Pancreatic Physiology

The pancreas serves exocrine and endocrine functions critical to normal digestion and metabolism. The exocrine components of the pancreas are arranged in clusters of acinar cells that produce and secrete an electrolyteenhanced alkaline solution rich in digestive enzymes into the duodenum via the pancreatic duct. A variety of neural and hormonal regulators of pancreatic secretion exist, with cholecystokinin and secretin being the ones most familiar to radiologists. Because pancreatic secretion is minimized during fasting, fasting plays an important role in the management of pancreatic pseudocysts communicating with the pancreatic duct. Fasting is also recommended before secretin-augmented magnetic resonance cholangiopancreatography (MRCP), a method of assessing pancreatic exocrine function in patients with suspected chronic pancreatitis.

The endocrine components of the pancreas are arranged into pancreatic islets that are scattered throughout the pancreas with a concentration toward the tail. Islet cells produce hormones critical to carbohydrate metabolism. Normal pancreatic islets cannot be resolved with current imaging modalities, and their importance in imaging extends from the occasional development of islet cell neoplasms.

Acute Pancreatitis

Acute pancreatitis refers to acute onset of pancreatic inflammation instigated by one or more of a variety of innate or acquired mechanical, chemical, or metabolic factors. Gallstones expelled into the common bile duct incite the majority of cases of acute pancreatitis. Other causes of acute pancreatitis include alcohol abuse, drug reactions, pancreatic and ampullary neoplasms, hypertriglyceridemia, hypercalcemia (caused by hyperparathyroidism), hypothermia, congenital anomalies, trauma, and parasites. Rarely, pancreatitis results from bites or stings of a variety of venomous organisms (our personal favorite is the Gila monster). Despite the proliferation of sophisticated imaging technologies in the last century, establishing the diagnosis of pancreatitis remains a clinical pursuit. Serum amylase and lipase levels are routinely checked when patients have abdominal pain and a compelling (and sometimes not so compelling) history and physical examination. Mild increases of amylase level occur with causes of abdominal pain other than pancreatitis, although a threefold increase of amylase level is specific for pancreatitis. Amylase levels are typically greater in gallstone pancreatitis than in alcohol-related pancreatitis, and only minimal increase is noted in many patients with hyperlipidemic pancreatitis. Normal amylase levels can be found in a small minority of patients with acute pancreatitis.

Serum lipase levels increase within 8 hours of onset of acute pancreatitis. Lipase levels may be significantly increased despite only mild increase of amylase levels in a patient with pancreatitis. Lipase levels also tend to remain increased longer than amylase levels. Although lipase levels can be increased out of proportion to amylase levels in patients with alcoholic pancreatitis, this finding is not as specific as once thought. Mild lipase level increase can occur with other causes of abdominal pain such as cholelithiasis and choledocholithiasis, ruptured aortic aneurysm, and small-bowel obstruction. A serum lipase level greater than three times normal makes a nonpancreatic cause of increased levels unlikely.

Other laboratory findings that can be associated with severe pancreatitis include hypocalcemia, hyperglycemia, hypoalbuminemia, hyperlipidemia, coagulopathy, and leukocytosis.

A variety of systemic complications of severe acute pancreatitis can occur, including diabetes, shock/hypovolemia, adult respiratory distress syndrome, disseminated intravascular coagulation, fat necrosis, and polyarthritis.

Chronic Pancreatitis

Patients with chronic pancreatitis often suffer from chronic, sometimes severe, epigastric or diffuse abdominal pain that can radiate to the back. Patients who do not suffer from continuous or intermittent abdominal pain can present clinically with symptoms of pancreatic insufficiency, including steatorrhea, weight loss, or diabetes.

Pancreatic Cancer

The peak incidence of ductal adenocarcinoma of the pancreas is in the seventh and eighth decades of life, although patients with hereditary pancreatitis are prone to earlier development of pancreatic cancer. Smokers and patients with chronic pancreatitis also appear to be at increased risk for development of pancreatic cancer. Patients often have nonspecific symptoms such as abdominal pain, weight loss, anorexia, or depression. Jaundice results from malignant obstruction of the distal bile duct and can be associated with pruritus, light-colored stools, and a palpable but nontender gallbladder. Diabetes can eventually ensue but is rarely a presenting symptom. Migratory thrombophlebitis and polyarthralgias are rare manifestations. Carcinoembryonic antigen (CEA) or CA 19-9 levels can be increased in patients with ductal adenocarcinoma of the pancreas but are nonspecific. CA 19-9 levels are less helpful in the setting of biliary obstruction and are often normal in patients with small tumors.

Neuroendocrine Tumor (Islet Cell Tumor)

A variety of functioning and nonfunctioning endocrine tumors arise in the pancreas. Many pancreatic neuroendocrine tumors occur sporadically, although neuroendocrine tumors of the pancreas also constitute one component of multiple endocrine neoplasia syndrome type 1 (MEN-1). In the setting of MEN-1, neuroendocrine tumors have a tendency to be multiple.

Symptomatic nonfunctioning neuroendocrine tumors tend to be large at presentation, because patients have symptoms of mass effect rather than clinical sequelae of excess hormone secretion. The various functional neuroendocrine tumors of the pancreas are listed in Table 14-1 with their associated clinical manifestations.

Table 14-1 Pancreatic Neuroendocrine Tumors

* Headache, light-headedness, confusion, abnormal behavior, seizures.

† Dermatitis that begins in groin and spreads to thighs, buttocks, and extremities.

The Normal Pancreas

Grossly, the pancreas is a lobulated extraperitoneal organ that resides in the anterior pararenal space. As such, it is surrounded by areolar tissue and lacks a distinct capsule. The pancreas is divided into the head and uncinate process, the neck, the body, and tail (Fig. 14-1). The divisions between these portions represent arbitrary boundaries that aid in communicating the location of abnormalities. These divisions do not separate anatomically or functionally distinct units.

Figure 14-1 Typical pancreas. SMV, Superior mesenteric vein.

The superior mesenteric vein (SMV) serves as a useful anatomic landmark. The pancreatic head is generally considered the portion of pancreas to the right of the SMV and resides within the c-loop of the duodenum. The uncinate process is the continuation of the head posterior to the SMV and normally has a triangular shape. The posteromedial border of the uncinate process should be concave or flat rather than rounded. The portion of pancreas immediately ventral to the SMV is considered the neck, whereas the body and tail continue to the left. No clear external landmark divides body and tail of the pancreas; therefore, most radiologists roughly divide the pancreas to the left of the SMV in half, designating the more midline portion the body. The pancreatic tail lies within the splenorenal ligament, which provides a conduit for tumor and inflammation between the pancreatic tail and the spleen. The exocrine pancreas generally diminishes with age, often becoming replaced by fat.

Lobulations of the lateral contour of the pancreatic head are commonly visualized on cross-sectional imaging studies of the pancreas. These protrusions of the pancreatic head are similar in echogenicity, attenuation, signal intensity, and enhancement characteristics to normal pancreas and should not be mistaken for pancreatic neoplasm.

The normal pancreatic echotexture is homogeneous and isoechoic to mildly hyperechoic compared with the normal liver on ultrasound (US) images (Fig. 14-2). Increased echogenicity of the pancreas occurs with fatty infiltration. The normal pancreatic parenchyma measures 40 to 50 HU on unenhanced computed tomographic (CT) images. The pancreas is higher in signal intensity than liver, spleen, or skeletal muscle on T1-weighted magnetic resonance (MR) images. The innately high signal intensity of the pancreas on fat-suppressed T1-weighted images makes such images valuable for detecting tumors (Fig. 14-3). The normal pancreas is only slightly higher in signal intensity than muscle on T2-weighted images. With CT or magnetic resonance imaging (MRI), maximum pancreatic parenchymal enhancement occurs at 35 to 45 seconds after intravenous contrast administration or approximately 15 seconds after the contrast bolus arrives in the abdominal aorta.

Figure 14-2 Transverse sonogram of the normal pancreas (arrows) in a patient without clinical evidence of pancreatic disease.

Figure 14-3 Unenhanced, fat-suppressed, T1-weighted (T1W), axial magnetic resonance image through the tail of the pancreas in a patient with pancreatic cancer. SI, Signal intensity.

Pancreatic Relationships

The pancreas is predominantly an extraperitoneal organ that resides in the anterior pararenal space immediately posterior to the lesser sac. The pancreas is separated from the stomach anteriorly by the lesser sac of the peritoneal cavity. The pancreatic tail courses in the splenorenal ligament along with the splenic vessels, rendering this portion of the pancreas intraperitoneal. The two layers of the transverse mesocolon (reflections of the posterior parietal peritoneum) split near the anterior surface of the pancreas providing a route for spread of tumor and inflammation between the pancreas and the transverse colon. The root of the small-bowel mesentery lies just inferior to the pancreas. These relationships provide anatomic continuity among the pancreas, transverse colon, and small bowel. The duodenum is intimately associated with the pancreas and frequently involved by tumor and inflammation arising within the pancreas. The intraperitoneal portion of the duodenum is connected to the pancreas by the dorsal mesoduodenum. The extraperitoneal portion is in the anterior pararenal space adjacent to the pancreas. The second portion of the duodenum courses along the right lateral pancreatic head. The third and fourth portions of the duodenum run dorsal to the pancreatic head, body, and tail.

Pancreatic Duct Anatomy

The main pancreatic duct forms when the dorsal pancreatic duct and ventral pancreatic duct join during embryologic fusion of the dorsal and ventral pancreas. The main duct (duct of Wirsung) runs the length of the pancreas and receives small branch duct tributaries at right angles along its entire length. Until recently, the normal branch ducts were rarely visible on cross-sectional imaging studies. Although this is changing with higher resolution CT scanning and MRI, numerous conspicuous branch ducts should be considered an abnormal finding on cross-sectional imaging studies. The main pancreatic duct gradually tapers from pancreatic head toward the tail without abrupt changes in caliber. The course of the main pancreatic duct varies in the region of the pancreatic neck and head. Some of the more common variants in duct course include a gradual caudal bend toward the ampulla, a “hockey-stick” configuration, a sigmoid or S-shaped course, and a looped appearance. These meanderings of the pancreatic duct are rarely important provided the duct maintains a smoothly tapering and nondilated appearance. The main pancreatic duct normally enters the duodenum with the common bile duct via the major papilla. In many individuals, the dorsal pancreatic duct persists as a smaller caliber accessory duct that extends from the main pancreatic duct near the neck of the pancreas to enter the duodenum at the minor papilla approximately 2 cm proximal to the major papilla (see Fig. 14-1). With state-of-the-art equipment, the normal accessory pancreatic duct can be routinely identified on multidetector CT and high-resolution MRI examinations (this duct is also referred to as the duct of Santorini). Usually, the accessory duct appears as a small rudimentary structure with CT and MRI, although it can be dominant in a small percentage of individuals. On secretin-stimulated MRCP examinations, the pancreatic ducts begin to enlarge approximately 1 minute after secretin administration and reach maximum diameter after approximately 20 minutes.

Vascular Anatomy of the Pancreas and Peripancreatic Vessels

The blood supply to the pancreas comes from branches of the celiac artery and superior mesenteric artery (SMA). The head of the pancreas is richly supplied by three arteries forming an intricate vascular arcade. The gastroduodenal artery (GDA) is a branch of the common hepatic artery that arises from the celiac artery. The GDA gives off the posterior and anterior superior pancreaticoduodenal arteries. These arteries anastomose with the posterior and anterior inferior pancreaticoduodenal arteries, which are branches of the inferior pancreaticoduodenal artery branch of the SMA. The inferior pancreaticoduodenal vessels supply the uncinate process and caudad portion of the head of the pancreas. The third vessel is the dorsal pancreatic artery, a branch of the splenic artery. These intricate vascular arcades that surround the pancreas play a critical role in providing collateral blood supply in the event of celiac axis or proximal SMA obstruction. The body and tail of the pancreas are supplied by the dorsal pancreatic artery, a branch of the splenic artery, and multiple other branches of the splenic artery.

The veins draining the head of the pancreas initially course with the arteries but eventually deviate from these paths. The posterior superior pancreaticoduodenal vein drains to the main portal vein, and the anterior superior pancreaticoduodenal vein drains to the gastrocolic trunk, which drains into the SMV ventrally at the level of the midpancreatic head. The gastrocolic trunk is formed by the junction of the right gastroepiploic vein and the right or middle colic vein. The inferior pancreaticoduodenal vein drains into the proximal jejunal vein that drains into the SMV dorsally at the level of the uncinate process. The pancreaticoduodenal venous arcades serve as a potential portoportal collateral pathway in the event of portal vein obstruction. Enlargement of the pancreaticoduodenal veins in the setting of pancreatic carcinoma is a secondary sign of portal vein compromise by tumor (Fig. 14-4).

Figure 14-4 Coronal reformation of a portal-phase enhanced computed tomographic scan through the upper abdomen of a patient with pancreatic cancer. Portal vein obstruction is bypassed by posterior pancreaticoduodenal veins (arrows).

The venous drainage of the body and tail of the pancreas is to the splenic vein. The splenic vein then joins with the SMV to form the portal vein.

The pancreatic blood supply and drainage are identifiable on vascular-phase, thin-slice, axial CT images. The SMA and SMV normally lie to the left of the pancreatic head. A fat plane surrounds the artery, whereas a fat plane is only occasionally visible between the right lateral margin of the SMV and the pancreatic head. The GDA is easily identified on imaging studies coursing along the right anterolateral border of the pancreatic head. The anterior superior pancreaticoduodenal artery continues caudally from the GDA along the anterolateral pancreatic head. The anterior superior pancreaticoduodenal vein usually drains into the gastrocolic trunk or right gastroepiploic vein and tends to be horizontally oriented on axial CT and MR images. The gastrocolic trunk is easily and consistently found on cross-sectional imaging studies just anterior to the midpancreatic head (Fig. 14-5). The posterior superior pancreaticoduodenal artery (first branch of the GDA) and vein are seen in the region of the distal bile duct between the pancreatic head and the proximal duodenum. The vein can often be seen in cross section on axial images and drains into the suprapancreatic portion of the portal vein within 2 cm of the portal confluence. The inferior pancreaticoduodenal vessels may be visible at the level of the uncinate process, although their small size makes them difficult to identify definitively.

Figure 14-5 Enhanced axial computed tomographic image through the abdomen demonstrates the gastrocolic trunk.

Developmental Anomalies of the Pancreas

The organogenesis of the pancreas occurs in concert with the formation of the liver and duodenum, and involves two separate components, dorsal and ventral, each with its own ductal system. During development, the ventral pancreas rotates posterior to the duodenum to join with the dorsal pancreas, forming a single organ. The two ductal systems also join to create the main pancreatic duct. Not surprising, given the complexity of this process, pancreatic variant anatomy is relatively common (Fig. 14-6).

Figure 14-6 Variant pancreatic ductal anatomy.

Agenesis of the dorsal anlage (dorsal agenesis) occurs when only the pancreatic head and uncinate process develop, and the accessory duct (Santorini) is absent (Fig. 14-7). Dorsal agenesis may be incomplete, resulting in the presence of a variable portion of the dorsal pancreas and accessory duct. Dorsal agenesis can be associated with polysplenia.

Figure 14-7 Enhanced axial computed tomographic images through the upper abdomen in a patient with dorsal agenesis of the pancreas show presence of the ventral pancreas (A) and complete absence of the dorsal pancreas (B).

Ectopic pancreatic tissue can be present within organs of entodermal origin (organs arising from the primitive gut). The gastric antrum and proximal duodenum are most commonly affected. In such cases, the ectopic tissue can consist of acinar cells, islet cells, and a small duct. Ectopic pancreas can also occur in other organs such as the remainder of the small bowel, colon, appendix, Meckel’s diverticulum, gallbladder, liver, and spleen. Rarely, ectopic pancreas occurs above the diaphragm. Abnormalities that affect the pancreas, such as neoplasia and inflammation, can also affect heterotopic pancreatic tissue.

Pancreas divisum is a relatively common anomaly (almost 10% of individuals) characterized by completely separate dorsal and ventral ductal systems draining the pancreas (Fig. 14-8). In divisum, the dorsal duct drains the body and tail of the pancreas via the minor papilla, whereas the ventral pancreatic duct drains the caudad portion of the head and uncinate process via the major papilla. This variant has been implicated in the development of pancreatitis, although many cases of pancreas divisum are discovered incidentally on high-resolution CT or MR images. Occasionally, the dorsal and ventral moieties are separated by a fat plane, but frequently the pancreas is normal in size and shape.

Figure 14-8 Volume-rendered magnetic resonance cholangiopancreatographic image demonstrating pancreas divisum in an asymptomatic patient.

Ansa pancreatica occurs when the normal communication between the accessory pancreatic duct and ventral (main) duct is replaced by a looping branch duct that courses from the region of the minor papilla to drain into the main pancreatic duct (see Fig. 14-6).

Annular pancreas is much less common than divisum. In the case of annular pancreas, the duodenum is completely encircled by pancreatic tissue. Pancreatic ducts can either encircle or drain directly into the duodenum. This anomaly manifests on upper gastrointestinal series in neonates as obstructive narrowing of the second portion of the duodenum. Occasionally, annular pancreas presents in adulthood as an incidental finding on CT or MRI (Fig. 14-9). The pancreatic tissue surrounding the descending duodenum maintains identical echogenicity, attenuation, signal intensity, and enhancement characteristics to the remainder of the pancreas. When the duodenum is not adequately distended with oral contrast material or fluid, the combination of collapsed duodenum and annular pancreas may simulate a neoplasm of the pancreatic head.

Figure 14-9 Annular pancreas. A, Contrast-enhanced computed tomography performed to evaluate the liver in a patient with cirrhosis shows an asymptomatic annular pancreas. B, A similar abnormality is seen on a noncontrast examination in a different patient.

One final pancreatic variant rarely described in the literature involves complete encasement of the portal vein by pancreatic tissue (Fig. 14-10). In such cases, pancreatic parenchyma surrounds the portal vein on all sides, potentially simulating a mass lesion or encasement of the portal vein by tumor. The main pancreatic duct can course anterior or posterior to the portal vein in such cases. Surgical resection of the pancreas can be potentially complicated by this variant.

Figure 14-10 Enhanced axial computed tomographic image through the pancreas of a patient with complete encasement of the portal vein by normal pancreatic tissue (arrows).

Acute Pancreatitis

Acute pancreatitis ranges in severity from mild inflammation beyond the limits of detection of most standard imaging examinations to extensive pancreatic necrosis. Although most patients are diagnosed before imaging, acute pancreatitis is being increasingly diagnosed on imaging studies used to evaluate nonspecific abdominal complaints (often in the place of thorough clinical and laboratory assessment). In cases of pancreatitis established clinically, imaging serves to establish the potential cause, predict the disease course, and detect complications of pancreatitis.

Imaging Findings of Acute Pancreatitis

RADIOGRAPHY

Conventional radiographs are not able to directly image pancreatic inflammation and rarely yield a specific diagnosis of pancreatitis. However, radiographs are often abnormal in the setting of acute pancreatitis (Fig. 14-11). The most common radiographic abnormalities include a focal or generalized ileus, pleural effusion (often left sided), and basal atelectasis. The “colon cutoff sign” originally referred to gaseous distention of the right colon with abrupt termination of the gas column to the left of the hepatic flexure. This sign has been generalized to include areas of narrowing anywhere in the colon related to mesocolic involvement with pancreatitis. Dilatation of the descending duodenum (“sentinel-loop”) can be a sign of pancreatic inflammation and is more suggestive of acute pancreatitis when accompanied by colonic involvement.

Figure 14-11 Abdominal radiograph of a patient with severe acute pancreatitis.

BARIUM

Barium examinations can demonstrate findings of acute pancreatitis or pathology mimicking acute pancreatitis such as peptic ulcer disease.

Upper gastrointestinal series can demonstrate widening of the duodenal c-loop because of an enlarged pancreatic head and thickening and spiculation of the duodenal mucosal folds, especially along the medial wall caused by mucosal edema.

Pancreatic inflammation can extend within the small-intestine mesentery, causing thickening of the small-bowel mucosal folds. These findings can extend to the cecum via the ileocolic mesentery.

Barium enema can demonstrate a dilated right and transverse colon, spasm (particularly common in the region of the splenic flexure), thickened spiculated fold pattern in the transverse colon, or effacement of the inferior haustra of the transverse colon.

ULTRASOUND

Diffuse acute pancreatitis manifests on US as decreased or heterogeneous echogenicity of the pancreas, which can appear enlarged. In the setting of pancreatitis, US has its greatest utility in the diagnosis of gallstones, choledocholithiasis, and biliary obstruction. Hypoechoic inflammation, acute fluid collections, and pseudocysts are easily revealed provided a suitable sonographic window exists (Fig. 14-12). Lesser sac collections are relatively easy to see anterior to the pancreas. Fluid accumulating in the superior recess of the lesser sac can be seen around the caudate lobe. Standard grayscale US is relatively insensitive for the diagnosis of pancreatic necrosis in the setting of acute pancreatitis. Table 14-2 lists some sonographic signs of acute pancreatitis.

Figure 14-12 Longitudinal sonogram of the right kidney demonstrates inflammation (arrows) inferior to the right kidney secondary to acute pancreatitis.

Table 14-2 Sonographic Abnormalities in Acute Pancreatitis

Finding	Prevalence Rate
Peripancreatic inflammation	60%
Heterogeneous parenchyma	56%
Decreased gland echogenicity	44%
Indistinct ventral margin	33%
Glandular enlargement	27%
Focal parenchymal echo change	23%
Peripancreatic fluid collection	21%
Focal mass (usually hypoechoic)	17%
Perivascular inflammation	10%
Pancreatic duct dilatation	4%
Venous thrombosis	4%

Adapted from Finstad TA, Tchelepi H, Ralls PW: Sonography of acute pancre-atitis: prevalence of findings and pictorial essay, Ultrasound Q 21:95-104, 2005, by permission.

COMPUTED TOMOGRAPHY

The initial diagnosis of acute pancreatitis is based on clinical and laboratory findings. However, pancreatitis occasionally presents with a confusing clinical picture. In such cases, CT findings can suggest the correct diagnosis. Furthermore, enhanced CT is of benefit in the initial evaluation of pancreatitis to assess its severity and to identify complications. Intravenous contrast media improve detection of pancreatic necrosis or complications such as pseudoaneurysm formation or venous thrombosis. Occasionally, CT will establish a cause for pancreatitis such as choledocholithiasis or aberrant pancreatic ductal anatomy (Fig. 14-13).

Figure 14-13 Enhanced axial computed tomographic image through the abdomen of a patient with gallstone pancreatitis and a small calcified stone impacted at the ampulla.

The CT findings of uncomplicated acute pancreatitis include focal or diffuse pancreatic enlargement with infiltration or stranding in the peripancreatic fat (Fig. 14-14). Peripancreatic fluid collections commonly occur and either resolve over time or organize to form pseudocysts. After administration of intravenous contrast material, the inflamed pancreas can enhance heterogeneously. Confluent areas of nonenhancing tissue suggest pancreatic necrosis.

Figure 14-14 Enhanced axial computed tomographic image through the upper abdomen of a patient with acute pancreatitis.

MAGNETIC RESONANCE IMAGING

MRI is rarely essential to the acute management of patients with pancreatitis. MRI is considerably less sensitive than CT for detection of calcifications and gas bubbles, but it excels at demonstrating the biliary and pancreatic ductal systems and pancreatitis-related fluid collections. MRI is also more sensitive than other modalities for the detection of pancreatic hemorrhage. In patients with contraindications to iodinated contrast media, gadolinium-enhanced MRI may be helpful in detecting pancreatic necrosis and vascular complications. MRCP aids in detecting stones within the gallbladder, common bile duct, and pancreatic duct. MRCP can also be helpful for defining ductal anatomy in suspected cases of pancreas divisum or annular pancreas. Secretin-augmented MRCP has been suggested as a means of evaluating the pancreatic duct for stricture, disruption, or continuity with pseudocysts. Secretin should be administered in a closely monitored setting to patients with acute pancreatitis because of the potential to exacerbate pancreatic inflammation.

Pancreatic edema results in a higher-than-normal signal intensity pancreas on T2-weighted images and lower-than-normal signal intensity pancreas on T1-weighted images. When sufficiently severe, acute pancreatitis causes diminished enhancement of the pancreas with gadolinium-based contrast administration. Absent enhancement suggests pancreatic necrosis. Uncomplicated acute peripancreatic fluid collections appear as irregularly shaped areas of low signal intensity on T1-weighted images and of very high signal intensity on T2-weighted images. Areas of hemorrhage appear relatively bright on T1-weighted images. Fluid collections complicated by hemorrhage or infection have variable signal intensity on T1- and T2-weighted MR images.

Complications of Acute Pancreatitis

Imaging plays an important role in the detection and management of complications related to pancreatitis. Pancreatic pseudocysts are collections of inflammatory fluid contained within a fibrous capsule (Fig. 14-15). Pseudocysts result from the maturation of acute peripancreatic fluid collections that fail to resolve over the course of several weeks. Many pseudocysts maintain a communication with the pancreatic duct, and this communication may be evident on thin-section CT or MRCP images. Pseudocysts that become symptomatic because of mass effect or infection are usually managed by percutaneous or endoscopic drainage. Pancreatic pseudocysts can exert mass effect on the posterior gastric wall visible with radiography or fluoroscopy (Fig. 14-16). The distinction between pseudocysts and other cystic pancreatic masses is discussed later in this chapter.

Figure 14-15 Axial T2-weighted magnetic resonance image through the level of the pancreatic tail in a patient with a large pancreatic pseudocyst.

Figure 14-16 Frontal radiograph from upper gastrointestinal series (A) and enhanced axial computed tomographic image (B) through the abdomen of a patient with a previous episode of acute pancreatitis and a large pancreatic pseudocyst that displaces the stomach upward and the transverse colon downward. This localizes the mass to the left supramesocolic compartment.

Pancreatic necrosis is present when one or more demarcated foci of pancreatic parenchyma fail to enhance on dynamic contrast-enhanced CT or MRI (≤30 HU at peak enhancement with CT) and occurs in up to a third of cases of acute pancreatitis (Fig. 14-17). Pancreatic necrosis increases mortality and may require necrosectomy when extensive. Focal acute fluid collections, fatty infiltration, or glandular atrophy should not be misinterpreted as pancreatic necrosis. Pancreatic necrosis can become infected, usually several weeks after onset of acute pancreatitis. Gas within an area of nonenhancing parenchyma suggests the diagnosis, although gas also results from fistulous communication with the bowel or prior intervention. Unlike pancreatic pseudocyst or abscess, sterile or infected pancreatic necrosis is difficult to manage via catheter drainage because of the presence of copious solid debris.

Figure 14-17 Enhanced axial computed tomographic image through the upper abdomen of a patient with extensive pancreatic necrosis and a large pancreatiform fluid collection replacing nearly the entire pancreas within the anterior pararenal space.

Pancreatic necrosis can involve the central portion of the pancreas, potentially resulting in interruption of the pancreatic duct because of necrosis of the duct epithelium (Fig. 14-18). In such cases, a variable amount of the pancreatic tissue proximal to the area of necrosis becomes isolated from the main ductal system. This potentially allows leakage of pancreatic secretions into the peripancreatic spaces. The imaging findings of a disconnected pancreatic duct include necrosis of at least 2 cm of pancreas, viable pancreatic tissue proximal to the disruption, and extravasation of contrast material injected at pancreatography. On CT and MR images, a large intrapancreatic fluid collection is often present in the setting of disconnected pancreatic duct, although this finding is nonspecific, because disruption of a pancreatic branch duct can also cause an intrapancreatic fluid collection. Although a branch duct disruption can often be treated with placement of a pancreatic stent, main duct disconnection often requires surgery.

Figure 14-18 Enhanced axial computed tomographic images through the head (A) and tail (B) of the pancreas in a patient with necrosis involving the central pancreas.

Pearl: Necrosis of the central portion of the pancreas can result in interruption of the pancreatic duct, isolation of the remaining viable pancreatic tissue in the tail, and leakage of pancreatic secretions into the peripancreatic spaces.

Pancreatic abscess is a well-defined collection of pus in or near the pancreas that demonstrates variable amounts of gas, a thick enhancing wall, and no central enhancement after administration of intravenous contrast material. Percutaneous aspiration may be necessary to confirm infection or identify an organism. Pancreatic abscess is more amenable to percutaneous drainage than infected pancreatic necrosis.

Hemorrhage associated with acute pancreatitis may occur within the pancreas, within the peripancreatic fat, or within a pancreatic pseudocyst. Hemorrhage within a pseudocyst results in internal echoes with US and increased attenuation of pseudocysts on CT images. Hemorrhage typically causes areas of increased signal intensity on T1-weighted MR images.

Venous thrombosis is relatively common in the setting of pancreatitis and most often involves the splenic vein because of its close relation with the pancreas. Splenic vein thrombosis should be suspected when the vein fails to enhance on CT or MR images after intravenous contrast administration, or when the vein fails to demonstrate flow with Doppler interrogation. Enlarged gastroepiploic veins often signify collateral flow in the setting of splenic vein thrombosis. Other veins to evaluate for evidence of thrombosis in the setting of pancreatitis include the superior mesenteric and portal veins (Fig. 14-19).

Figure 14-19 Enhanced axial computed tomographic image through the abdomen of a patient with severe necrotizing pancreatitis and superior mesenteric vein (SMV) thrombosis.

Pseudoaneurysm formation results from weakening of an arterial wall by pancreatic enzymes. Pseudoaneurysms are typically round and demonstrate arterial-phase enhancement on CT and MRI (Fig. 14-20). Depending on the timing of the scan, some pseudoaneurysms may not completely fill until the second contrast-enhanced phase of a dynamic study; therefore, all vascular phases should be routinely consulted. Pseudoaneurysms will demonstrate evidence of flow on color Doppler images. Whenever a round, potentially fluid-filled structure is identified in the region of the pancreas in a patient with acute pancreatitis, one must always consider the possibility of pseudoaneurysm before attempting aspiration or drainage. Table 14-3 lists some additional potential complications resulting from pancreatitis.

Figure 14-20

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