

a


15/22


b

Insulinomas are usually benign and solitary pancreatic lesions, while gastrinomas tend to be

malignant and multiple.

Insulinomas represent the most frequently found functioning neuroendocrine tumors of the

pancreas (about 60% of all neuroendocrine tumors), benign (85%99%) and single (93%

98%) [(42;43)] in the majority of cases. Insulinoma appears as hypoechoic pancreatic

nodules, usually capsulated.

At the time of clinical presentation 50% of the tumors are smaller than 1.5 cm [(40)]. When

malignant their diameter is generally >3 cm and about a third of these have metastases at the

time of diagnosis [(42;43)]. The mean diameter of insulinomas is


16/22


which only the pancreatic side is correctly explorable by US [(39;40)]. Identification of

pancreatic gastrinomas can be easy considering their moderate size [(40;45)]. Liver metastatic

lesions are present in 60% of cases at the time of diagnosis [(40;46)].

Nonfunctioning islet cell tumors represent up to 33% of neuroendocrine tumors of the

pancreas [(47)], ranging from 1 to 20 cm in diameter and showing a high malignancy rate, up

to 90% [(47;48)]. However they are less aggressive than adenocarcinomas. These tumors,characterized by predominantly expansive growth, are not clinically apparent until adjacent

viscera and structures have become involved. At US they appear well marginated and usually

easy to detect, thanks to their size. Due to their dimensions, necrosis and hemorrhage can be

present, developing a typical inhomogeneous appearance, sometimes accompanied by very

small intralesional calcifications. Larger nonfunctioning islet cell tumors show cystic

degeneration or cystic changes [(39)]. The finding of numerous intratumoral vascular spots is

typical of neuroendocrine pancreatic tumors at color-Doppler. In particular, a spot pattern

can be demonstrated in both large and small endocrine tumors [(39)]. However, while positive

Doppler results predict hypervascularization of the lesion, a Doppler silence can also be

present in hypervascular endocrine tumors because of the small size of the tumoral vascular

network.At CEUS, different enhancement patterns can be observed in relation to the size of tumors

and tumoral vessels. Voluminous endocrine tumors show a rapid and intense enhancement in

the early contrast-enhanced phase [Figure 13b], with the exception of necrotic intralesional

areas [(39;49;50]. In moderate-sized neuroendocrine pancreatic tumors, a capillary blush

enhancement can be present in the early contrast-enhanced phase, then becoming hypoechoic

in the late contrast-enhanced phase [(39;49;50].

Nonfunctioning neuroendocrine tumors can also be hypovascularized, depending on the

amount of stroma inside the lesion which is dense and hyalinized [(22)].

LymphomaPancreatic lymphoma is represented by the non-Hodgkin B-cell histotype and usually

associated with lymph nodes or lesions in other organs. US shows focal or diffuse pancreatic

enlargement, hypoechoic relative to the normal pancreatic parenchyma. [(36)]

Metastases

Pancreatic metastases are rare. Primary tumors that most frequently metastasize to the

pancreas are from lung, breast, kidney and the melanoma [(51)]. Pancreatic metastases can

appear as focal or multifocal, often as well demarcated lesions in patients with a known

primary neoplasm. [(36)].

CEUS may well demonstrate the enhancement of pancreatic metastases from renal cellcarcinoma, as they are clearly hypervascular, allowing differential diagnosis against ductal

adenocarcinoma. However, their features cannot be differentiated from that of endocrine

tumors and the differential diagnosis is therefore based on the clinical history and symptoms

and finally on cytology [(52;53)].

Pancreatic cystic neoplasm

Serous cystadenoma

Serous cystadenoma (SCA) is a benign lesion. It is usually located in the head of the pancreas

and generally characterized by tiny cysts of


17/22


glycogen-rich serous, transonic at US. If extremely microcystic SCA can have a solid

appearance at US and CT.

In up to 15% of cases, the tumor contains a central scar, which may calcify. US imaging can

show the microcystic appearance of this lesion related to the sponge macroscopic aspect. The

central scar, if present, is often visible as a central solid echogenic portion of the tumor,

sometimes containing calcifications. The contours of the SCA are always quite sinuous andthe wall is thin. The internal septa normally are well orientated and centrally directed,

reaching the central scar with a definitive typical aspect of the skeleton of this cystic lesion.

Numerous thin septa with a radial arrangement give to the lesion its typical microcystic

aspect.

SCAs do not communicate with the main pancreatic duct. The demonstration of that is

fundamental, especially when the lesion is large, because it might compress the main

pancreatic duct, so upstream dilated [36].

At CEUS, intralesional septa enhancement improves the identification of the microcystic

features of the lesion. The less common oligocystic or macrocystic types of serous

cystadenoma present features indistinguishable from those of the other macrocystic tumors of

the pancreas [(55;56)].

Mucin producing neoplasms

Mucin producing neoplasms of the pancreas may originate either from the peripheral ducts

(mucinous cystic tumors) or from the main pancreatic duct and its collateral branches

(intraductal papillary mucinous neoplasms; IPMNs) [(57)].

Mucinous cystoadenoma

Mucinous cystic neoplasm is a potentially malignant lesion. It is most often located in the

body or tail of the pancreas in middle-aged women. The content of the cyst is mucin. At US,

it appears as round or ovoid, usually unilocular lesionwith thick wall and septa andoccasionally peripheral calcifications. The mucinous content is viscous and may generate fine

echoes in the internal part of the lesion that covers the internal wall of the cystic tumor and

may hale the inclusion such as internal septa and/or solid papillary projections. The number

and the thickness of intralesional septa and nodules are not always related to the grade of

malignancy. Mucinous tumors may spread, involve lymph nodes and produce liver metastases

[(58;59].

CEUS may significantly improve the ultrasonographic detection of parietal nodules. The

vascularization of septa and nodules can be demonstrated beaming hyperechoic [Figure 14],

standing out against the lesional background, anechoic during the dynamic imaging.

Therefore CEUS examination improves ultrasonographic differential diagnosis between MCA

and pseudocyst, thanks to the identification and study of inclusions vascularization in cystic

masses of the pancreas [(60)].


18/22


Figure 14 Mucinous cystadenoma. Ultrasound oblique scan of the pancreatic body showsrounded cystic mass with small enhancing septa.

Mucinous cystoadenocarcinoma

Mucinous cystoadenocarcinoma represents the malignant neoplastic transformation of

mucinous cystoadenoma. Compared to the latter it is characterized by thicker wall and septa,

disomogeneous content and a greater number of nodules [Figure 15], whose significant cell

proliferation is responsible for wall and then peripheral structures invasion, leading to lymph

nodes involvement and liver metastases development [(58;59)].

Figure 15 Mucinous cystadenocarcinoma. Ultrasound oblique scan of the pancreatic bodyshows huge rounded cystic mass with thick wall and several enhancing septa andnodules.


19/22


IPMN

Intraductal papillary mucinous neoplasm (IPMN) is recognized as a dilation of the main

pancreatic duct and/or its branches or cyst formation with proliferation of pancreatic ductal

epithelium and excessive production of mucin. IPMNs are classified into the main duct type,

branch duct type, or a combination of the two [(61)]. The main duct type can be localized or

diffuse. The localized main duct type of IPMN is characterized by highly inhomogeneous

masses, related to neoplastic intraductal proliferation, with upstream dilation of the main

pancreatic duct. The diffuse main type may be difficult to distinguish from chronic

pancreatitis.

The branch duct mucinous tumor is characterized by cystic ectasia of one or more branches,

forming masses. At US examination the mucin of IPMN, especially the ductectatic mucin-

hypersecreting variant of the branch ducts, may not be easily differentiated from the solid

portions of the tumor, which can therefore be mistakenly reported as solid. Harmonic

imaging, with its better contrast resolution [(62;63)], may lead to better identify the non solid

part of the leison, thanks to the demonstration of more or less sharp intralesional interfaces.

However, at US, final diagnosis of IPMN by demonstrating the communication with thepancreatic duct is difficult [(64)].

CEUS examination of the IPMNs may allow identification of intraductal papillary tumoral

vegetations, especially in the papillary-villous variant, demonstrating its vascularization.

CEUS can be a safe method to follow-up the border-line lesions evaluating changes in

dimensions and vascularization of the inclusion. Considering that, in this setting, CEUS has

the great advantage of being a noninvasive and low-cost technique [(55)].

References

1.

Rumack C, Wilson SR, Charboneau JW. Diagnostic ultrasound. New York: Mosby YearBook 1991; 145177.

2. Mittelstaedt CA. Abdominal ultrasound. New York: Mosby 1987; 163176.3. Weissleder R, Rieumont MJ, Wittenberg J Primer of diagnostic imaging. 2nd ed. New

York: Mosby Year Book 1997; 220228.

4. Lorn I, Lasson A, Fork T, et al. New sonographic imaging observations in focalpancreatitis. Eur Radiol 1999; 9:862867.

5. DOnofrio M, Zamboni G, Tognolini A, Malag R, Faccioli N, Frulloni L, Pozzi MucelliR. Mass-forming pancreatitis: value of CEUS. World J Gastroenterol 2006; 12:4181

4184.

6. Numata K, Ozawa Y, Kobayashi N, Kubota T, Akinori N, Nakatani Y, Sugimori K,Imada T, Tanaka K. Contrast-enhanced sonography of autoimmune pancreatitis:comparison with pathologic findings. J Ultrasound Med 2004; 23:199206.

7. Freeny P, Lawson T. Radiology of the pancreas. New York: Springer-Verlag 1982, 449.8. Bolondi L. Sonography of chronic pancreatitis. Radiol Clin North Am 1989; 27:815833.9. Alpern MB, Sandler MA, Kellman GM, Madrazo BL. Chronic pancreatitis: ultrasonic

features. Radiology 1985; 155:215219.

10.Bolondi L, Priori P, Gullo L, et al. Relationship between morphological changes detectedby ultrasonography and pancreatic esocrine function in chronic pancreatitis. Pancreas

1987; 2:222229.

11.Lankisch PG, Banks PA Chronic pancreatitis: etiology. In: Lankisch PG, Banks PA (eds)Pancreatitis. New York: Springer Verlag 1998; 199208.


20/22


12.Lecesne R, Laurent F, Drouillard J, et al. Chronic pancreatitis. In: Baert AL, Delorme G,Hoe LVan (eds) Radiology of the pancreas. 2nd rev ed. New York: Springer Verlag 1999;

145180.

13.Husband JE, Meire HB, Kreel L. Comparison of ultrasound and computer tomography inpancreatic diagnosis. Br J Radiol 1977; 50:855863.

14.Remer EM, Baker MB. Imaging of chronic pancreatitis. Radiol Clin N Am 2002;40:12291242.15.Lees WR, Vallon AD, Denyer ME, et al. Prospective study of ultrasonography in chronic

pancreatic disease. BMJ 1979; 1:162164.

16.Foley WD, Stewart ET, Lawson TL, et al. Computer tomography, ultrasonography andechoscopic retrograde cholangiopancreatography in the diagnosis of pancreatic disease: a

comparative study. Gastrointestinal Radiol 1980; 5:2935.

17.Grant TH, Efrusy ME. Ultrasound in the evaluation of chronic pancreatitis. JAMA 1981;81:183188.

18.Homma T, Harada H, Koizumi M. Diagnostic criteria for chronic pancreatitis by the JapanPancreas Society. Pancreas 1997; 15:1415.

19.Niederau C, Grendell JH. Diagnosis of chronic pancreatitis. Gastroenterology 1985;88:19731995.

20.Hessel ST, Siegelman SS, McNeil BJ, et al. A prospective evaluation of computertomography and ultrasound of the pancreas. Radiology 1982; 143:129133.

21.Furukawa N, Muranaka T, Yasumori K, et al. Autoimmune pancreatitis: radiologicfindings in three histologically proven cases. J Comput Assist Tomogr 1998; 22:880883.

22.Faccioli N, Crippa S, Bassi C, D'Onofrio M. Contrast-enhanced ultrasonography of thepancreas. Pancreatology. 2009; 9(5):560-6.

23.Okazaki K. Autoimmune-related pancreatitis. Curr Treat Options Gastroenterol 2001;4:369375.

24.Kamisawa T, Yoshiike M, Egawa N, Nakajima H, Tsuruta K, Okamoto A. Treatingpatients with autoimmune pancreatitis: results from a long-term follow-up study.

Pancreatology 2005; 5:234240.

25.Kim T, Murakami T, Takamura M, Hori M, Takahashi S, Nakamori S, Sakon M, Tanji Y,Wakasa K, Nakamura H. Pancreatic mass due to chronic pancreatitis: correlation of CT

and MR imaging features with pathologic findings. AJR Am J Roentgenol 2001; 177:367-

371.

26.D'Onofrio M, Zamboni G, Faccioli N, Capelli P, Pozzi Mucelli R. Ultrasonography of thepancreas. 4. Contrastenhanced imaging. Abdom Imaging 2007; 32:171-181.

27.Takeda K, Goto H, Hirooka Y, Itoh A, Hashimoto S, Niwa K, Hayakawa T. Contrast-enhanced transabdominal ultrasonography in the diagnosis of pancreatic mass lesions.Acta Radiol 2003; 44:103-106.

28.Procacci C, Biasiutti C, Carbognin G, Capelli P, El-Dalati G, Falconi M, Misiani G,Ghirardi C, Zamboni G. Pancreatic neoplasms and tumor-like conditions. Eur Radiol

2001; 11Suppl2:S167-S192

29.Cubilla Al, Fitzgerald PJ. Tumors of the esocrine pancreas. 2nd Series. Ed. Washington,DC: Armed Forces Institute of Pathology 1984.

30.O Connor TP, Wade TP, Sunwoo YC, et al. Small cell undifferentiated carcinoma of thepancreas. Report of a patient with tumor marker studies. Cancer 1992; 70:1514-1519

31.Tryka AF, Brooks JR. Histopathology in the evaluation of total pancreatectomy for ductalcarcinoma. Ann Surg 1979; 190:373-381.

32.Yeo CJ, Cameron JL, Lillemoe KD, et al. Pancreaticoduodenoctomy for cancer of thehead of the pancreas. 201 patients. Ann Surg 1995; 221:721-733.
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Faccioli%20N%22%5BAuthor%5Dhttp://www.ncbi.nlm.nih.gov/pubmed?term=%22Crippa%20S%22%5BAuthor%5Dhttp://www.ncbi.nlm.nih.gov/pubmed?term=%22Bassi%20C%22%5BAuthor%5Dhttp://www.ncbi.nlm.nih.gov/pubmed?term=%22D%27Onofrio%20M%22%5BAuthor%5Dhttp://www.ncbi.nlm.nih.gov/pubmed?term=%22D%27Onofrio%20M%22%5BAuthor%5Dhttp://www.ncbi.nlm.nih.gov/pubmed?term=%22Bassi%20C%22%5BAuthor%5Dhttp://www.ncbi.nlm.nih.gov/pubmed?term=%22Crippa%20S%22%5BAuthor%5Dhttp://www.ncbi.nlm.nih.gov/pubmed?term=%22Faccioli%20N%22%5BAuthor%5D


21/22


33.Bertolotto M, D'Onofrio M, Martone E, Malag R, Pozzi Mucelli R. Ultrasonography ofthe pancreas. 3. Doppler imaging. Abdom Imaging 2007; 32:161-170.

34.Koito K, Namieno T, Nagakawa T, Hirokawa N, Ichimura T, Syonai T, Yama N, SomeyaM, Nakata K, Sakata K, Hareyama M. Pancreas: imaging diagnosis with color/power

Doppler ultrasonography, endoscopic ultrasonography, and intraductal ultrasonography.

Eur J Radiol 2001; 38:94-104.35.Ueno N, Tomiyama T, Tano S, Wada S, Miyata T. Color Doppler ultrasonography in the

diagnosis of portal vein invasion in patients with pancreatic cancer. J Ultrasound Med

1997; 16:825-830

36.A. Martnez-Noguera, M. DOnofrio Ultrasonography of the pancreas. 1. Conventionalimaging Abdom Imaging 2007; 32(2):136-149.

37.Faccioli N, DOnofrio M, Malag R, Zamboni G, Falconi M, Capelli P, Mucelli RP.Resectable pancreatic adenocarcinoma: depiction of tumoral margins at CEUS. Pancreas

2008; 37:265268.

38.Oshikawa O, Tanaka S, Ioka T, Nakaizumi A, Hamada Y, Mitani T. Dynamic sonographyof pancreatic tumors: comparison with dynamic CT. AJR Am J Roentgenol 2002;

178:11331137.39.DOnofrio M, Mansueto GC, Falconi M, Procacci C. Neuroendocrine pancreatic tumor:

value of contrast enhanced ultrasonography. Abdom Imaging 2004; 29:246258.

40.Ros PR, Mortele KJ. Imaging features of pancreatic neoplasms. JBR-BTR 2001;84(6):239249.

41.Buetow PC, Miller DL, Parrino TV. Islet cell tumors of the pancreas: clinical, radiologic,and pathologic correlation in diagnosis and localization. Radiographics 1997; 17:453

472.

42.Liu TH, Tseng HC, Zhu Y. Insulinoma. An immunohistochemical and morphologicanalysis of 95 cases. Cancer 1985; 56:14201429.

43.Stefanini P, Carbonni M, Patrassi N. Beta islet-cell tumors of the pancreas: result of astudy on 1067 cases. Surgery 1974; 75:597.

44.Pereira PL, Wiskirchen J. Morphological and functional investigations of neuroendocrinetumors of the pancreas. Eur Radiol 2003; 13(9):21332146.

45.Semelka RC, Cumming MJ, Shoenut JP, Magro, et al. Islet cell tumors: comparison ofdynamic contrast-enhanced CT and MR imaging with dynamic gadolinium enhancement

and fat suppression. Radiology 1993; 186(3):799802.

46.Mergo PJ, Helmberger TK, Buetow PC, et al. Pancreatic neoplasm: MR imaging andpathologic correlation. Radiographics 1997; 17:281301.

47.Fugazzola C, Procacci C, Bergamo Andreis IA, Iacono C, et al. The contribution ofultrasonography and computed tomography in the diagnosis of nonfunctioning islet cell

tumors of the pancreas. Gastrointest Radiol 1990; 15(2):139144.48.Eckhauser FE, Cheung PS, Vinik AI, et al. Nonfunctioning malignant neuroendocrinetumors of the pancreas. Surgery 1986; 100:978988.

49.Malag R, DOnofrio M, Zamboni GA, Faccioli N, Falconi M, Boninsegna L, MucelliRP. Contrast-enhanced sonography of nonfunctioning pancreatic neuroendocrine tumors.

AJR Am J Roentgenol 2009; 192:424430.

50.DOnofrio M, Malag R, Zamboni G, Vasori S, Falconi M, Capelli P, Mansueto G. CEUSbetter identifies pancreatic tumor vascularization than helical CT. Pancreatology 2005;

5:398402.

51.Merkle EM, Braz T, Kolkythas O, et al. Metastases to the pancreas. Br J Radiol 1998;71:12081214.


22/22


52.Flath B, Rickes S, Schweigert M, Lochs H, Possinger K, Wermke W. Differentiation of apancreatic metastasis of a renal cell carcinoma from a primary pancreatic carcinoma by

echo-enhanced power Doppler sonography. Pancreatology 2003; 3:349-351.

53.Megibow AJ. Secondary pancreatic tumors: imaging. In:Procacci C, Megibow A, editors.Imaging of the pancreas: cystic and rare tumors. Berlin: Springer-Verlag 2003; 277-288.

54.Procacci C. Pancreatic neoplasms and tumor-like conditions. Eur Radiol 2001;11Suppl2:S167S192.55.DOnofrio M, Megibow AJ, Faccioli N, Malag R, Capelli P, Falconi M, Mucelli

RP:.Comparison of contrast-enhanced sonography and MRI in displaying anatomic

features of cystic pancreatic masses. AJR Am J Roentgenol 2007; 189:14351442.

56.DOnofrio M, Caffarri S, Zamboni G, Falconi M, Mansueto G. CEUS in thecharacterization of pancreatic mucinous cystadenoma. J Ultrasound Med 2004; 23: 1125

1129.

57.Procacci C, Graziani R, Bicego E, et al. Intraductal mucinproducing tumors of thepancreas: imaging findings. Radiology 1996; 198:249257.

58.Tham RT, Heyerman HG, Falke TH, et al. Cystic fibrosis: MR imaging of the pancreas.Radiology 1991; 179:183186.

59.Ros PR, Hamrick-Turner JE, Chiechi MV, et al. Cystic masses of the pancreas.Radiographics 1992; 12:673686.

60.DOnofrio M, Zamboni G, Malago` R, Martone E, Falconi M, Capelli P, Mansueto G.Pancreatic pathology. In: Quaia E (ed) Contrast media in ultrasonography. Springer-

Verlag: Berlin 2005; 335347.

61.Procacci C, Megibow AJ, Carbognin G, et al. Intraductal papillary mucinous tumor of thepancreas: a pictorial essay. Radiographics 1999; 19:14471463.

62.Shapiro RS, Wagreich J, Parsons RB, et al. Tissue harmonic imaging sonography:evaluation of image quality compared with conventional sonography. AJR 1998;

171:1203-1206.

63. Bennett GL, Hann LE. Pancreatic ultrasonography. Surg Clin North Am 2001; 81:259281.

64.Procacci C, Schenal G, Dalla Chiara E, et al. Intraductal papillary mucinous tumors:imaging. In: Procacci C, Megibow AJ (eds) Imaging of the pancreas cystic and rare

tumors. Berlin: Springer Verlag 2003; 97137.

Documents

Ecb Ch04 Pancreas