). The midgut (which includes the duodenum) then rotates clockwise, and the ventral bud rotates along with it and fuses with the dorsal pancreatic bud from behind. The fused pancreas now lies completely to the left of the duodenum. The dorsal duct (duct of Santorini∗) from the original dorsal bud now drains the tail, body, and upper head and for a while drains into the minor papilla. The ventral duct (from the original ventral bud), also known as duct of Wirsung,† drains the lower head and uncinate into the major papilla along with the common bile duct. Normally, the ventral and proximal dorsal ducts fuse to form the main pancreatic duct, which drains into the major papilla (papilla of Vater). The remaining distal remnant of the dorsal duct usually regresses and drains into the accessory duct of Santorini.
Figure 9-1 Schematic representation of embryological development of the pancreas. The ventral and dorsal buds are originally separate (A). The ventral pancreas then rotates clockwise to fuse with the dorsal pancreas (B and C).
Annular Pancreas
Annular pancreas is a rare anomaly resulting from abnormal or failed rotation of the ventral bud and/or rotation of the duodenum embryologically (Fig. 9-2) such that the bud fails to achieve its position to the left of the duodenum and instead forms a partial or complete ring of pancreatic tissue around the second part of the duodenum. It can also result when the bifid ventral ducts encircle the duodenum rather than fuse together. Many patients are asymptomatic, but annular pancreas can present early in childhood because it is commonly associated with other congenital atretic anomalies, including those of the esophagus, duodenum, and anus. Furthermore, the resulting ring can cause duodenal strictures, which if severe can be recognized in the neonate because of copious vomiting from duodenal obstruction, often requiring surgery to remove the stricture. Presentation in adults is usually after repeated episodes of epigastric pain, early satiety, and vomiting from subacute duodenal obstruction.
Figure 9-2 Schematic representation of an annular pancreas. The ventral pancreas rotates abnormally to variable degrees and either partially or whole envelops the second part of the duodenum.
The diagnosis was formerly made with an upper gastrointestinal (GI) series, in which the second part of the duodenum appears strictured to a variable degree depending on the degree of the anomaly and associated with loss of the normal duodenal fold pattern (Fig. 9-3). Depending on the degree of stricture formation, the proximal duodenum may be distended or dilated. However, annular pancreas is now detected primarily by CT because of its increased use. The CT findings are characteristic of pancreatic tissue passing to the right and encircling the second part of the duodenum, which is sometimes better visualized on multiplanar imaging (Fig. 9-4). The diagnosis can also be made with ERCP that shows the ventral duct (Wirsung) completely encircling the duodenum. Annular pancreas is associated with an increased incidence of pancreatitis and peptic ulcer disease, both of which may be identified by CT.
Figure 9-3 Upper GI series in a 44-year-old woman with narrowing of the second part of the duodenum (arrow) caused by an annular pancreas.
Agenesis of the Dorsal Pancreas
Complete pancreatic agenesis, defined as absence of the neck, body, tail, duct of Santorini, and minor papilla, is extremely rare, particularly because many with this condition are stillborn or die of multiple other congenital anomalies as neonates. More commonly the agenesis is partial, with the neck, body, or tail missing (Figs. 9-5 and 9-6). Many patients are asymptomatic, but if present, symptoms include abdominal pain and an increased incidence of pancreatitis. Depending on the degree of agenesis, patients can also present with pancreatic insufficiency (diabetes mellitus and steatorrhea).
Figure 9-5 Axial contrast-enhanced CT in a 38-year-old woman with a congenitally short pancreas and missing tail (arrow).
Figure 9-6 Axial contrast-enhanced CT in a 41-year-old woman with a pancreatic uncinate (arrow) but no body or tail because of partial agenesis.
On imaging, pancreatic agenesis can be identified by a short pancreas, but the findings may be subtle. ERCP or MCRP, which will identify a ventral (Wirsung) duct but little or no accessory (Santorini) duct, confirms the diagnosis.
Pancreas Divisum
Pancreas divisum is far more common than other pancreatic anomalies, with up to 10% of the population showing some variant, depending on the degree of ductal fusion anomalies. Essentially, despite normal rotation of the ventral bud, its duct (Wirsung) fails to fuse appropriately with the dorsal duct (Santorini), so a single pancreatic duct is not formed (Fig. 9-7). With complete lack of fusion, the dorsal duct now drains exclusively into the minor papilla, which remains patent, and the body and upper pancreatic head drain through the minor papilla. The ventral duct continues to drain into the major papilla, draining the uncinate and lower half of the pancreatic head.
Figure 9-7 Axial and coronal contrast-enhanced CT in a 76-year-old man with pancreas divisum. The minor pancreatic duct (Santorini; large arrow) remains anterior to the bile duct and major pancreatic duct (Wirsung; small arrow).
Many patients are asymptomatic, but others have intermittent pain, which usually appears between 30 and 50 years of age and results from mild and occasionally severe pancreatitis, possibly because of the restricted drainage of the bulk of pancreatic fluid through the smaller minor papilla. Therefore pancreatitis, when present, is usually of the neck, body, and tail, although pancreatitis of the uncinate caused by reflux of bile into a short ventral duct can also occur.
The diagnosis of pancreas divisum can be challenging. At ERCP, injection of contrast material into the major papilla opacifies only the duct of Wirsung (Fig. 9-8). Ideally the minor papilla is also cannulated, but because of its small size, this sometimes fails. Should it prove successful, a long dorsal, noncommunicating duct is outlined. Imaging with MRCP, which demonstrates the anatomical anomaly in most patients noninvasively, may therefore be preferable (Fig. 9-9). Imaging with CT is less sensitive, and the anomaly is often missed unless the pancreatic ductal anatomy is closely scrutinized. The pancreatic head may be enlarged, and sometimes there is a subtle fatty cleft between the uncinate process and the remaining pancreas, but this is rarely observed and nonspecific. With thin-section and multiplanar imaging, the two distinct noncommunicating ducts can be observed (Fig. 9-10). Evidence of pancreatitis, a relatively common feature of pancreas divisum, may also be present (Fig. 9-10).
Figure 9-8 A and B, ERCP in a 53-year-old man with initial injection into the major duodenal papilla outlining only the duct of Wirsung (arrow). Subsequent cannulation of the minor papilla fills a dilated duct of Santorini (small arrow) owing to chronic pancreatitis resulting from pancreatic divisum. There are changes of chronic pancreatitis with a dilated irregular duct of Santorini.
Figure 9-9 MRCP in a 43-year-old woman demonstrating drainage of the duct of Santorini (small arrow) via the minor papilla duct of Wirsung into the common bile duct and major papilla (large arrow).
Figure 9-10 Axial contrast-enhanced CT in a 43-year-old woman with pancreatic divisum and pancreatic head enlargement, peripancreatic inflammation, and calcification caused by an acute flare-up of chronic pancreatitis from pancreatic divisum. The ventral duct (small arrow) is just identifiable separate from the dorsal duct (large arrow).
Secretin Stimulation Test
The secretin stimulation test is designed to determine any functional obstruction of the pancreatic duct. Secretin is a powerful hormonal stimulant for pancreatic bicarbonate production (required for duodenal neutralization of gastric acid). When injected, it causes a temporary increase in the production and therefore volume of pancreatic fluid, which should pass normally into the duodenum. Typically, in the healthy patient, after 0.4 µg/kg is injected, the duct dilates slightly (from a normal 1 to 3 mm to between 4 and 6 mm) but returns rapidly to normal. Conversely, the duct remains dilated for up to 30 minutes in the presence of a functional obstruction. Measurements are made using US or, more commonly, coronal MRCP (Fig. 9-11).
Figure 9-11 Secretin MRCP in a 63-year-old woman with papillary dysfunction. The pancreatic duct (small arrow) measured 3 mm at baseline (A), which increased to 5 mm at 5 minutes (B) and returned to 3 mm at 10 minutes (C). The distal duct is tortuous (large arrow) due to previous episodes of pancreatitis.
Ectopic Pancreas
The true incidence of ectopic pancreas is unknown, but some figures put the incidence surprisingly at 10% of the population, although the condition is rarely seen in clinical practice. Ectopic pancreas is also known as pancreatic rest or aberrant pancreas. Small areas of pancreatic tissue come to “rest” in an ectopic position, usually in the distal gastric antrum along the greater curvature or near the pancreatic ampulla in the second portion of the duodenum. They can, however, be detected in more disparate locations, including other intestinal locations and even the pelvis, liver, and spleen.
Patients are usually asymptomatic, but ectopic pancreas can cause gastric or duodenal hemorrhage and, if large enough, biliary obstruction or even small bowel intussusception. Rests that are identified at imaging are usually in the expected location of the stomach or duodenum and found mostly with upper GI series because they are too small to be identified by cross-sectional imaging techniques (although they may be inferred from the presence of a small hypodense and cystic mass). The characteristic appearance is of a 1- to 2-cm submucosal mass, either round or eccentric in shape, sometimes lobular, with a central pit or depression that fills with contrast material in the dependent position.
Fatty Pancreatic Replacement
Fatty pancreatic replacement can be a normal aging process as the pancreas becomes increasingly atrophic and fatty replaced (Fig. 9-12).
Figure 9-12 Axial noncontrast CT in a 79-year-old woman with an age-related atrophic fatty-replaced pancreas (small arrows) that has tiny punctate calcifications (arrows).
Cystic Fibrosis
Cystic fibrosis is an autosomal-recessive disease with a number of abdominal complications, including diffuse pancreatic insufficiency when severe. The pancreatic tissue becomes largely fatty replaced, sometimes with small cystic change. On US the fatty change is hyperechoic, but on CT the pancreas is partially replaced by fat (Fig. 9-13) or may not be seen at all, the fatty replacement merging into the surrounding retroperitoneal fat (Fig. 9-14). Other features may include small bowel dilatation and cecal thickening (see discussion in Chapters 4, on the small bowel, and 5, on the colon). The pancreas in cystic fibrosis can also become diffusely calcified or undergo cystosis (see later in the chapter).
Figure 9-13 Axial contrast-enhanced CT in a 24-year-old woman with a partially fatty-replaced pancreas (arrow) resulting from cystic fibrosis. The pancreatic head and uncinate are normal (small arrow).
Figure 9-14 Axial noncontrast CT in a 39-year-old man with cystic fibrosis and complete pancreatic fatty replacement (arrows).
Uneven Lipomatosis
Fatty pancreatic replacement can be either diffuse (Fig. 9-15) or focal, termed “uneven” (Fig. 9-16). It is of little clinical significance, except that it has been associated with pancreas divisum and can be confused with a pancreatic neoplasm. Fat-suppressed MRI can be helpful in distinguishing between the two.
Figure 9-15 Transverse US of the pancreas in a 44-year-old woman with diffuse echogenicity (arrows) secondary to a fatty pancreas.
Figure 9-16 Axial contrast-enhanced CT in a 65-year-old man demonstrating a nondeforming hypodense anterior pancreatic head (arrows) consistent with uneven lipomatosis.
Pancreatic Lipomatous Pseudohypertrophy
Pancreatic lipomatous pseudohypertrophy is of unknown but possibly congenital origin, causes pancreatic hypertrophy with focal or diffuse fatty replacement, and is readily identified with CT or MRI (Fig. 9-17). It is, however, often associated with chronic liver disease (i.e., cirrhosis), which may therefore be contributory. It is also associated with cystic fibrosis but should be distinguished from diffuse pancreatic fatty replacement, which is also seen in cystic fibrosis but shows no pancreatic hypertrophy.
Figure 9-17 Axial noncontrast CT in a 28-year-old woman with cystic fibrosis and diffusely enlarged fatty pancreas (arrows) caused by pancreatic lipomatous pseudohypertrophy.
Pancreatic Lipoma
Lipomas are very rare in the pancreas, being much more common in the intestinal tract. In the pancreas, as elsewhere, lipomas are relatively straightforward to diagnose with CT because of their fat content, which is confined to the pancreas and is well circumscribed (Fig. 9-18).
Figure 9-18 Axial contrast-enhanced CT in a 44-year-old woman with a 4-cm pancreatic hypodense fatty mass (arrow) that represents a pancreatic lipoma.
Pancreatitis
Pancreatitis represents acute or chronic inflammation of the pancreas caused by release of pancreatic enzymes, mainly trypsin, into the pancreatic parenchyma rather than the duodenum. Pancreatitis has numerous precipitating factors (Box 9-1), but gallstones cause the majority of cases of acute pancreatitis, whereas alcohol is mainly responsible for chronic pancreatitis. The diagnosis is based on the clinical history, elevated serum amylase and lipase levels, and imaging. However, clinical symptoms and presentation vary widely and range from mild to severe. Patients with milder forms present with pain, vomiting, and abdominal tenderness, whereas those with severe forms present with shock, organ failure, and hemorrhage. The severe hemorrhagic clinical signs have been well recognized for more than a century. Grey Turner∗ sign is flank bruising, and Cullen† sign is periumbilical bruising, resulting from acute pancreatitis. Clinical severity is ranked by either Ranson or APACHE II criteria.
Many patients with pancreatitis have no imaging abnormalities. When pancreatitis is more severe, however, plain radiographs may demonstrate ileus, particularly a sentinel loop, representing a distended loop of small bowel immediately adjacent to the inflamed pancreas. A colon “cut-off” sign represents a distended transverse colon, with paucity of air from the splenic flexure distally because of colonic spasm (Fig. 9-19). Upper GI studies often demonstrate thickened and spiculated duodenal and gastric folds representing secondary edematous transmural enteric changes (Fig. 9-20). On US the pancreas can appear enlarged with a heterogeneous echo texture mixed with prominent hypoechoic regions (Fig. 9-21), although contrast-enhanced CT is usually performed to evaluate pancreatitis. Not all patients with clinical and biochemical pancreatitis have abnormal CT findings, although the majority of patients show abnormalities to a variable degree. The pancreas is typically enlarged, sometimes focally, with effacement of the normal indented pancreatic border combined with peripancreatic edematous changes (Fig. 9-22). The latter can be severe with widespread edema throughout the retroperitoneal space, producing single or multiple acute fluid collections (Fig. 9-23). Sometimes pancreatic adenocarcinoma has a similar appearance, and a useful CT sign is preservation of perivascular fat planes (unlike pancreatic adenocarcinoma, in which they are often obliterated), which strongly favors a benign diagnosis (Fig. 9-24). The reverse is not always true in that the peripancreatic inflammation in severe pancreatitis can sometimes obliterate this fat plane. Unless contraindicated, contrast-enhanced CT is administered to evaluate the vascular viability of the pancreatic parenchyma. Pancreatic necrosis is recognized by single or multiple focal hypodensities (or diffuse depending on the severity) surrounded by normally enhancing pancreas (Fig. 9-25). These hypodensities represent the hypovascularized or nonvascularized pancreatic parenchyma, which has been destroyed by the acute inflammatory process. Depending on the degree of pancreatic necrosis, it may be termed necrotizing pancreatitis if more than 50% of the gland is involved.
Figure 9-19 CT scout view in a 43-year-old man with distended transverse colon (small arrows) and a colon cut-off sign (arrow).
Figure 9-20 Upper GI series in a 66-year-old man with a “puckered” appearance to the greater curvature of the stomach (arrows) caused by inflammation from pancreatitis.
Figure 9-21 Transverse US in a 17-year-old male with acute pancreatitis, demonstrating an edematous, heterogeneously enlarged pancreas (arrows) with anterior peripancreatic fluid (small arrow).
Figure 9-22 Axial contrast-enhanced CT in a 37-year-old man with hypertriglyceridemia-induced pancreatitis. The liver is markedly fatty, and pancreatic enlargement without necrosis (small arrow) and diffuse peripancreatic inflammation (large arrow) are present.
Figure 9-23 Axial contrast-enhanced CT in a 27-year-old man with acute pancreatitis demonstrating evolution of acute pancreatitis. A, Enlarged and inflamed pancreas (arrows) with diffuse peripancreatic inflammation (small arrows). B, Axial contrast-enhanced CT 1 month later demonstrating partial necrosis and partial loss of pancreatic tail (small arrow) and an organizing peripancreatic collection (arrows). C, Axial contrast-enhanced CT 2 months after B, demonstrating pancreatic body and tail of formation of a capsule (arrow) around the peripancreatic collection as a result of pseudocyst formation.
Figure 9-24 Axial contrast-enhanced CT in a 38-year-old man with acute pancreatitis and preservation of the fat plane (large arrow) surrounding the superior mesenteric artery (small arrow).
Figure 9-25 Transverse US (A) and axial (B) and coronal (C) contrast-enhanced CT in an 80-year-old man with acute pancreatitis. The pancreas is enlarged (arrows) and markedly heterogeneous at US with an anterior peripancreatic acute fluid collection (small arrows) confirmed by CT. CT also demonstrates almost complete pancreatic necrosis (arrowheads), except for the pancreatic tail (thin arrows), and a large peripancreatic acute fluid collection (small arrows).
Documentation of pancreatic necrosis is critical because it places the patient in a much higher risk category than those with simple fluid collections. Necrotic areas can also become infected, which has an even higher mortality rate. Surgical debridement is the treatment of choice. Necrosis is usually associated with pancreatic and peripancreatic fluid collections (Figs. 9-23 through 9-25). There may be evidence of acute fluid collections in the retroperitoneum, which may also become infected and form an abscess. If contrast material is not administered, the pancreas is typically diffusely hypodense. MRI also demonstrates an enlarged gland with areas of necrosis that fail to enhance after IV administration of contrast medium. The terminology used in pancreatitis is defined in Table 9-1.
Table 9-1
Definition of Findings in Pancreatitis
| Pancreatic necrosis | Single or multiple nonenhancing intrapancreatic regions (necrotizing pancreatitis with >50% necrosis). |
| Exudative pancreatitis | Predominantly peripancreatic fluid collections with normally enhancing pancreas. It is synonymous with peripancreatic fat necrosis. |
| Acute fluid collection | Intrahepatic or extrahepatic fluid collections without defined wall in acute phase. Caused by inflammation or peripancreatic fat necrosis. May or may not be infected. |
| Pseudocyst | Fluid collection with defined fibrous capsule; develops 4-6 weeks after acute event. May or may not be infected. |
The severity of acute pancreatitis can be staged by contrast-enhanced CT (Table 9-2) and corresponds reasonably closely to the clinical course. When the percentage of gland necrosis is also included (0 to 30%, 30% to 50%, >50%), a CT severity index can be calculated, which corresponds even more closely to the clinical course (Table 9-3). However, the CT severity index does not always match the clinical course, and therefore its use in clinical practice is variable. The most important CT finding is pancreatic necrosis, which markedly increases morbidity and mortality rates associated with disease. Acute hemorrhagic pancreatitis is a particularly severe form of pancreatitis with, as its name suggests, hemorrhage within the pancreas (which might not be recognized if IV contrast medium has been administered) along with diffuse pancreatic inflammation, enlargement, and necrosis. Splenic and portal vein thromboses (Fig. 9-26) and aneurysm formation, particularly of the splenic artery (Fig. 9-27), are other recognized complications of severe pancreatitis.
Table 9-2
CT Staging of Pancreatitis
Table 9-3
CT Severity Index
| Index Point | Necrosis |
| 0 | None |
| 2 | 0-30% |
| 4 | 30%-50% |
| 6 | >50% |
Figure 9-26 Axial contrast-enhanced CT in a 53-year-old woman with complete thrombosis of the splenic and superior mesenteric veins (arrows) secondary to acute pancreatitis.
Figure 9-27 Axial contrast-enhanced CT in a 44-year-old woman with a 6-cm hyperenhancing left upper quadrant mass due to a splenic artery aneurysm (arrow) as a complication of acute pancreatitis.
Mild or moderate pancreatitis usually involves pancreatic inflammation and enlargement that may or may not be focal (grades B and C). With more severe forms, peripancreatic fluid collections develop acutely, representing pancreatic fluid collections. Unlike chronic fluid collections (pseudocyst), they have no encapsulation or wall (Fig. 9-23). These collections can also occur within the pancreas or in other retroperitoneal locations. Many resolve spontaneously, but approximately 50% evolve into pseudocysts (see below).
Pancreatic Pseudocyst
Pancreatic pseudocyst is a complication of pancreatitis (usually acute but also chronic) and is defined as a well-circumscribed, rounded, and fibrous encapsulated pancreatic or peripancreatic fluid collection, rich in blood, necrotic material, and pancreatic enzymes. A pancreatic pseudocyst can be hard to differentiate from acute fluid collections, so the diagnosis is usually made by temporally relating the finding to the onset of symptoms. There is no radiological definition as to when an acute fluid collection becomes a pseudocyst, although the surgical definition is 6 weeks from the onset of symptoms. If ERCP is performed, a connection with the pancreatic duct is seen in up to 50% of patients.
Patients often have upper abdominal pain (radiating to the back) and, because pseudocysts can be quite large, a palpable mass. About 50% of pseudocysts resolve spontaneously with no treatment. Approximately 20% remain without further complications, but about 30% cause local complications, including erosion or dissection into adjacent organs, hemorrhage (erosion into vessels), aneurysm formation, rupture and peritonitis, and duodenal or biliary obstruction. Pseudocysts can also become infected and develop into pancreatic abscesses. These can be suitably drained percutaneously, unlike infected necrosis, which requires surgical debridement.
At imaging by CT, a rounded homogeneous hypodense and encapsulated mass is seen (acute fluid collections are not encapsulated) (Fig. 9-28). If the pseudocyst has become secondarily infected (with or without gas) or undergone hemorrhage, the contents of the mass may be heterogeneous. The fibrous rim usually shows fine enhancement on contrast-enhanced CT. MRI features match the CT findings, with hypointense contents on T1-weighted imaging and hyperintense contents on T2-weighted imaging (Fig. 9-29). Less commonly, US is performed, the results of which usually show the cyst filled with complex echoes because of the internal debris and blood.
Figure 9-28 Axial (A) and coronal (B) contrast-enhanced CT in a 44-year-old woman with a 10-cm well-contained encapsulated fluid collection (arrows) representing a pancreatic pseudocyst.
Figure 9-29 Axial T2-weighted (A) and coronal T1-weighted (B) fat-saturated postcontrast MRI in a 53-year-old man with a 5-cm pancreatic pseudocyst (arrows).
Chronic Pancreatitis
Chronic pancreatitis, as its name suggests, is secondary to repeated bouts of acute pancreatitis, most often in unremitting alcoholics, although many of the causes of acute pancreatitis are also responsible for chronic pancreatitis (Box 9-1). The episodes of pancreatitis range from mild to severe, but the repeated injury to the pancreas ultimately takes its toll with irreversible parenchymal damage. Patients usually admit to episodes of acute pancreatitis and have recurrent or chronic abdominal pain, sometimes jaundice, and signs of pancreatic insufficiency (diabetes mellitus, steatorrhea) with malabsorption and weight loss. Serum amylase and lipase levels are typically elevated, although not usually to the degree seen in acute pancreatitis. The secretin stimulation test by ERCP has high sensitivity for the diagnosis but is not often performed, having been replaced by US or an MRCP technique (Fig. 9-11). Because of pancreatic dysfunction, pancreatic duct bicarbonate production is decreased.
In addition to the clinical features, the diagnosis is often made by cross-sectional imaging, although plain radiography may show diffuse pancreatic calcification (Fig. 9-30) and upper GI studies may show thickened duodenal folds and luminal narrowing. On CT there is usually diffuse dystrophic calcification (Fig. 9-31) within an atrophic gland and a dilated pancreatic duct, which may also contain calcifications or stones. Pancreatic enhancement is variable depending on the degree of fibrosis. The chronic inflammatory change often causes splenic vein thrombosis and consequent splenic varices and splenomegaly. Sometimes intrapancreatic or extrapancreatic pseudocysts are observed. Findings at ERCP include a dilated irregular duct, sometimes beaded in both the main and side branches (Fig. 9-32), although the duct can also be narrowed, usually tapered rather than abruptly constricted as is seen in pancreatic adenocarcinoma. Both the pancreatic duct and bile duct may be strictured in the head of the pancreas, giving a “double-duct” appearance in which there is proximal biliary and pancreatic duct dilatation to the stricture in the pancreatic head. This feature is far more commonly associated, however, with pancreatic carcinoma. Filling defects are usually secondary to pancreatic stones.
Figure 9-30 Plain abdominal radiograph and axial contrast-enhanced CT in a 47-year-old woman with chronic pancreatitis and diffuse pancreatic calcification (arrows). A plastic biliary stent (small arrow) is present because of an inflammatory biliary stricture.
Figure 9-31 Axial contrast-enhanced CT in a 42-year-old man with an acute episode of chronic pancreatitis, demonstrating diffuse pancreatic calcification (large arrow), peripancreatic inflammatory changes (small arrow), and a focally enlarged pancreatic duct (arrowhead). Splenomegaly is caused by chronic splenic vein thrombosis.
Figure 9-32 ERCP (A) and axial contrast-enhanced CT (B) in a 55-year-old man with a diffusely dilated and irregular pancreatic duct (arrows) from chronic pancreatitis.
Autoimmune Pancreatitis
Autoimmune pancreatitis is a poorly understood entity that is also a form of chronic pancreatitis but with no discrete cause. Most patients have elevations of immunoglobulin 4 (IgG4) levels (a specific sign for the disease) and antinuclear antibody levels, which are associated with many other autoimmune diseases, hence the term autoimmune pancreatitis. The pancreas is filled with a lymphoplasmocytic infiltrate. Characteristically, the normal lobulated pancreatic external contour is effaced, producing a more tubular or sausage-shaped outline (Fig. 9-33). Usually the whole gland is affected, but the disease can be focal (Fig. 9-34). After IV contrast administration at CT, capsule-like enhancement that surrounds a low-density band or halo is demonstrated (Fig. 9-35). Peripancreatic adenopathy or inflammatory lesions elsewhere are sometimes observed (Fig. 9-36). The pancreatic duct, if evaluated with ERCP or MRCP, is typically irregularly narrowed and strictured, which may also affect the intrahepatic ducts and resemble primary sclerosing cholangitis.
Figure 9-33 Axial (A) and coronal (B) contrast-enhanced CT in a 32-year-old man with a diffusely enlarged pancreas (arrows) and subtle peripancreatic inflammation caused by autoimmune pancreatitis. The pancreas is sometimes described as “sausage” shaped.
Figure 9-34 Axial contrast-enhanced CT in a 29-year-old woman with smooth enlargement of the pancreatic tail caused by autoimmune pancreatitis with a sharp margination from the normal pancreas (arrow).
Figure 9-35 Axial contrast-enhanced CT in a 62-year-old man with raised IgG4 levels showing a smoothly enlarged body and tail of the pancreas with a peripancreatic halo (arrow) characteristic of autoimmune pancreatitis.
Figure 9-36 Axial contrast-enhanced CT in a 46-year-old woman with an enlarged and heterogeneous pancreatic body and tail (large arrow) and hypodense hepatic IgG4 inflammatory pseudotumors (small arrows) concomitant with autoimmune pancreatitis.
Chronic Segmental Pancreatitis (Groove Pancreatitis)
Chronic segmental pancreatitis is a specific form of chronic pancreatitis confined to the pancreaticoduodenal groove (hence its common name “groove pancreatitis”), defined as the area between the head of the pancreas and the second portion of the duodenum. Its exact cause is unknown, but it is associated with excessive and chronic alcohol abuse (similar to chronic pancreatitis), minor papilla strictures (either congenital or caused by neoplasm), and chronic inflammation of the lower common bile duct resulting from prior surgery. Most patients present between 30 and 50 years of age with postprandial pain and vomiting and sometimes with weight loss and mild jaundice. In the correct clinical setting the imaging features at CT are highly suggestive, with separation between the head of the pancreas and the duodenal C-loop because of an intervening hypodense inflammatory mass (or hypointense on T1-weighted MRI) that is often associated with cystic change (Fig. 9-37).
Figure 9-37 Axial contrast-enhanced CT in a 47-year-old woman with diffuse inflammation (arrows) in the duodenal pancreatic groove caused by “groove” pancreatitis.
Solid Pancreatic Mass Lesions (Box 9-2)
Pancreatic Adenocarcinoma
Pancreatic adenocarcinoma is the most common pancreatic neoplasm (90% of malignant pancreatic tumors) and the fourth most common cause of cancer death in the United States. Patients with this type of cancer still have a dismal prognosis (20% 5-year survival rate with surgery and 5% without). The tumor arises from the ductal epithelium of the exocrine pancreas, with two thirds in the head and the remainder in the body and tail. Patients are typically in their seventies and generally present with central abdominal or back pain, weight loss, and jaundice. The Courvoisier∗ sign is painless jaundice in the presence of a distended and palpable gallbladder secondary to biliary obstruction, an ominous sign. Rarer presentations include GI bleeding, diabetes mellitus, and pancreatitis. Pancreatic adenocarcinoma is staged according to the TNM classification (Table 9-4).
Table 9-4
TNM Classification of Pancreatic Adenocarcinoma
SMA, Superior mesenteric artery; SMV, superior mesenteric vein.
A primary reason for the grim prognosis is that most patients present late, when the tumor is already advanced and inoperable. This is compounded by the difficulty in detecting small lesions at imaging. Lesions less than 2 cm are notoriously difficult to detect, even with a dedicated pancreatic CT protocol. However, contrast-enhanced CT is still the initial imaging investigation of choice. The key to maximizing lesion detection and assessing resectability is pancreatic-phase scanning, which maximizes normal pancreatic parenchymal enhancement while the pancreatic tumor remains relatively unenhanced. This increase in tumor conspicuity is best evaluated with a 40- to 45-second scan delay after the initiation of IV contrast material. At that time, celiac and superior mesenteric arteries are well enhanced, so that local encasement by tumor can also be assessed (Fig. 9-38). Furthermore, sufficient delay for the mesenteric veins to be opacified has usually occurred, so any vascular encasement can be evaluated at the same time. Portal venous–phase scanning at 60 to 70 seconds adds additional diagnostic information about the mesenteric veins and, more important, about the presence of any potential hepatic metastases that were not optimally imaged during the earlier pancreatic-phase scanning.
Figure 9-38 Axial pancreatic phase (A) and portal venous phase (B) contrast-enhanced CT in a 70-year-old woman with a pancreatic head adenocarcinoma. On pancreatic-phase imaging, the tumor (large arrows), celiac axis (small arrows), and superior mesenteric vein (thin arrows) are all visualized to better effect.
When a tumor is detected at contrast-enhanced CT, there may or may not be mass effect, depending on the size of the tumor. Lack of a pancreatic mass effect should not deter the diagnosis, but larger tumors will inevitably distort the normal pancreatic outline. Tumors are typically hypodense (particularly during the pancreatic phase) because of the central hypovascularity of the tumor (Fig. 9-38). As the tumor enlarges, recognition of hypodensity becomes easier, and large tumors may show frank necrosis (Fig. 9-39). As the mass grows in size, pancreatic duct dilatation becomes more evident, particularly if the tumor is in the head, resulting in upstream ductal dilatation (Fig. 9-40). Smaller tumors in the uncinate may cause little ductal dilatation because of their distance from the main pancreatic duct. Ultimately, the common bile duct may also become obstructed with large pancreatic head tumors (Fig. 9-41), which may progress to a “double-duct” sign when both the pancreatic and biliary ducts are dilated. This is best visualized by ERCP or MRCP (Fig. 9-42). The double-duct sign indicates that the likelihood of a pancreatic adenocarcinoma in the head of the pancreas is very high, even if the tumor is not visualized. Uncommonly, chronic pancreatitis can also cause a double-duct sign, but there should be other signs of chronic pancreatitis at CT and a prolonged clinical history. As the tumor extends beyond the pancreas, the peripancreatic fat becomes invaded or obliterated, which is recognized by increased (sometimes hazy) inflammatory change (i.e., stranding) (Fig. 9-43). Often the tumor causes local pancreatitis, further adding to the peripancreatic inflammation so that it is sometimes difficult to differentiate changes due to tumor from those due to pancreatitis. The local extension into the peripancreatic fat can abut and then surround key vascular structures, particularly the superior mesenteric artery (Fig. 9-44) or vein and sometimes both (Fig. 9-45). The superior mesenteric vein (SMV), however, is often compressed by tumor mass effect as it courses through the pancreas rather than becoming invaded and encased (Fig. 9-46). Multiplanar images can offer better depiction of the relationship of the tumor to the adjacent vessels (Fig. 9-47) and are often used to determine surgical resectability of the mass. Local invasion of splenic, celiac, and mesenteric vessels may preclude operability but will depend on the local surgical expertise. Tumors with more than 50% encasement of the SMV or portal vein (Figs. 9-46 through 9-48) are generally unresectable, although some surgeons are more aggressive and have shown some success with up to 75% circumferential encasement. Splenic vein invasion is not a contraindication to surgery. Celiac axis (celiac or hepatic artery or both) and superior mesenteric artery encasement greater than 25% is generally unresectable (Figs. 9-45 through 9-47). Splenic and gastroduodenal artery encasement is not a contraindication to surgery. Tumors with distant metastases, which are common in pancreatic cancer because of its late presentation, are unresectable. However, it is becoming increasingly apparent that some newer neoadjuvant therapies (e.g., FOLFIRINOX with or without radiation therapy) cause a dramatic reduction in tumor size and residual perivascular soft tissue changes now represent fibrosis rather than active tumor. Radiologists should therefore hesitate before assuming inoperability in these patients (Fig. 9-49). Contrast-enhanced CT has a high predictive value (close to 100%) for unresectability but only 75% to 80% for tumor resectability. Hence, when the CT features suggest unresectability, the radiologist is usually correct. The converse is not true, as a number of tumors deemed resectable by CT turn out not to be. Pancreatic positron emission tomography (PET)/CT does not usually add value to the diagnosis of the primary tumor because of variable fluorodeoxyglucose uptake (Fig. 9-50), but it can sometimes be useful to evaluate extrapancreatic disease, particularly regional adenopathy.
Figure 9-39 Axial (A) and coronal (B) contrast-enhanced CT in a 76-year-old man with a large pancreatic adenocarcinoma having a central hypodense necrotic area (large arrows). The tumor also obstructs the duodenum (small arrows).
Figure 9-40 Axial reformatted contrast-enhanced CT in a 60-year-old man with a subtle 2-cm uncinate mass (large arrow) that obstructs the pancreatic duct (small arrow).
Figure 9-41 Axial contrast-enhanced CT (A) and ERCP (B) in a 53-year-old man with chronic pancreatitis and a new pancreatic head mass caused by adenocarcinoma (large arrow). A stricture is present in the lower bile duct (small arrow), as well as calcification (arrowheads).
Figure 9-42 MRCP in a 61-year-old with dilated pancreatic and biliary ducts (double-duct sign) (arrows) resulting from an obstructing pancreatic adenocarcinoma.
Figure 9-43 Axial pancreatic-phase contrast-enhanced CT in a 78-year-old man with an adenocarcinoma of the midpancreatic body (large arrow) with upstream pancreatic duct dilatation (small arrow) and peripancreatic extension of tumor. The tumor has extended to encase the celiac axis (thin arrows), rendering the patient inoperable.
Figure 9-44 Axial pancreatic-phase contrast-enhanced CT in a 73-year-old woman with soft tissue encasement by pancreatic adenocarcinoma of the superior mesenteric artery (arrows), but the superior mesenteric vein is unaffected (small arrow). This patient was inoperable.
Figure 9-45 Axial contrast-enhanced CT in a 71-year-old with pancreatic adenocarcinoma and almost complete encasement of the superior mesenteric artery (large arrow) and approximately 50% of the superior mesenteric vein (small arrow), which has lost its normal ovoid shape. This patient proved inoperable.
Figure 9-46 Axial pancreatic-phase contrast-enhanced images in a 66-year-old woman with a 1.5-cm subtle hypodense mass in the junction of the head and uncinate that abuts the superior mesenteric vein between the 6 and 11 o’clock positions with effacement of the normal fat plane (arrows) but preservation of vessel caliber. This patient was operable.
Figure 9-47 Axial (A) and coronal (B) contrast-enhanced CT in a 54-year-old man with inoperable pancreatic adenocarcinoma and complete encasement of the superior mesenteric artery (arrows).
Figure 9-48 Axial (A) and coronal (B) contrast-enhanced CT in a 63-year-old woman with pancreatic adenocarcinoma showing complete encasement of the superior mesenteric vein (arrows).
Figure 9-49 Axial contrast-enhanced CT in a 49-year-old woman with what was initially thought to be inoperable pancreatic cancer by imaging (A) as evidenced by encasement of the superior mesenteric artery (large arrow). After treatment with FOLFIRINOX (B), the mass has significantly reduced in size (small arrow). Even though there is some residual tissue around the superior mesenteric artery, this was proven to be fibrosis and no residual tumor at Whipple operation.
Figure 9-50 Axial contrast-enhanced CT (A) and PET (B) in a 63-year-old woman with pancreatic adenocarcinoma. A 5-cm hypodense mass in the body of the pancreas (arrowheads) completely surrounds the superior mesenteric artery (large arrow). There are also superior mesenteric vein occlusion and collateral formation (small arrow). PET shows increased fluorodeoxyglucose uptake in the pancreatic mass (arrowhead).
Further extension of pancreatic tumor may involve local organs, including the stomach, small bowel, spleen, and even the kidneys. More regional extension frequently involves local lymphadenopathy, and further distant metastases often involve the liver and peritoneum and less frequently the lungs.
The tumor can be visualized with MRI, being hypointense on T1-weighted imaging, particularly with added fat suppression, which increases the contrast between the tumor and higher signal healthy pancreas. On contrast-enhanced MRI the pancreas and tumor show features similar to those with contrast-enhanced CT. Should these techniques fail to detect any lesion and with a high index of clinical suspicion, endoscopic US should detect most small tumors unrecognized on CT or MRI (Fig. 9-51). Furthermore, tissue sampling can be performed during the procedure. However, endoscopic US generally usually cannot detect distant metastases.
Figure 9-51 Endoscopic US in a 65-year-old woman with an ill-defined 2-cm hypoechoic mass (arrows) in the head of the pancreas that proved to be ductal adenocarcinoma at biopsy (small arrow).
Pancreatic Neuroendocrine Tumor
Pancreatic neuroendocrine tumors (PNETs) are also known as islet cell tumors or amine precursor and uptake decarboxylation tumors. They can hypersecrete various hormones (insulin, glucagon, gastrin, and somtatostatin), producing unusual but classic clinical findings. The amine precursor and uptake decarboxylation cells are embryonic and migrate from the neural crest to the pancreas and also to the intestinal tract, thyroid, parathyroid, and adrenal gland. They are classified as either functioning (85% of all islet cell tumors) or nonfunctioning (15%) if no excessive hormones are produced. If hyperfunctioning, they may be part of a multiple endocrine neoplasia syndrome 1 (MEN 1), an autosomal-dominant disease associated with endocrine hyperplasia or neoplasia in disparate organs (Table 9-5). They can be benign or malignant (Table 9-6), although the most common type of tumor, insulinoma, is usually benign.
Table 9-6
Features of Pancreatic Neuroendocrine Tumors
WDHA, Watery diarrhea, hypokalemia, and achlorhydria.
Insulinoma
Insulinomas are the most common islet cell tumors that are either functioning, producing insulin from hyperactivity of alpha cells, or nonfunctioning, without significant insulin elevation. Most tumors are small (<2 cm), isolated (70%), benign (90%), and hypervascular (70%). The resulting hyperinsulinemia leads to classic symptoms when florid, but milder forms can go clinically undetected for many years. Typical features are those of hypoglycemia with weakness, confusion, loss of consciousness, and even seizures. Because insulinomas are hypervascular, anyone suspected of having this tumor should undergo dedicated arterial-phase (rather than pancreatic-phase) multidetector CT pancreatic imaging. The lesion, particularly if small (as they frequently are), is often detected only during the arterial phase. Many are missed if the timing of the IV bolus is suboptimal. Classically, optimal CT scanning shows a small, uniform, hyperenhancing mass in the pancreas (Fig. 9-52), which rapidly washes out on portal venous–phase or later imaging, so much so that the sometime-lesion disappears. Dedicated contrast-enhanced MRI has slightly higher accuracy for islet cell tumor detection (especially with fat-saturated techniques) (Fig. 9-53), but if it is still not detected when there is a very high index of suspicion, selective angiography can delineate the hypervascular mass or excessive insulin at pancreatic venous sampling. Alternatively, endoscopic US has proved more accurate than either CT or MRI for the detection of small lesions (Fig. 9-54). Because lesions have high levels of somatostatin receptors, the somatostatin analogue indium-111 pentetreotide (octreotide) can help locate and characterize these pancreatic lesions (Fig. 9-55) as neuroendocrine in origin (insulinoma or otherwise). Ultimately, an exploratory laparotomy with intraoperative US may be required if the index of suspicion remains very high and noninvasive imaging tests fail to identify the mass (Fig. 9-56).
Figure 9-52 Axial arterial-phase contrast-enhanced CT in a 54-year-old man with a 2-cm enhancing mass in the pancreatic head (large arrow) that represents a functioning insulinoma. An additional hypervascular liver mass is in segment II of the liver (small arrow).
Figure 9-53 Axial arterial-phase CT (A) and T1-weighted fat-saturated arterial phase MRI (B) and portal venous–phase T1-weighted fat-saturated MRI (C) in a 50-year-old woman with a 1.2-cm pancreatic head neuroendocrine tumor (arrow) identified only on arterial-phase MRI (B). A segment II hepatic metastasis (arrowheads) is barely visible on arterial-phase CT (D) and portal venous–phase CT (E) and fat-saturated PVP MRI (F) but is clearly visible on arterial-phase T1-weighted fat-saturated MRI (G).
Figure 9-54 Endoscopic US in a 44-year-old woman with a normal CT and a 1.4-cm hypoechoic mass (large arrows) in the pancreatic tail that represents an insulinoma. A biopsy needle is inserted into the mass (small arrow).
Figure 9-55 Axial (A) and coronal (B) contrast-enhanced CT and pentetreotide study (C) in a 66-year-old man with a 1.5-cm hypervascular neuroendocrine tumor in the pancreatic tail (large arrows). The lesion is hyperactive on pentetreotide imaging (small arrow). Other activity (arrowhead) is normal in the left kidney.
Figure 9-56 Intraoperative US in a 32-year-old woman with clinical signs of insulinoma. Contrast-enhanced CT was negative, but the hypoechoic tumor (arrows) was imaged perioperatively.
Not all islet cell tumors are hypervascular. Some are isodense or hypodense on CT imaging (even in the arterial phase) and may therefore occasionally be confused with adenocarcinoma. However, they tend to be more well circumscribed (Fig. 9-57) without peripancreatic extension unless very large with a late presentation. Others are heterogeneous and either partially cystic (Fig. 9-58) or almost completely cystic (Fig. 9-59).
Figure 9-57 Axial contrast-enhanced CT in arterial (A) and portal venous (B) phases in a 55-year-old man with a proven neuroendocrine tumor in the pancreatic head (arrows). The 2.5-cm tumor enhances in neither phase.
Figure 9-58 Axial contrast-enhanced CT in a 47-year-old woman showing a 2.5-cm complex partially cystic pancreatic neuroendocrine tumor in the body of the pancreas (arrow).
Figure 9-59 Axial contrast-enhanced CT in a 63-year-old woman with a 3.5-cystic insulinoma (arrow) in the pancreatic tail.
Nonfunctioning insulinomas can be more sinister and indolent because they often present late owing to the lack of hormone production and early clinical signs. They are therefore usually larger at presentation with mass-like symptoms (pain, obstruction, and invasion of other organs) (Fig. 9-60). Because they are large, insulinomas are often necrotic, but the active periphery of the tumor can enhance avidly like other islet cell tumors. They can also be cystic in appearance, like functioning tumors, and calcification is present in 20% (Fig. 9-61). They are often metastatic (80% to 90%), either locally or distantly (hypervascular liver metastases), and consequently patients have a relatively poor 5-year survival rate (45%).
Figure 9-60 Axial (A) and coronal (B) contrast-enhanced CT in a 72-year-old man with a 9-cm complex pancreatic head mass (arrows) representing a nonfunctioning islet cell tumor. As the tumor was nonfunctioning, the patient presented late with abdominal pain.
Figure 9-61 Axial contrast-enhanced CT in a 63-year-old woman with a 4.5-cm complex pancreatic tail mass (arrow) with partial calcification (arrowhead) that proved to be a cystic insulinoma tumor by pathological study.
Gastrinoma
Gastrinomas are the second most common pancreatic neuroendocrine tumors and are associated with MEN1 in approximately 20% to 40% of patients. They arise from alpha-1 cells and typically reside in the pancreas but can be ectopic in the second part of the duodenum or stomach. They are often small, like insulinomas, but are more likely to be multiple (75%). Investigation of the patient is triggered by clinical symptoms (also known as Zollinger-Ellison∗ syndrome) that result from profuse ulceration of the gastric, duodenal, and even proximal jejunal mucosa because of gastrin hyperproductivity (Fig. 9-62). This peptide hormone normally stimulates gastric parietal cells to secrete hydrochloric acid, so with excessive hormonal production, profuse upper intestinal tract inflammation and ulceration ensue.
Figure 9-62 Axial (A) and coronal (B) contrast-enhanced CT in a 54-year-old man with a 4.5-cm hypervascular gastrinoma just posterior to the uncinate process (large arrows). Coronal images demonstrate marked gastric and small bowel mucosal thickening secondary to diffuse gastritis resulting from Zollinger-Ellison syndrome (small arrows).
Because of their sometimes ectopic location outside the pancreas, gastrinomas are more frequently missed than insulinomas, and careful evaluation along the medial border of the second part of the duodenum is required. With optimal bolus timing and dedicated arterial multidetector CT, most tumors should be detected. Metastases are far more common (approximately 60% of gastrinomas) than with insulinomas (10%) (Fig. 9-63) and can also secrete gastrin, and palliative treatment involves gastrectomy or H2-blocker therapy.
Figure 9-63 Axial arterial-phase contrast-enhanced CT in a 66-year-old man with a 2.5-cm pancreatic head gastrinoma (arrow) and an obstructed pancreatic duct. There are multiple subtle hepatic metastases (small arrows).
Glucagonoma
Glucagonomas are rarer than either insulinomas or gastrinomas and arise from alpha-2 islet cells. Even though they secrete glucagon, glucagonomas often present late and large, and up to 80% are metastatic to the liver or regional lymph nodes at the time of diagnosis. They are usually located in the body and tail of the pancreas (Fig. 9-64). Clinical findings are secondary to the elevated glucagon levels and include diabetes mellitus, anemia, weight loss, hypoaminoacidemia, and a characteristic necrolytic migratory erythema.
Figure 9-64 Axial arterial-phase contrast-enhanced CT in a 66-year-old man with a 1.5-cm hypervascular mass in the head of the pancreas (A; arrowhead) representing glucagonoma. Images of the liver during the same scan demonstrate three hypervascular metastases (B; arrows).
VIPoma
VIPomas secrete vasoactive intestinal polypeptide (VIP) from delta-1 islet cells, producing the WDHA (or WDHH) syndrome of watery diarrhea, hypokalemia, and achlorhydria and hypovolemia. Up to 50% are malignant, and most occur in the body and tail of the pancreas. Like other pancreatic neuroendocrine tumors at imaging, they are hypervascular and most likely to be detected during arterial-phase imaging (Fig. 9-65).
Figure 9-65 Axial T1-weighted fat-saturated postcontrast MRI in a 44-year-old woman with a 2-cm subtle and complex pancreatic tail mass (arrows) caused by a VIPoma.
Somatostatinoma
Somatostatinomas are the rarest of the islet cell tumors, with excess somatostatin produced from delta islet cells. Most are malignant, cause diarrhea and weight loss, and can be confused with VIPomas. At imaging, they are also relatively large and hypervascular and confined mostly to the pancreas. They can, however, occur in the chest and brain. Many have metastasized at the time of diagnosis, mainly to the liver and mesentery (Fig. 9-66).
Figure 9-66 Axial contrast-enhanced CT in a 77-year-old woman with a 3.5-cm calcified mesenteric mass from metastatic somatostatinoma (arrows).
Lymphoma
Primary pancreatic lymphoma is rare and usually non-Hodgkin. The pancreas is more commonly involved by direct invasion from extrapancreatic disease. When present, however, lymphoma presents with either an isolated relatively avascular homogeneous mass (Fig. 9-67) or diffuse pancreatic involvement with peripancreatic extension. As is common with lymphoma elsewhere, the tumor does not obliterate the immediate vasculature. Rather, vessels tend to course relatively normally through the tumor (Fig. 9-67). PET or PET/CT is useful to document response to treatment.
Figure 9-67 Axial contrast-enhanced CT in a 44-year-old man with pancreatic lymphoma and a large pancreatic head mass (large arrow). As with lymphoma elsewhere, vascular patency (hepatic artery) is preserved (small arrow). There are subtle liver metastases (thin arrows).
Metastases
Local extension from adjacent malignancies (e.g., colon or stomach) is most common. When hematogenous, metastases can be either hypervascular (Fig. 9-68) or hypovascular (Fig. 9-69), depending on the primary tumor, and also multiple. Multiplicity may give a clue to the diagnosis because without a history of malignancy, these metastases could be confused with pancreatic neuroendocrine or pancreatic adenocarcinoma (Fig. 9-70). The most common primary malignancies are renal cell, lung, breast, colon, and melanoma. Renal cell metastases may occur many years after removal of the primary lesion.
Figure 9-68 Axial arterial-phase contrast-enhanced CT (A) in a 70-year-old woman with a hypervascular renal cell metastasis (large arrows), poorly visualized on portal venous–phase images (B). Note surgical clips from prior right nephrectomy (small arrows).
Figure 9-69 Axial contrast-enhanced CT in a 66-year-old woman with a 1.8-cm low-density cystic breast metastasis (arrow) in the pancreatic tail.
Figure 9-70 Axial contrast-enhanced CT in a 62-year-old man with a 3.8-cm hypodense lung metastasis in the pancreatic head and uncinate (arrow). This could be confused with a pancreatic adenocarcinoma.
Pancreaticoblastoma
Pancreaticoblastomas are rare tumors of early childhood but can rarely present in adults. They are usually indolent and slow growing and are therefore large at the time of initial presentation. They tend to be soft and gelatinous, so may not produce obstructive symptoms (i.e., ductal obstruction). Pancreaticoblastomas are associated with Beckwith-Wiedemann∗ syndrome, a spectrum usually seen in childhood with multiple congenital defects and increased incidence of malignancies. On contrast-enhanced CT, in addition to usually being large, pancreaticoblastomas show a multilobulated mass separated by enhancing septa (Fig. 9-71).
Figure 9-71 Axial contrast-enhanced CT in an 18-year-old man with a multilobulated pancreatic mass (arrow) caused by pancreaticoblastoma.
Colloid Carcinoma
Colloid carcinomas are rare pancreatic tumors that were previously classified as either adenocarcinoma or mucinous cystadenocarcinoma. Despite the usual large size of colloid carcinomas at presentation, patients with these tumors have a much better prognosis than do those with ductal adenocarcinoma. Even without surgical removal, patients can live for years. With contrast-enhanced CT, it can be understood why these tumors were confused with other tumors, because they often demonstrate large necrotic and cystic regions (Fig. 9-72).
Figure 9-72 Axial contrast-enhanced CT in a 67-year-old woman with a large predominantly necrotic and cystic mass (arrowheads) caused by colloid carcinoma. There is a biliary metallic stent in situ (arrow).
Acinar Cell Carcinoma
Acinar cell carcinomas are very rare pancreatic neoplasms arising from acinar cells, which are usually responsible for exocrine enzyme production. Therefore they often oversecrete lipase, causing widespread fat necrosis, which may present clinically as subcutaneous nodules. Patients with these carcinomas have a slightly better prognosis than those with ductal adenocarcinomas. On contrast-enhanced CT the tumors have no distinguishing features and are often large and heterogeneous with areas of necrosis (Fig. 9-73). Occasionally they appear cystic and may be confused with other cystic pancreatic neoplasms.
Figure 9-73 Axial (A) and coronal (B) contrast-enhanced CT in a 44-year-old woman with acinar cell carcinoma of the pancreas. There is a large heterogeneous pancreatic mass (large arrows) with multiple varices caused by splenic and portal vein thrombus (small arrows). There is an incidental hepatic cyst.
Anaplastic Carcinoma
Anaplastic carcinomas are rare malignant pancreatic masses that are highly aggressive and readily metastasize to the liver and lungs. They are usually seen in the elderly and present in patients with a relatively short history of pain and general loss of well-being, particularly if they are metastatic. At imaging, the mass is usually found in the body and tail and is large and highly heterogeneous with areas of hypervascularity and necrosis.
Small Cell Carcinoma
Small cell carcinomas are rare pancreatic tumors that are usually large at presentation but generally less aggressive than anaplastic carcinomas. They respond relatively well to chemotherapy. Small cell carcinomas are usually found in the pancreatic head.
Giant Cell Carcinoma
Giant cell carcinoma is another type of rare malignant pancreatic tumor, characteristically presenting as a relatively large complex mass at presentation, but often appearing similar to mucinous neoplasms in that it can be exophytic and multicystic, with multiple internal septa and calcification of the wall and septa. Giant cell carcinomas rarely metastasize, so the prognosis is usually good in these patients if the primary tumor is removed surgically.
Cystic Pancreatic Masses
Cystic Pancreatic Neoplasms
Approximately 90% of cystic pancreatic neoplasms are benign, with the remaining malignant 10% arising predominantly arising from mucinous tumors. Many lesions appear similar at imaging, however, and the challenge for the radiologist is to determine which lesions need to be monitored more closely than others. With modern imaging techniques, it is possible to differentiate many by their location, size, and internal architecture along with the sex and age of the patient (Box 9-3 and Table 9-7). However, some lesions can be identified only by endoscopic US and biopsy or complete surgical removal.
Table 9-7
Differentiation of Pancreatic Cystic Neoplasms
IPMN, Intraductal papillary mucinous neoplasms.
Simple Pancreatic Cysts
Simple pancreatic cysts are uncommon and may be congenital in origin, since they are more commonly seen in neonates. At imaging, they are usually thin walled and less than 2 cm, without septa, mural nodules, or thickening, and are therefore innocent (Fig. 9-74). They are usually single but can be multiple. Up to 10% of patients with adult polycystic kidney disease show simple pancreatic cysts, as do 50% of patients with von Hippel-Lindau∗ disease (Fig. 9-75). Pancreatic cysts can also be seen in patients with Beckwith-Wiedemann syndrome.
Figure 9-74 Axial contrast-enhanced CT in a 71-year-old woman with three smooth-walled simple pancreatic cysts (arrows).
Figure 9-75 Axial T2-weighted MRI in a 32-year-old woman with von Hippel-Lindau disease. There are numerous simple pancreatic (arrow) and renal cysts (arrowhead).
Pancreatic Enteric Duplication Cyst
Pancreatic enteric duplication cysts are rare and most commonly found in children. They are usually incidental but can present with complications of pancreatitis and therefore can be confused with pancreatic pseudocyst. They are, however, usually well circumscribed and cystic in appearance and tend to be larger than simple cysts (Fig. 9-76).
Figure 9-76 Transverse US (A) and T2-weighted (B) and postcontrast (C) MRI of the pancreatic body in a 24-year-old man demonstrating a uniform hypoechoic, nonenhancing, cystic, 3-cm mass (arrows) representing a pancreatic duplication cyst.
Pancreatic Cystosis
In patients with cystic fibrosis, the pancreas typically becomes fatty replaced (Figs. 9-13 and 9-14) or less commonly calcified. In some patients, however, pancreatic epithelial cysts develop because some exocrine function remains, but their ducts are blocked by the viscous inspissated secretions (Fig. 9-77). The older the individual is, the more likely these cysts are to develop.
Serous Microcystic Pancreatic Neoplasm
Serous microcystic pancreatic neoplasms are of uncertain cause but are considered benign. Their walls consist of cuboidal epithelium and secrete glycogenic-type material. They are more common in women (4:1) and in patients with von Hippel-Lindau disease. They are much less common than mucinous tumors and account for approximately 15% of cystic pancreatic neoplasms. They are difficult to differentiate from other cystic neoplasms, particularly when small, but as they enlarge, these neoplasms may show characteristic features (Table 9-7). They are usually discovered incidentally but if large can produce symptoms of bowel or biliary duct obstruction.
At imaging, the lesion is usually well circumscribed and positioned in the pancreatic head. Multiple small (<2 cm, often <1 cm) lace-like cysts are identified, giving them their well-known “honeycomb” and microcystic appearance (seen in approximately 90% of serous cystadenomas) (Fig. 9-78). Approximately 10% show larger cysts and are termed oligocystic or macrocystic (not to be confused with macrocystic mucinous cysts). The cyst walls may enhance and show a central scar, which can calcify, a useful differentiating feature from mucinous tumors (Fig. 9-79). The tumor typically does not cause pancreatic duct dilatation. Imaging with MRI may delineate the size and number of cysts better than CT, particularly in small lesions, because of MRI’s better contrast characteristics with T2-weighted images (particularly when fat saturated) (Fig. 9-80). Cyst wall and central scar enhancement is also noted after gadolinium administration.
Figure 9-78 Axial contrast-enhanced CT in a 44-year-old woman with a 6-cm multicystic mass in the head of the pancreas (arrow). The numerous small cysts are consistent with a serous cystadenoma.
Figure 9-79 Axial contrast-enhanced CT in a 48-year-old woman with an 8-cm pancreatic tail mass (arrowheads) with central scar calcification (arrow) characteristic of serous cystadenoma. There are multiple other pancreatic cystic changes caused by chronic pancreatitis in the head.
Figure 9-80 Axial contrast-enhanced CT (A) and T2-weighted MR images (B) in a 64-year-old woman with a 2-cm pancreatic tail serous cystadenoma (arrow). The multiple small septa (arrowhead) are better appreciated with fat-saturated T2-weighted MRI.
Once the cystic lesion is detected, usually by CT, and before a definitive diagnosis is made, the main concern is whether it is serous or mucinous. Mucinous lesions require more aggressive management because of their propensity to become malignant. Despite this conundrum, these lesions can be managed less aggressively (partly because they occur in the elderly) and are generally not removed unless they are large and produce symptoms, even if a simple-appearing mucinous tumor has not been totally excluded. The lead time for mucinous tumors to become malignant is usually sufficiently long that delaying surgical removal (a procedure not without complications) may be prudent if the lesion shows no malignant features. Definitive diagnosis may require endoscopic US (Fig. 9-81), which can often show the multiple small cystic masses to even better advantage than MRI. Percutaneous aspiration of cyst contents is then usually performed and yields negative carcinoembryonic antigen values.
Figure 9-81 Endoscopic US in a 78-year-old woman with a serous cystadenoma. The mass has multiple small cystic components (arrow).
Mucinous Pancreatic Neoplasms
Mucinous pancreatic neoplasms are differentiated into mucinous cystic neoplasms and intraductal pancreatic mucinous neoplasms because both produce mucin.
Mucinous Cystic Neoplasms
Mucinous cystic neoplasms result from mucinous production from tall columnar epithelium and are far more common than serous tumors. They most commonly occur in the pancreatic tail (90%) and in middle-aged women (40 to 60 years of age; 9:1). The diagnosis therefore should be considered mucinous until proven otherwise in a middle-aged woman with a cystic tail pancreatic lesion. However, when small, these neoplasms may be very difficult to differentiate from other cystic neoplasms. Given this, and their 10% chance of malignant transformation, the threshold for needle aspiration (endoscopic US) is relatively low. The neoplasms are then usually surgically removed if mucinous. Sometimes, benign-appearing lesions are periodically followed with imaging (6 months to 1 year) if the patient is elderly because the chance of malignancy is still low and surgical removal is not without risks.
At imaging, several features distinguish mucinous cystic neoplasms from other cystic pancreatic neoplasms (Table 9-7). Cysts are generally fewer (<6) and may sometimes even be unilocular. The cysts are usually larger (>2 cm) than those seen in serous cystic pancreatic neoplasms. Enhancement can be seen in the cyst walls, including any internal septa. Wall or septal calcification is observed in approximately 15% of lesions (Fig. 9-82). Cyst walls may contain mural nodules, which markedly increase the likelihood of malignancy, particularly if they enhance (Fig. 9-83). The mass more commonly causes proximal pancreatic duct dilatation than do serous neoplasms. On MRI with T1-weighted imaging, the cyst contents can be of mixed signal if contents are proteinaceous or hemorrhagic, but they are generally hyperintense on T2-weighted imaging (Fig. 9-84). Endoscopic US is often performed to evaluate cyst features and to aspirate fluid contents. Elevated carcinoembryonic antigen 19-9 levels are commonly observed and are specific for mucinous cystic neoplasms (Fig. 9-85).
Figure 9-82 Axial contrast-enhanced CT in a 76-year-old man with a 10-cm macrocystic lesion (large arrow) in the pancreatic tail representing a mucinous cystadenoma. Septa separating larger cysts are seen (arrowheads), and there are two punctate areas of calcification (small arrows).
Figure 9-83 Axial contrast-enhanced CT in a 66-year-old woman with a 12-cm complex cystic mass in the pancreatic tail representing a malignant cystadenocarcinoma. Note scattered calcification (small arrows) and mural nodules (large arrow).
Figure 9-84 Axial T2-weighted fat-saturated MRI in a 75-year-old woman with a unilocular 7-cm mucinous cystadenoma in the pancreatic tail (arrow).
Figure 9-85 Endoscopic US of a 57-year-old woman with a 4-cm macrocystic neoplasm of the pancreas. The cysts are few in number and relatively larger than microcystic disease (arrows).
Intraductal Papillary Mucinous Neoplasms
Intraductal papillary mucinous neoplasms (IPMNs) are also known as intraductal papillary mucinous tumors (IPMTs). These are not as rare as once thought and are relatively frequently detected with high-resolution cross-sectional imaging. They are ductal epithelial in origin, arising either from the side (30%) or combined main and side (70%) pancreatic ducts and producing excessive thick mucin (hence, mucinous-producing tumor), which almost always obstructs the immediate duct or main duct with resulting ductal dilatation.
Most IPMNs are asymptomatic, occurring in elderly men in the head and uncinate of the pancreas (Fig. 9-86) (approximately 55%), with a minority (10%) in the tail. The remainder (35%) are multiple and diffusely located throughout the pancreas (Fig. 9-87). Most are small and cyst like, but main duct variants simply cause duct dilatation owing to excessive mucin production. Main duct IPMNs can involve either the entire duct or a segment (Fig. 9-88). They are more frequently detected by MRCP because of the high T2 mucin signal characteristics (Fig. 9-88), and side branch lesions can often be observed to communicate with the main pancreatic duct (Figs. 9-86 and 9-87).
Figure 9-86 Axial contrast-enhanced CT in a 79-year-old man with two 8-mm cystic lesions in the uncinate (arrows) consistent with side branch IPMNs.
Figure 9-87 MRCP in a 74-year-old man demonstrating three small side branch IPMNs (arrows).
Figure 9-88 Axial contrast-enhanced CT (A) and MRCP (B) in an 80-year-old woman with a main duct IPMN and dilatation of a segment of the main pancreatic duct in the head (arrows).
The lesions are premalignant, with up to 25% showing hyperplastic features, 50% showing dysplastic features, and 25% showing frank adenocarcinoma. Malignant degeneration is more common in main duct tumors than in side branch lesions, and features include presence or development of a solid mass, pancreatic duct dilatation greater than 10 mm, mucin calcification, and polypoid main duct lesions (Fig. 9-89). Therefore annual follow-up is recommended for incidentally detected IPMNs, especially if the patient is younger. Follow-up should ideally be performed with MRCP rather than CT because of better contrast characteristics and avoidance of ionizing radiation. The management of small IPMNs, particularly the more common side branch lesions, in the elderly is more challenging given that they are relatively common and the risk of malignant degeneration may be small. Less frequent monitoring is therefore sometimes practiced.
Figure 9-89 Axial contrast-enhanced CT in a 78-year-old man with a malignant IPMN demonstrates a multicystic complex mass (arrows) and a soft tissue mass projecting into the duodenum (arrowhead).
Cystic Pancreatic Neuroendocrine Tumors
Some PNETs are predominantly cystic (Figs. 9-60 and 9-62), whether functioning or nonfunctioning. Larger nonfunctioning PNETs may undergo central necrosis and appear cystic at presentation (Fig. 9-90).
Figure 9-90 Axial contrast-enhanced CT in a 57-year-old man with a 9-cm complex predominantly low-density necrotic mass (arrows) representing a nonfunctioning pancreatic neuroendocrine tumor.
Acinar Cell Tumor
Acinar cell tumors are usually heterogeneous, but some are predominantly cystic and can be confused with other pancreatic cystic neoplasms (Fig. 9-91). These tumors are, however, extremely rare, and the diagnosis may be made only after biopsy or surgery.
Figure 9-91 Axial (A) and coronal (B) contrast-enhanced CT in a 65-year-old man with a 4-cm complex cystic mass in the head of the pancreas (arrows) owing to acinar cell carcinoma.
Cystic Teratoma of the Pancreas
Cystic teratomas of the pancreas are extremely rare. They usually present late and large and are discovered because of their mass effect on adjacent organs. They tend to be homogeneous and uniform with a rounded, smooth-walled mass, sometimes with rim calcification, but like teratomas elsewhere, they can present with fat, soft tissue, and coarse calcification.
Pancreatic Lymphangioma
Pancreatic lymphangioma, a very rare presentation of lymphangioma, is usually identified in the neck or axilla, retroperitoneum, or mesentery. Similar to lymphangiomas elsewhere, pancreatic lymphangiomas are multicystic with thin septa and uniformly hypodense cyst contents.
Solid and Papillary Epithelial Neoplasm
Solid and papillary epithelial neoplasms (SPENs), also known as solid and pseudopapillary neoplasms, papillary cystic carcinoma tumors, papillary epithelial neoplasms, and Frantz∗ tumors, are composed of epithelial tissue. These tumors are rare, more common in younger women (90%; often non-Caucasians), and usually large at initial imaging presentation because of their indolent growth pattern. At imaging they are usually located in the pancreatic body and tail. They show complex solid and cystic masses (with or without calcification) and a well-defined capsule, which often avidly enhances. They can therefore appear similar to other cystic pancreatic neoplasms, particularly mucinous tumors (Fig. 9-92). Internal hemorrhage is common because they are highly vascular masses, which can be observed after administration of IV contrast medium, helping to differentiate the lesion from mucinous tumors (Fig. 9-93). Despite these rather alarming imaging features, only 10% are malignant. Most are removed for formal diagnosis because of their complex imaging features.
Figure 9-92 Axial contrast-enhanced CT in a 17-year-old woman with an 8-cm complex cystic mass (arrow) representing a solid and papillary epithelial neoplasm of the pancreas, not dissimilar to mucinous pancreatic neoplasms.
Figure 9-93 Axial contrast-enhanced CT in a 24-year-old woman with a 10-cm complex solid and cystic pancreatic head mass (arrow) caused by a solid and papillary epithelial neoplasm.
Pancreatic Calcification (Box 9-4)
The most common cause of pancreatic calcification is chronic pancreatitis, usually presenting with multiple variably sized coarse calcifications, which lie within the distorted ducts (Figs. 9-10 and 9-30 through 9-32). The walls of chronic pseudocysts can calcify and are typically thicker and more circumferential than those observed in pancreatic cystic mucinous neoplasms (15% of cases). Calcification is also curvilinear, or sometimes possibly septal (Fig. 9-83), but is not usually circumferential. Calcification in serous tumors is more stellate with a calcification of the central scar (Fig. 9-79).
Congenital calcification from cystic fibrosis and hereditary pancreatitis tends to lie within pancreatic ducts. Cystic fibrosis affects the pancreas by developing thick inspissated mucous plugs that “plug” the pancreatic ducts with consequent calcification (Fig. 9-94). Over the longer term the pancreas becomes atrophic and fatty replaced (Figs. 9-12 and 9-15), and patients usually develop diabetes mellitus. Hereditary pancreatitis is a rare autosomal-dominant disease characterized by recurrent bouts of pancreatitis. The resulting chronic pancreatitis and development of ductal pancreatic calcification are typically larger than those seen in other, more common forms of chronic pancreatitis.
Figure 9-94 Axial contrast-enhanced CT in a 27-year-old woman with diffuse pancreatic calcification secondary to cystic fibrosis (large arrow). There is also pancreatic cystosis (small arrow).
Intrapancreatic Accessory Spleen
An accessory spleen (splenules or splenunculi) is relatively common, usually in the region of the splenic hilum, but occasionally is present in the pancreas, particularly the pancreatic tail (Fig. 9-95). Accessory spleens are usually small and enhance similarly to the spleen and may therefore be confused with hypervascular pancreatic tumors, particularly neuroendocrine tumors. Diagnosis may require 99mTc sulfur colloid imaging to identify the mass as splenic tissue (see Chapter 7).
Figure 9-95 Axial T2-weighted fat-saturated (A) and T1-weighted fat-saturated arterial- (B) and portal venous–phase (C) postcontrast images in a 29-year-old man with a 1.5-cm pancreatic tail lesion (arrows) with similar signal characteristics to the spleen (arrowheads) on all pulse sequences, which proved to be an intrapancreatic accessory spleen.
Pancreatic Trauma
Pancreatic trauma is either penetrating (e.g., stab or gunshot) or blunt (e.g., motor vehicle accident). Contrast-enhanced CT is the investigation of choice, and depending on the severity of the trauma, the pancreas can be enlarged and inflamed because of contusion, although more severe injuries lead to laceration and even transection (Fig. 9-96). With more severe trauma, there may be areas of nonvascularization with the consequent lack of enhancement. Patients with laceration or transection should be evaluated intraoperatively with contrast pancreatography to determine the integrity of the pancreatic duct. Longer term complications include pancreatitis, pancreatic fluid collections, fistula, and abscess formation.
Figure 9-96 Axial contrast-enhanced CT in a 38-year-old man with a pancreatic fracture (arrow) and diffuse hemorrhage (arrowheads).
Postsurgical Pancreas
The Whipple∗ procedure, the standard surgical maneuver to remove pancreatic head tumors, involves resection of the pancreatic head, duodenum, gastric antrum, and usually gallbladder. A pylorus-sparing Whipple procedure is often performed, which preserves the stomach and pylorus to normalize gastric emptying. With either procedure, a loop of jejunum is used to connect to the bile ducts (choledochojejunal anastomosis) and the remaining pancreas (pancreaticojejunal anastomosis), which usually is referred to as the afferent loop. At follow-up imaging, the radiologist should recognize normal postoperative findings. The normal afferent loop is often partially fluid filled but can appear mass like and should not be mistaken for local recurrence (Fig. 9-97).
Figure 9-97 Axial contrast-enhanced CT in a 56-year-old man with a right upper quadrant mass (arrows) caused by a normal afferent loop after a Whipple procedure.
Complications of the Whipple procedure include delayed gastric emptying (common to other anastomotic gastric procedures), pancreatic fistula (usually resolves spontaneously), pancreatitis (Fig. 9-98), hemorrhage (Fig. 9-99), abscess, and biliary strictures (common to all biliary-enteric procedures). The afferent loop can become obstructed because of edema, tumor, or adhesions (Fig. 9-100).
Figure 9-98 Axial contrast-enhanced CT in a 66-year woman after pancreatic tail resection for adenocarcinoma. A large postoperative fluid collection (arrow) in the operative bed is due to a combination of pancreatitis and a pancreatic duct transection.
Figure 9-99 Axial contrast-enhanced CT in a 50-year-old man with distal pancreatic resection and splenectomy and a hematoma in the operative bed (arrow).
Figure 9-100 Coronal contrast-enhanced CT in a 71-year-old man with an obstructed afferent loop (arrows) after a Whipple procedure. There is also intrahepatic duct dilatation caused by the obstructed loop (small arrow) and intraabdominal ascites (arrowheads).
Other pancreatic procedures include the Puestow∗ procedure, performed to facilitate pancreatic duct drainage (usually from chronic pancreatitis) by filleting the pancreas along its length and oversewing a loop of small bowel onto it (pancreaticojejunostomy). The imaging appearances are similar to those of a Whipple procedure, except the pancreatic head is preserved.
Pancreatic Transplant
Pancreatic transplant is an innovative procedure that is performed primarily for patients with type 1 diabetes mellitus. The pancreas is transplanted alone or more commonly with simultaneous renal transplantation. With older surgical transplants the pancreatic duct drainage occurred into the bladder via a duodenal interposition with the vascular supply to the pancreas delivered from the iliac arteries. More recently, the procedure has enabled drainage directly into a loop of small bowel with pancreatic vascularization from the iliac vessels. Pancreatic transplantation usually occurs on the right side, and renal transplantation occurs on the left.
The follow-up imaging of the transplant is preferentially performed with US or MRI because of potential renal complications from iodinated contrast material, although with normal posttransplant function, smaller doses of iodinated contrast are not contraindicated. Complications include pancreatitis (Fig. 9-101), thrombosis, hemorrhage, infection, and rejection. For patients who have undergone this procedure, the 5-year allograft survival rate approaches 70%.
Figure 9-101 Axial and coronal contrast-enhanced CT in a 43-year-old woman with a combined renal (arrowheads) and pancreas transplant with pancreatic swelling and peripancreatic inflammation (stranding) (arrows) caused by transplant pancreatitis.
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∗ Abraham Vater (1684-1751), German anatomist.
∗ Paul Langerhans (1847-1888), German pathologist.
∗ George Grey Turner (1877-1951), British surgeon.
∗ Johann Georg Wirsung (1600-1643), German physician.
∗ George Grey Turner (1877-1951), British surgeon.
∗ Thomas S. Cullen (1868-1953), Canadian-American gynecologist.
∗ Ludwig Georg Courvoisier (1843-1918), Swiss surgeon.
∗ Robert Milton Zollinger (1903-1992), American surgeon; Edwin H. Ellison (1918-1970), American surgeon.
∗ John Bruce Beckwith (1933- ), American pathologist; Hans Rudolf Wiedemann (1915-2006), German pediatrician.
∗ Eugen von Hippel (1867-1939), German ophthalmologist; Arvid Vilhelm Lindau (1892-1958), Swedish pathologist.
∗ Virginia Kneeland Frantz (1896-1967), American surgical pathologist.
∗ Allen Whipple (1881-1963), American surgeon.
∗ C.B. Puestow (1902-1973), American surgeon.
