Imaging features of benign and malignant pancreatic disease

Introduction to pancreatic imaging

Transabdominal ultrasound (US) is a noninvasive, inexpensive, and rapid method of evaluating morphologic changes in the pancreas and may be used as an initial investigation in the setting of abdominal pain or suspected obstructive jaundice. However, considerable limitations reduce its diagnostic utility; these include overlying bowel gas obscuring the pancreas and limitations related to the patient’s body habitus. If a pancreatic mass or parenchymal abnormality is found at US, further assessment with contrast-enhanced computed tomography (CT) or magnetic resonance imaging (MRI) should be performed. If CT is performed in the workup of a pancreatic mass, particularly in suspected pancreatic ductal adenocarcinoma (PDAC), it should be performed as a multiphase pancreatic protocol study, with imaging in the pancreatic parenchymal/late arterial phase and the portal venous phase. MRI with Magnetic resonance cholangiopancreatography (MRCP) is also a mainstay of pancreatic imaging and can provide detailed assessment of the pancreatic and bile ducts. Secretin-enhanced MRCP is an advanced imaging technique, with limited availability. The technique can be used to improve visualization and assessment of the pancreatic ductal system and to assess exocrine gland function.

Congenital conditions, variants, and benign alterations

Pancreatic divisum

Pancreatic divisum is the most common congenital pancreatic ductal anatomic variant, resulting from failure of fusion of the ventral and dorsal pancreatic anlages ( Fig. 17.1 ; see Chapters 1 and 53 ). This results in the majority of pancreatic parenchyma draining via the dorsal duct into the minor papilla. The ventral duct, which generally does not communicate with the dorsal duct, joins the common bile duct to empty into the major papilla. Pancreas divisum may be seen on high-spatial-resolution and thin-section multidetector CT ; however, MRI is generally superior in visualizing the pancreatic duct, with T2 sequences offering similar visualization to dedicated MRCP sequences. MRI will demonstrate the dominant dorsal duct emptying into the minor papilla, superior to the level of the bile duct, with the ventral duct sometimes too small to discretely visualize on MRI or even absent.

Annular pancreas

Annular pancreas is present when a complete or incomplete ring of pancreatic tissue encircles the second portion of the duodenum (D2; Fig. 17.2 ; see Chapters 1 and 53 ). MRI will demonstrate the encircling, or partially encircling pancreatic tissue, and sometimes the small associated annular duct that drains the annular portion. An incomplete ring is demonstrated by pancreatic tissue extending in both a posterolateral and anterolateral direction around the D2 or, in some cases, only in the posterolateral direction. Pancreatic tissue extending only in an anterolateral direction around the D2 is less specific for incomplete annular pancreas.

Fatty infiltration

Fatty replacement of pancreatic tissue may be focal or diffuse and can occur in diabetic, obese, or elderly patients. ^, Complete fatty replacement of the pancreas is seen most commonly in patients with cystic fibrosis or Schwachman-Diamond syndrome. ^, In severe cases, the pancreas will be clearly visible and will have the same density (CT) or signal (MRI) to the mesenteric fat ( Fig. 17.3 ). In this setting, the presence of the ductal system differentiates fatty replacement from agenesis. Fatty replacement may not be homogeneous, with the anterior pancreatic head more severely affected, compared with the posterior pancreatic head peribiliary tissue, which can be spared. ^, This nonhomogeneous fatty replacement may mimic a mass or neoplasm on CT ( Fig. 17.4 ); however, MRI can usually differentiate fatty replacement changes from neoplasm.

FIGURE 17.3, Axial computed tomography (CT) in portal venous phase demonstrating extensive fatty replacement of the pancreas, appearing isodense to the mesenteric fat. Minimal pancreatic acinar tissue is visible in the posterior aspect of the pancreatic head (arrow), where there can be peribiliary sparing.

FIGURE 17.4, Fatty infiltration with pseudomass.

Pancreatitis

Acute pancreatitis

The 2012 revised Atlanta classification provides standardized clinical and radiologic nomenclature for acute pancreatitis and associated complications. The classification defines two distinct types of acute pancreatitis: interstitial edematous pancreatitis (IEP) and necrotizing pancreatitis (NP), depending on the absence or presence of necrosis, respectively (see Chapters 55 and 56 ). ^,

Imaging of the pancreas is not necessarily required in the setting of mild cases of acute pancreatitis because the diagnosis can be based on clinical symptoms and serology. ^, Nevertheless, imaging may be required to make the diagnosis if one of the aforementioned factors is negative or to assess for a causative factor, the most common being gallstones (see Chapter 33 ). ^, Early US can be performed with a limited purpose of identifying gallstones or to demonstrate bile duct dilatation; however, stones in the distal duct may not be identified. Standard contrast-enhanced CT (CECT) abdomen is the most common modality used, and a multiphase pancreatic protocol is typically unnecessary. MRI/MRCP may also be used, particularly in the setting of iodinated contrast allergy, renal failure, or suspicion of choledocholithiasis. ^, Nevertheless, MRI scan time is long compared with CT, and the availability of MRI should be considered. Imaging in pancreatitis should ideally be performed five to seven days after pain onset, when necrosis is clearly definable and local complications have developed. Earlier imaging within the first few days after pain onset may miss or be equivocal for necrosis and correlates poorly with clinical severity. ^,

The CT Severity Index (CTSI) and later modified CT Severity Index (mCTSI) both define specific radiologic criteria for grading the severity of acute pancreatitis and complications. The CTSI score is based on pancreatic changes, the presence and amount of necrosis (none, ≤30%, 30%–50%, and >50%), and peripancreatic fluid collections. The mCTSI includes similar criteria, with a simplified definition of the amount of necrosis (none, ≤30%, and >30%), and includes extrapancreatic findings, such as pleural effusions and ascites. ^, A study involving almost 400 patients demonstrated no significant difference between CTSI and mCTSI in evaluating the severity of acute pancreatitis.

Interstitial edematous pancreatitis

IEP is the more common form of acute pancreatitis and, at imaging, usually appears as diffuse or focal pancreatic enlargement with a small amount of peripancreatic fluid ( Fig. 17.5 ). The pancreatic parenchyma will generally enhance less than a normal pancreas because of the presence of interstitial edema. However, there should be no nonenhancing parenchymal regions or peripancreatic necrotic collections; if these are present, the diagnosis of NP should be made.

According to the 2012 revised Atlanta criteria, any peripancreatic fluid collection occurring within the first 4 weeks of IEP is classified as an “acute peripancreatic fluid collection” (APFC; see Chapter 54 ). Because there is no necrosis in IEP, the APFC will contain only fluid and appear as homogeneous fluid attenuation (0–20 HU) at CT and fluid signal intensity on T2-weighted MRI imaging, conforming to the retroperitoneal structures, and without a well-defined wall. ^, These usually resolve spontaneously without intervention and most APFC will remain sterile. In 10% of cases, the peripancreatic collections persist for more than four weeks, and these are termed pancreatic pseudocysts (see Chapter 54 ). Like APFC, pseudocysts should not include any solid components or debris. Pseudocysts will appear as homogeneous fluid attenuation CT and hyperintense on T2, with a well-defined enhancing capsule. A connection between the pseudocyst and the main pancreatic duct may be present, best visualized on MRI/MRCP ( Fig. 17.6 ). On transabdominal US, pseudocysts typically appear as a circumscribed, smooth-walled spherical anechoic lesion with posterior acoustic enhancement.

FIGURE 17.6, Pseudocyst communication with main duct.

Necrotizing pancreatitis

Necrotizing pancreatitis (NP) is defined by necrosis involving the pancreatic parenchyma and/or the peripancreatic soft tissues. Involvement of both parenchyma and peripancreatic soft tissues is the most common form, occurring in 75% of cases. Involvement of the peripancreatic tissues alone without parenchymal necrosis occurs in 25%, and pancreatic necrosis alone without peripancreatic collections is the least common, occurring in 5%.

At early imaging within the first few days of pain onset, NP will appear as patchy enhancement, potentially indistinguishable from IEP, and with potential underestimation of the eventual extent of necrosis. At around five to seven days, the necrotic, nonenhancing parenchyma will become demarcated, and peripancreatic necrotic collections may develop ( Fig. 17.7 ). If parenchymal necrosis is present, the amount of necrosis should be estimated according to either the CTSI or mCTSI systems. ^, Parenchymal necrosis predominantly affects the neck and body, and the head and tail may be spared. If there is confluent necrosis extending over 2 cm at the head, neck, or body, the pancreatic duct may be disrupted and pancreatic fluid from the isolated non-necrotic distal body or tail will leak into soft tissues, causing fistulas and collections. The disrupted duct may be best identified with ERCP or secretin MRCP. The isolated duct may not be dilated.

FIGURE 17.7, Axial computed tomography (CT) in the portal venous phase.

Pancreatic and peripancreatic fluid collections occur in NP, and these have different and specific terms to the fluid collections found in IEP. A collection present within the first four weeks of NP is termed an “acute necrotic collection” (ANC). These can occur within the pancreas or peripancreatic tissue, are often multiple, loculated, and can extend into the pelvis. ANC contain a variable amount of fluid, debris, and necrotic tissue. At imaging, the debris and necrotic tissue will appear as nonenhancing solid components or fat globules. The term ANC is still used in NP to describe any fluid collection, even if the collection lacks debris. After four weeks, the collections will become encapsulated with a well-defined, thick enhancing wall, termed “walled off necrosis” (WON). These can occur in both the pancreatic parenchyma and peripancreatic tissues and may form coalescent collections. MRI is superior to CT in demonstrating the internal debris present with WON. The internal debris usually appears as dependant, nonenhancing T2 hypointense material on MRI, and as soft tissue or high attention on CT ( Fig. 17.8 ). Infected necrosis does not have specific imaging findings; air within the necrotic areas can indicate infection but may also be secondary to fistula.

Leaked pancreatic proteolytic enzymes can cause weakening of vessel walls and the formation of pseudoaneurysms, most commonly involving the splenic, gastroduodenal, and pancreaticoduodenal arteries, and may lead to life-threatening hemorrhage (see Chapter 115 ). If hemorrhage is clinically suspected, a multiphase CT with both arterial and portal venous phases should be performed. On imaging, pseudoaneurysms will show a connection to an adjacent vessel and enhance similar to arteries. Other local complications that may be evident on imaging include splenic or portal vein thrombosis, gastric outlet obstruction, and colonic necrosis.

You're Reading a Preview

Become a Clinical Tree membership for Full access and enjoy Unlimited articles

Become membership

If you are a member. Log in here