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MRI of the Pancreas and Spleen
▪ Pancreas
Anatomy and Function
The pancreas is a nonencapsulated organ of the digestive system located within the retroperitoneum, posterior to the stomach and anterior to the spine. The pancreas is approximately 2 inches wide and 6 to 8 inches in length. The pancreas can be subdivided into the head, uncinate process, neck, body, and tail ( Fig. 5.1 ). The head and uncinate process are cradled by the duodenum. Its body sits posterior to the body of the stomach. The tail of the pancreas tickles the hilum of the spleen.
The pancreas possesses exocrine and endocrine function. The exocrine tissues of the pancreas (acinar cells) constitute approximately 95% of the pancreatic tissue and are made up of acinar cells. The acinar cells produce pancreatic enzymes, which flow through the pancreatic duct and enter the duodenum via the ampulla of Vater (at the major papilla) to aid in digestion. (In a minority of patients, the minor papilla, situated slightly cephalad to the major papilla, also transmits digestive fluids into the duodenal lumen.) The remaining 5% of the pancreatic tissue is responsible for the endocrine function of the gland and is made up of small clusters of cells throughout the gland, called islets of Langerhans . The endocrine tissues produce hormones that are released into the bloodstream.
Normal Appearance
The normal pancreas has the highest signal intensity of the abdominal organs in in-phase T1-weighted gradient recalled-echo images (except in the presence of hepatic steatosis) owing to the aqueous proteins in the glandular elements, intracellular paramagnetic substances (like manganese), and abundant endoplasmic reticulum in the pancreatic exocrine cells ( Fig. 5.2A ). The relative signal intensity of the pancreas increases in fat-suppressed T1-weighted images owing to the increased dynamic range ( Fig. 5.2B ). Normal pancreas is slightly hyperintense to muscle in T2-weighted images ( Fig. 5.3A ). With the addition of fat suppression, there is minimal contrast between normal pancreatic parenchyma and the surrounding suppressed fat ( Fig. 5.3B ).
Owing to the highly vascular nature of the pancreas, the normal pancreatic parenchyma demonstrates a homogeneous blush shortly after the arrival of gadolinium in the abdominal aorta. Because the liver receives the majority of its blood flow via the portal system, the pancreas is hyperintense to the liver and fat during the arterial phase ( Fig. 5.4 ).
▪ Imaging Techniques
Optimal imaging of the pancreas demands high-field-strength systems with an adequate fat-water frequency shift for chemically selective fat suppression (≥1 Tesla) and high-performance gradients that enable the use of fast magnetic resonance (MR) sequences. Protocols should include axial T1-weighted imaging with and without fat suppression (either breathhold gradient recalled-echo or breathing signal-averaged spin-echo sequences). T1-weighted images with fat suppression are ideal for depicting the extent of extrapancreatic involvement of inflammatory and neoplastic processes (ie, vascular encasement). As discussed previously, fat suppression increases the dynamic range and improves the detection of small pancreatic lesions by providing the greatest contrast between normal and abnormal pancreatic tissues. Fat-suppressed T2-weighted imaging is useful for depicting ductal anatomy, cystic pancreatic lesions, islet cell tumors, peripancreatic fluid collections, and hepatic metastases.
Two-dimensional (2-D) or three-dimensional (3-D) dynamic, postgadolinium, fat-suppressed T1-weighted gradient recalled-echo sequences aid in the characterization of pancreatic masses, diffuse inflammatory pancreatic processes, and vascular involvement. Postcontrast imaging involves imaging of both the pancreatic parenchymal and the peripancreatic vascular phases. In general, this can be accomplished by imaging at 15 seconds and 35 to 45 seconds after the arrival of gadolinium in the abdominal aorta.
▪ Congenital/Developmental Anomalies of the Pancreas
During normal development, the ventral and dorsal pancreatic buds rotate about the duodenum and fuse. The ventral pancreatic bud constitutes the posteroinferior pancreatic head and the uncinate process. The dorsal pancreatic bud constitutes the anterior head, body, and tail. Following rotation and fusion of the ventral and dorsal pancreatic buds, there is fusion of the main pancreatic duct (Wirsung) and the accessory pancreatic duct (Santorini) ( Fig. 5.5 ). Migrational disturbances result in a variety of congenital lesions marked by different structural deformities in pancreatic anatomy.
Annular Pancreas
Annular pancreas is a rare congenital anomaly that results when there is abnormal migration and rotation of the ventral bud of the pancreas, resulting in a ring of pancreatic tissue that completely or partially encircles the duodenum ( Fig. 5.6 ). The majority of patients with annular pancreas present with gastric outlet obstruction during infancy. Infants with symptomatic annular pancreas also tend to have associated anomalies, such as trisomy 21, duodenal atresia, and tracheoesophageal fistula. Adults with annular pancreas present with peptic ulcer disease and pancreatitis.
During imaging, annular pancreas demonstrates a ring of normal pancreatic parenchyma (high T1-weighted signal intensity) about the duodenum and an aberrant pancreatic duct encircling the duodenum and joining the main pancreatic duct (best seen by magnetic resonance cholangiopancreatography [MRCP]).
Pancreas Divisum
Pancreas divisum is the most common congenital variant of the pancreatic duct, representing the failure of fusion of the ducts of the ventral and dorsal pancreatic buds ( Fig. 5.7 ). The clinical significance of this congenital variant is controversial because most patients are asymptomatic. However, in a subset of these patients with recurrent pancreatitis or abdominal pain, functional stenosis of the minor papilla with resultant obstruction of the exocrine juices causing increased intraductal pressure, ductal distention, and recurrent pancreatitis is believed to be the pathogenesis. These patients often benefit from endoscopic or surgical drainage of the minor papilla.
Variation in pancreatic ductal anatomy potentially simulates pancreas divisum ( Fig. 5.8 ). Aberrations in embryologic fusion of the pancreatic anlage result in different pancreatic ductal configurations and potential persistent patency of the duct of Santorini through the minor papilla.
Agenesis
Complete agenesis of the pancreas is a very rare condition and incompatible with life. Partial agenesis is rare, with either the ventral or the dorsal segment of the pancreas failing to develop. Partial agenesis of the pancreas is associated with polysplenia and intrathoracic abnormalities. Patients with agenesis of the dorsal bud or hypoplasia are more common, but also rare. Agenesis of the dorsal bud is related to a mutation in the gene for insulin promoter factor-1 (IPF-1). Patients with pancreatic hypoplasia generally have a normal development of the pancreas, but later in life, they have replacement of the normal glandular elements with fatty tissue and present with exocrine insufficiency and normal endocrine function.
▪ Diffuse Pancreatic Disorders
Lipomatosis
Severe pancreatic lipomatous depositions can occur in adult patients with severe obesity, senile atrophy, or cystic fibrosis. The pancreatic parenchyma demonstrates some degree of atrophy with preservation of the pancreatic margins and normal lobulations.
Pancreatitis
Pancreatitis is the most common benign disease of the pancreas. The majority of cases are caused by cholelithiasis or alcohol abuse (∼80% of cases), but a wide variety of uncommon etiologic factors have been identified ( Table 5.1 ). The diagnosis of pancreatitis is clinical, based on laboratory abnormalities and clinical presentation. The role of magnetic resonance imaging (MRI) is to identify possible etiologies (eg, choledocholithiasis) or complications (necrosis, peripancreatic inflammation and fluid collections, pseudocysts, hemorrhage, abscess, pseudoaneurysm, and/or venous thrombosis). However, when the cause of abdominal pain is unclear, imaging findings help establish the diagnosis of pancreatitis.
TABLE 5.1
Etiologies of Pancreatitis
| Drugs | Infectious | Inherited | Mechanical | Metabolic | Toxins | Other |
|---|---|---|---|---|---|---|
| Furosemide | CMV | Cystic Fibrosis | Gallstones | Hypertriglyceridemia | Alcohol | Pregnancy |
| ACE inhibitors | Mumps | Autosomal dominant PRSS1 mutation | ERCP | Hypercalcemia | Methanol | Groove pancreatitis |
| Sulfa drugs | Salmonella | Pancreatic or ampullary carcinoma | Tropical pancreatitis | |||
| Azathioprine | Coxsackie B | Pancreas divisum | Post renal transplant | |||
| Pentamidine | Sphincter of Oddi stenosis | Ischemia (ie, hypotension) | ||||
| Valproate | Choledochal cyst | |||||
| Asparaginase |
ACE , angiotensin-converting enzyme; CMV , cytomegalovirus; ERCP , endoscopic retrograde cholangiopancreatography.
Acute Pancreatitis
Acute pancreatitis encompasses a wide spectrum from mild inflammation of the pancreatic parenchyma to severe disease, possibly including hemorrhage, necrosis, and/or superimposed infection ( Fig. 5.9 ). As such, the imaging appearance is varied ranging from normal homogeneous T1 hyperintensity to heterogeneous T1 hypointensity with glandular enlargement, heterogeneous enhancement, and loss of the normal pancreatic contours with thickening of the left anterior pararenal fascia (see Fig. 5.9 ).
With pancreatic inflammation, the gland focally or diffusely enlarges. Associated peripancreatic fluid is best detected in fat-suppressed T2-weighted images with even trace T2 hyperintense peripancreatic fluid standing out from the intermediate-to-low T2-weighted signal intensity of the pancreatic parenchyma and the signal suppressed peripancreatic fat. As the severity of pancreatitis increases, there is decreased T1-weighted parenchymal signal intensity with blunted heterogeneous early phase contrast enhancement ( Fig. 5.10 ).
In the majority of severe cases of pancreatitis, there is a reaction to the pancreatic inflammatory process resulting in the development of fluid collections within the pancreatic parenchyma, peripancreatic tissues, lesser sac, and paracolic gutters. The majority of these fluid collections are resorbed in 4 to 6 weeks; however, approximately 10% develop a capsule and eventually become pseudocysts ( Fig. 5.11 ).
Pancreatic necrosis is a complication of severe pancreatitis in which there is either focal or diffuse nonviable pancreatic parenchyma ( Fig. 5.12 ). Absent enhancement, superimposed in findings of acute pancreatitis, indicates necrosis. Pancreatic necrosis tends to involve the body and tail of the pancreas and spare the head owing to its abundant vascular supply. The potential for abscess development and the high morbidity of pancreatic necrosis usually necessitate percutaneous drainage or surgical débridement. When 75% or more of the gland is necrotic or there is progression of pancreatic necrosis on serial examinations, necrosectomy is generally performed owing to the high morbidity.
Leakage of pancreatic enzymes from the inflamed pancreas can result in autodigestion of the arterial wall with subsequent pseudoaneurysm formation ( Fig. 5.13 ). The most commonly involved artery is the splenic artery, followed by the pancreaticoduodenal and gastroduodenal arteries.
The most common vascular complication of pancreatitis is venous thrombosis. The close proximity of the splenic vein to the body and tail of the pancreas renders it the most susceptible to thrombosis. However, the superior mesenteric vein and portal confluence can also be involved.
Chronic Pancreatitis
Chronic pancreatitis is a progressive inflammatory disease of the pancreas with irreversible morphologic changes of the pancreatic parenchyma, eventually resulting in loss of endocrine and exocrine function of the gland.
Imaging stigmata of this disease process include decreased T1-weighted signal intensity of the gland, owing to a decreased protein content as a result of glandular atrophy and fibrosis (also contributing to T1 hypointensity). Furthermore the fibrotic changes of the parenchyma result in attenuation of the vascular supply, reflected by decreased enhancement in immediate postgadolinium images. The spectrum of changes in the pancreatic duct are broad, including dilatation, stricture, stenosis, intraductal calculi, and occasionally side branch duct dilatation (“chain of lakes” or “string of pearls” appearance) ( Fig. 5.14 ). The most pathognomonic imaging feature of chronic pancreatitis is parenchymal calcification; however, this occurs late in the disease process and is best seen by computed tomography (CT) imaging ( Fig. 5.15 ).
Autoimmune Pancreatitis
Autoimmune pancreatitis (AIP, also known as lymphoplasmacytic sclerosing pancreatitis) is a rare form of chronic pancreatitis. The autoimmune inflammatory process is marked by a lack of classic acute attacks of pancreatitis with a predilection for older males (over 50 years of age). Because of the uniquely dramatic response to steroids, consider AIP in the appropriate clinical setting.
Imaging findings also differ from other forms of pancreatitis. AIP tends to be mass-forming, with either focal or diffuse pancreatic enlargement, minimal peripancreatic inflammation, and has an absence of vascular encasement or calcification. Diffuse irregular narrowing of the main pancreatic duct and a peripancreatic hypointense hypovascular rind are characteristic features. These imaging features occasionally simulate the appearance of pancreatic carcinoma ( Fig. 5.16 ). Abrupt ductal caliber change with upstream dilatation and glandular atrophy and vascular encasement favor pancreatic carcinoma. Elevated IgG and autoantibody levels and clinical response to corticosteroids favor AIP.
Groove Pancreatitis
Groove pancreatitis is a form of segmental pancreatitis occurring between the pancreatic head, the common bile duct, and the duodenum. Although usually occurring in young men with a history of alcohol abuse, the etiology and pathogenesis of groove pancreatitis remain unknown. The imaging is similar to that of acute pancreatitis; however, the focal nature of this process makes differentiation from a periampullary tumor difficult ( Figs. 5.17 and 5.18 ). The characteristic MRI findings include a sheet-like mass between the second segment of the duodenum and the pancreatic head, often with superimposed cysts (frequently in the duodenal wall), duodenal stenosis, and a widening of the space between the distal common bile/pancreatic ducts and the duodenal lumen (best seen on MRCP) ( Fig. 5.18 ).
Hereditary Pancreatitis
Hereditary pancreatitis is a rare autosomal dominant disease with variable penetrance leading to exocrine dysfunction. This disease arises from mutations in the trypsinogen gene. The natural history is very similar to that of chronic alcoholic pancreatitis; however, symptom onset occurs at an earlier age and there is a higher prevalence of pseudocyst formation. There is an elevated risk for the development of pancreatic adenocarcinoma with smoking (∼50–60 times), increasing the risk and lowering the age of onset. Prominent pancreatic duct calcifications are a hallmark of this disease and are similar to those seen in chronic alcoholic pancreatitis; however, affliction of a much younger age group distinguishes hereditary pancreatitis ( Fig. 5.19 ).
▪ Genetic Disorders
Cystic Fibrosis
Cystic fibrosis is an autosomal recessive disease characterized by secretory dysfunction of the exocrine pancreas. Impaired mucociliary transport results in mucous plugging of the exocrine glands. MRI findings encompass a spectrum of imaging appearances, including pancreatic enlargement with complete fatty replacement, with or without loss of the normal lobulated contour, pancreatic atrophy with partial fatty replacement, and diffuse atrophy of the pancreas without fatty replacement. Superimposed pancreatic cysts secondary to duct obstruction are another manifestation of cystic fibrosis. Enlargement of the pancreas with complete fatty replacement is the most common imaging appearance ( Fig. 5.20 ). Fatty replacement imitates the appearance of retroperitoneal (macroscopic) fat with uniform T1 hyperintensity and signal loss in fat-suppressed images.
Primary (Idiopathic) Hemochromatosis
Primary (idiopathic or genetic) hemochromatosis is an autosomal recessive disease caused by a mutation that results in excessive iron absorption from the gastrointestinal tract with deposition of iron in the liver, heart, anterior pituitary, pancreas, joints, and skin (see Chapter 3 ). Cardiac and pancreatic deposition progresses over time. The presence of iron deposition in the pancreas correlates with irreversible changes of cirrhosis in the liver.
MR images demonstrate decreased T1- and T2-weighted pancreatic parenchymal signal intensity (lower than skeletal muscle) as a result of the paramagnetic effects of iron. These paramagnetic effects are exaggerated in gradient recalled-echo images with increasing echo times; therefore, in the in-phase T1-weighted images, the pancreas will lose signal compared with the out-of-phase images ( Fig. 5.21 ).
![▪ FIG. 5.21, Hemochromatosis. Out-of-phase ( A , time to excitation [TE] = 2.3 msec), in-phase ( B , TE = 4.6 msec), and long echo ( C , TE = 9.4 msec) T1-weighted gradient recalled-echo images demonstrate decreased signal intensity of the liver, spleen, and pancreas with increasing echo times.](https://storage.googleapis.com/dl.dentistrykey.com/clinical/MRIofthePancreasandSpleen/20_3s20B9780323431415000057.jpg "▪ FIG. 5.21, Hemochromatosis. Out-of-phase ( A , time to excitation [TE] = 2.3 msec), in-phase ( B , TE = 4.6 msec), and long echo ( C , TE = 9.4 msec) T1-weighted gradient recalled-echo images demonstrate decreased signal intensity of the liver, spleen, and pancreas with increasing echo times.")
Von Hippel–Lindau Disease
Von Hippel–Lindau disease is an autosomal dominant condition with variable penetration (see Chapter 6 ). This condition is characterized by cerebellar, spinal cord, renal, and retinal hemangioblastomas and is associated with renal angioma, renal cell carcinoma, and pheochromocytoma.
Pancreatic lesions include single or multiple cysts, cystic replacement of the pancreas, microcystic adenomas, and islet cell tumors. Cysts are the most common pancreatic manifestation ( Fig. 5.22 ).
Schwachman-Diamond Syndrome
Schwachman-Diamond syndrome is a rare congenital disorder of pancreatic insufficiency, growth retardation, and other congenital abnormalities. Imaging demonstrates extensive replacement of the pancreatic tissue with fat.
Johanson-Blizzard Syndrome
Johanson-Blizzard syndrome is an autosomal recessive disorder of ectodermal dysplasia with both endocrine and exocrine insufficiency. The primary defect is in the acinar cells with fatty replacement occurring over time.
Both Schwachman-Diamond and Johanson-Blizzard syndromes have preserved ductal output of fluid and electrolyes.
▪ Focal Pancreatic Lesions
Focal pancreatic lesions stratify into two basic categories: cystic and solid ( Fig. 5.23 ). The distinction helps lower the suspicion of malignancy—solidity usually implies malignancy. Solid tissue raises the specter of pancreatic adenocarcinoma—the diagnosis of exclusion. Cystic etiology incurs a better prognosis, but still threatens malignancy in the form of intraductal papillary mucinous neoplasm (IPMN), cystic metastases, and other conditions. T2-weighted sequences and postcontrast imaging collude to establish cystic versus solid tissue. Marked hyperintensity in T2-weighted sequences, indicating free water protons, characterizes cystic lesions. Postcontrast images bear binary information: enhancement = solid (enhancement) versus cystic (absent enhancement). The discrimination between lesions within cystic and solid categories becomes more difficult. Specific features within each category (discussed in the following subsections on solid and cystic lesions) narrow the differential diagnosis.
Solid Pancreatic Lesions
The two most common solid pancreatic neoplasms are adenocarcinoma and neuroendocrine tumors. These lesions have drastically different enhancement patterns and establish the archetypal enhancement categories—hypovascular and hypervascular, respectively. These designations depend on comparison with the background pancreatic parenchyma ( Fig. 5.24 ). Under normal circumstances, the pancreatic parenchyma avidly enhances, approximating the hypervascularity of islet cell tumors and significantly out-enhancing hypovascular pancreatic adenocarcinoma. However, with coexistent pancreatitis, pancreatic parenchymal enhancement (and precontrast signal intensity) drops, closely simulating adenocarcinoma. For this reason, the pancreatic lesion assessment depends on the status of the background pancreatic parenchyma.
Pancreatic Adenocarcinoma
Pancreatic adenocarcinoma is the most common pancreatic malignancy, accounting for approximately 95% of all pancreatic malignant tumors. Based on incidence rates from 2010 to 2012, approximately 1.5% of all men and women born today will be diagnosed with pancreatic adenocarcinoma at some time during their lifetime. Pancreatic adenocarcinoma is the third leading cause of cancer death in the United States, mainly attributable to the extremely poor survival: less than 20% of newly diagnosed patients survive the first year. There is an overall dismal prognosis with a 5-year survival rate of approximately 7.2%. Patients with localized disease at diagnosis have improved survival rates relative to those with advanced disease at diagnosis (27.1% 5-year survival for those with localized disease versus 2.4% for those with distant metastases). Pancreatic adenocarcinoma predominantly affects the elderly population, with 88.3% of patients diagnosed being older than 55 years of age, with the median age at diagnosis being 71. The majority of cases of pancreatic adenocarcinoma occur within the head of the pancreas and present with either jaundice, weight loss, pain, or nausea. Carbohydrate antigen 19-9 (CA 19-9) has been shown to be an effective diagnostic serum tumor marker with good sensitivity and specificity.
Pancreatic adenocarcinoma is typically hypointense compared with the normal pancreatic parenchyma in T1-weighted images ( Fig. 5.25 ; see also Fig. 5.24 ). Fat suppression increases lesion conspicuity by increasing the dynamic range between the low signal intensity tumor and the higher signal intensity of the normal parenchyma. Tumors have variable signal intensity in T2-weighted imaging depending on the degree of hemorrhage, necrosis, and inflammatory changes. In general, T2-weighted imaging is less helpful than T1-weighted imaging because of the poor contrast between the mass and the normal pancreas. Pancreatic adenocarcinoma is usually hypovascular to the normal glandular tissue in arterial phase imaging followed by gradual enhancement in delayed imaging, related to its desmoplastic content (see Fig. 5.24 ). Immediate contrast-enhanced imaging is the most sensitive for detecting pancreatic adenocarcinoma, especially in lesions that are small or do not deform the contour of the normal pancreas ( Fig. 5.26 ). Obstruction of the main pancreatic duct is one of the most common findings in pancreatic adenocarcinoma ( Fig. 5.27 ). Contiguous obstruction of the pancreatic and common bile ducts, as a result of the presence of a pancreatic head mass, is known as the “double duct” sign and is highly suggestive of malignancy ( Fig. 5.28 ). Because pancreatic adenocarcinomas frequently progress undetected until inciting symptoms, distal gland atrophy is often associated with the aforementioned duct dilatation.
In the setting of underlying pancreatitis, detecting underlying adenocarcinoma is problematic because both the tumor and the surrounding pancreas demonstrate similar T1 hypointensity. However, immediate contrast-enhanced images better delineate the size and extent of pancreatic adenocarcinomas, which tend to enhance less than adjacent inflamed pancreatic parenchyma (see Fig. 5.24 ). However, focal pancreatitis presents diagnostic difficulty because focal pancreatic enlargement, distortion of the normal glandular contour, ductal dilatation, and abnormal enhancement simulate pancreatic adenocarcinoma. Short-term follow-up imaging after resolution of the acute illness hopefully eliminates equivocation.
For the majority of cases, the diagnosis of pancreatic adenocarcinoma is straightforward and the role of imaging is to determine resectability ( Box 5.1 ). Among the factors preempting resectability and surgical cure, distant metastases and local spread account for most cases (40% each). Because the pancreas lacks a capsule to obstruct neoplastic spread and because most lesions arise in the pancreatic head, densely surrounded by adjacent structures, regional spread proceeds rapidly ( Fig. 5.29 ). Pancreatic continuity with the superior mesenteric vessels promotes vascular encasement of these vessels, which also precludes curative surgical resection. Vessel enhancement of 180 degrees constitutes vascular encasement (see Fig. 5.29 ). Metastatic spread progresses from regional lymph nodes to the liver and, uncommonly, to the lungs. In addition to direct invasion of adjacent structures, such as the duodenum and stomach, spread to any peritoneal surface is at risk for peritoneal dissemination.
BOX 5.1
Factors Predisposing to Unresectability in Pancreatic Cancer
-
Liver metastases
-
Vascular encasement (180 degrees)
-
Peritoneal implants
-
Peripancreatic spread
-
Size >3 cm
-
Adenopathy
-
Retroperitoneal
-
-
Mesenteric
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