22 Pancreas


22 Pancreas

Herzog\, Christopher

A diagram of computed tomography (CT) landmarks of the pancreas and its surrounding organs is presented in Fig. 22.1. Size, shape, and retroperitoneal position of the pancreas show a marked variation in individuals. Usually the diameter of the pancreatic head does not exceed the transverse diameter of the adjacent vertebral body. In general, the pancreatic head-to-vertebra ratio is ~0.7 and pancreatic body-to-vertebra ratio ~0.3. Thus, the pancreas reduces harmonically from head to tail in sagittal diameter. Benchmark diameters are 3 cm for the head, 2.5 cm for the body, and 2 cm for the tail. There is gradual diminution of the pancreatic size with advancing age. The contour of the pancreas is smooth in ~80% of individuals (Fig. 22.2) and lobulated in ~20% (Fig. 22.3).

The main duct of the pancreas (duct of Wirsung) lies centrally in the longitudinal axis of the organ and does not exceed 3 to 4 mm in diameter; > 5 mm in diameter is regarded as pathological. The auxiliary pancreatic duct (duct of Santorini) and side branches of the main duct usually are not visible on CT scans.

Inhomogeneous fatty replacement (attenuation from − 40 to − 10 HU, Fig. 22.4) of pancreatic tissue is more common in the anterior aspect of the head of the pancreas, whereas the posterior aspect and the area around the common bile duct tend to be spared. It represents a common tissue abnormality of the pancreas and typically is associated with age and obesity, less frequently with cystic fibrosis, diabetes mellitus, and pancreatitis. The annular pancreas is a ring of pancreatic tissue surrounding and encasing the descending or transverse part of the duodenum. It is a congenital abnormality due to hypertrophy of the dorsal and ventral pancreatic duct or abnormal migration of the left ventral pancreatic bud to the right of the duodenum rather than to the left. Pancreas divisum is observed in patients with insufficient fusion of the dorsal and ventral bud of the pancreas. Although it may be a cause for otherwise inexplicable recurrent pancreatitis, it is often missed.

The portal vein is formed behind the neck of the pancreas by the confluence of the splenic and superior mesenteric veins. The uncinate process of the pancreas head extends between the superior mesenteric vein and the inferior vena cava. Occasionally, the tail or head is congenitally absent.

Differentiation from the adjacent duodenum is critical for sufficient evaluation of the pancreas. Patients should drink 1l oz pure water (Hydro-CT) prior to the CT examination. This not only makes the duodenum appear hypodense in comparison to surrounding tissue, but also allows identification of hyperdense gallstones in the ampulla of Vater, which may otherwise be obscured by oral contrast medium. Differentiation may even be optimized by asking the patient to drink 300 mL water immediately before the exam and to subsequently rest on the right side for ~5 min before scanning is started. Additional administration of spasmolytic drugs (Buscopan) significantly decreases bowel motion and therefore has a direct impact on image quality. On precontrast scan, attenuation values of normal pancreatic tissue range from 30 to 50 HU.

Neoplasms usually are iso- to hypodense to normal pancreatic tissue and thus are masked on both precontrast and delayed postcontrast scans. Optimal visualization of malignancies is usually achieved on portal venous scans, when pancreatic tumors appear hypodense in contrast to typically strong enhancing pancreatic tissue. Endocrine-active tumors typically are enhancing—and thus discernible—only during the early arterial phase (AP).

In patients with acute pancreatitis, contrast enhancement helps to differentiate vital—and therefore attenuating—pancreatic tissue from nonenhancing necrotic tissue. Intravenous contrast administration is useful to distinguish pancreatic parenchyma from adjacent blood vessels, abdominal organs, or ligaments.

CT evaluation for neoplasms of the pancreas should be based on at least four contrast phases: noncontrast, or nonenhanced, CT; arterial phase (AP); portal venous phase (PVP); and parenchymal phase (PP). AP scans usually are acquired 25 to 30 seconds after the beginning of contrast injection, PVP immediately following this scan, and PP about 70 seconds after the beginning of contrast injection. For all other indications, three phases—nonenhanced, PVP, and PP—are sufficient. For follow-up examinations, usually only PVP and PP scans are necessary. Use of double-barrel power injectors, high-contrast flow (≥ 3.5 mL/s), and application of bolus chaser technique with 50 mL saline following contrast media injection are critical to achieve optimal image contrast. It is also preferable to use contrast media concentrations of 350 mg I/mL or higher. The total amount of contrast media should not exceed 70 to 90 mL.

Fig. 22.1 Anatomy of the pancreas and its surroundings. (Modified after Webb.)




inferior vena cava


left renal vein


superior mesenteric artery


superior mesenteric vein

Fig. 22.2 Smoothly delineated normal pancreas. Parenchyma attenuation is isodense to many neighboring organs in this nonenhanced image.

To identify even small pancreatic lesions and also be able to evaluate pancreatic ducts (ranging from 2.0 to 6.5 mm in diameter) on multidetector-row CT scanners, beam collimations < 1.5 mm and a slice thickness < 3 mm are required. The pancreatic duct is not always visible in all patients (Fig. 22.5). Optimal visualization of pancreatic ducts may often be achieved by using minimum intensity projection (MinIP) reformations.

The differential diagnoses of pancreatic abnormalities are discussed in Table 22.1.

Fig. 22.3 Atrophic pancreas. Lobulated, somewhat atrophic pancreas with fat between lobules and fatty replacement of the pancreas body. Modest atrophy of pancreas is normal in the elderly.
Fig. 22.4 Fatty replacement of the pancreas.
Fig. 22.5 A 10-mm slice through the body of the pancreas. The body, tail, and distal part of the head are visualized. The pancreatic duct (PD, arrow) is only barely visible within the body.

Table 22.1 Abnormal pancreas


CT Findings



Pancreatic abscess

Fig. 22.6

Well-defined cystic lesion in the pancreas.

Scan recommendation:

Biphasic CT (nonenhanced CT, parenchymal phase [PP]).

Nonenhanced CT: Near-water fluid collection. Intracystic gas present in 30% to 50% of cases.

PP: Slight rim enhancement.

Diagnostic pearls: Well-defined cystic mass with intracystic gas in a patient with a known history of pancreatitis.

Rare, but severe complication of acute pancreatitis. In 30% of cases, there are multiple abscesses. Fistulous tracts are often responsible for intralesional gas collection. Without the presence of gas, abscesses often are indistinguishable from noninfected (pseudo-) cysts. Treatment: PAD, surgery (high mortality without).


Pancreas divisum

Fig. 22.7a, b

Nonfusion of dorsal and ventral pancreatic buds.

Scan recommendation:

Biphasic CT (nonenhanced CT, PP).

Nonenhanced CT: Large pancreatic head. Separation of ventral and dorsal pancreatic segment sometimes with a visible fatty cleft between both. Nonfusion of ducts visible on thin-slice minimum intensity projection (MinIP).

PP: Hypoattenuation of necrotic areas (if present).

Diagnostic pearls: Large pancreatic head with separate duodenal drainage of nonfused long (dorsal) and short (ventral) pancreatic duct in a patient with recurrent pancreatitis.

Failure of ventral pancreas in rotation during embryogenesis posteriorly to the duodenum to come (physiologically) into contact with the dorsal pancreas.

Typical clinical symptoms are epigastric pain with or without vomiting in young patients due to recurrent episodes of idiopathic pancreatitis.

Treatment (only in symptomatic patients): sphincteroplasty or surgery.

Usually not diagnosed on CT scans. Magnetic resonance cholangiopancreatography (MRCP) modality of choice.

Annular pancreas

Fig. 22.8a, b

Encasement of descending duodenum through ringlike pancreatic tissue.

Scan recommendation:

Biphasic CT (nonenhanced CT, PP).

NECT: Obstructing band of pancreas tissue around descending duodenum with dilatation of stomach and proximal duodenum.

PP: Better delineation of pancreatic tissue.

Hypoattenuation of necrotic areas (if present).

Either due to hypertrophy of the dorsal and ventral pancreatic duct or to abnormal migration of the left ventral pancreatic bud to the right of the duodenum rather than to the left.

Typically diagnosed during childhood.

Clinical symptoms are epigastric pain with or without vomiting due to recurrent episodes of idiopathic pancreatitis, but pancreatitis is observed only in 20% to 30% of cases.

Differential diagnosis: pancreatic or duodenal carcinoma.

Agenesis of dorsal pancreas

Congenital absence of tail, body, and neck of pancreas.

Scan recommendation:

Biphasic CT (nonenhanced CT, PP).

Nonenhanced CT: Normal pancreatic head, absence of tail, and partial to complete absence of body.

PP: No additional information.

Diagnostic pearls: In cases with partial absence of the body, consider pancreatic atrophy.

Rare. Familial occurrence is indicative of potential hereditary mechanism. Agenesis is most likely a defect of the dorsal pancreatic bud.

Typically asymptomatic, incidental finding. Symptomatic patients may present with recurrent abdominal pain and diabetes mellitus.


Pancreas laceration

Fig. 22.9a, b

Traumatic laceration of the pancreas usually affecting either the neck or body.

Scan recommendation:

Biphasic CT (nonenhanced CT, PP).

Nonenhanced CT: Hypodense cleft at side of laceration. Blood may appear hyperdense.

PP: No additional information.

Diagnostic pearls: (Hyperdense) peripancreatic fluid in a patient with seat-belt injury.

Typical complication in car accidents due to seat-belt injuries. Short-lasting but severe encasement between the spine dorsally and the compressed peritoneal cavity ventrally (through the seat belt) in combination with abrupt anteflexion of the body (due to abrupt braking) typically effects laceration within the body of the pancreas.

Laceration is a severe posttraumatic injury that may easily be missed or misinterpreted on initial scans.


Acute pancreatitis

Fig. 22.10a–c

Acute inflammation of the pancreas with various etiologies.

Scan recommendation:

Biphasic CT (nonenhanced CT, PP).

Nonenhanced CT: Focal diffuse pancreas swelling (edema). Hypodense peripancreatic fluid/hyperdense stranding of peripancreatic fat.

PP: Pancreatic tissue usually enhances homogeneously. Hypodense regions are indicative of necrosis. Rim attenuation is typical for abscess/phlegmon.

Diagnostic pearls: Diffuse swelling of the pancreas, nonenhancing (necrotic) intrapancreatic regions, and peripancreatic fluid collection.

May be accompanied by pleural effusions and fluid along the fascia of Gerota/within the pelvis (space of Douglas). Renal halo sign refers to inflammatory infiltration of the pararenal space with sparing of the perirenal space.

Pancreatic hemorrhage can be seen as hyperdense peripancreatic fluid collection (> 60 HU).

Etiology includes alcohol abuse, trauma, cholelithiasis, penetrating peptic ulcer, hyperlipoproteinemia, hypercalcemia, and infection.

Clinical severity and CT changes may not correlate. On CT scans, differentiation is possible between edematous (swelling of the pancreas and stranding of peripancreatic fat), exudative (peripancreating fluid collections), and necrotic (hypodense intrapancreatic regions within normal attenuating pancreatic tissue) pancreatitis.

Phlegmonous extension is seen in ~20% of cases (mainly affecting patients with severe symptoms from the start). Any phlegmon may develop into a pseudocyst through progressive liquefaction of contents and development of a fibrous capsule. Hemorrhage/necrosis occurs in ~5% of cases, is associated with high mortality, and usually results from vessel erosion or occlusion.

Pancreatic phlegmon usually extends into the lesser sac or to the left anterior pararenal space, less frequently to the transverse mesocolon and small bowel mesentery.

Chronic pancreatitis

Fig. 22.7 , p. 723

Irreversible glandular atrophy and dysfunction due to recurrent episodes of inflammation.

Scan recommendation:

Biphasic CT (nonenhanced CT, PP).

Nonenhanced CT: Calcifications within atrophic pancreas (i.e., fatty degeneration).

PP: Irregular dilation of the main pancreatic bile duct (best visible on thin-slice CT). May show hypodense thrombosis within otherwise hyperdense splenic vein or well-defined hypodense pancreas pseudocysts.

Diagnostic pearls: Irregularly dilated main pancreatic duct, glandular atrophy, pseudocysts, and tissue calcifications.

Typically associated with alcohol abuse, but also observed in patients with recurrent cholelithiasis, pancreas divisum, or annular pancreas.

Tissue calcifications arise from reaction and precipitation of pancreas enzymes with Ca++ (from pancreatic tissue).

Often leads to glandular dysfunction with diabetes mellitus type II and fatty stool.

Pancreatic duct dilation due to pancreatic carcinoma occurs in 80% of cases confined to the pancreas head or body and appears less irregular.

Intraductal papillary mucinous neoplasm (IPMN) as another differential diagnosis may simulate chronic pancreatitis clinically and radiologically.

Pancreatic pseudocyst

Fig. 22.11

Fibrous encapsulated fluid collection of inflammatory pancreatic exudate.

Scan recommendation:

Biphasic CT (nonenhanced CT, PP).

Nonenhanced CT: Well-defined hypodense omental or retroperitoneal cystic lesion. Low-density intracystic gas bubbles seen in secondary infection. Cyst walls may calcify.

PP: Rim attenuation of pseudocyst.

Diagnostic pearls: Rim-enhancing, low-attenuating fluid collection in a patient with signs of chronic pancreatitis or following pancreas surgery/interventions.

Histologically, a collection of necrotic tissue, blood, and enzymatic pancreatic fluid, encapsulated by granulation tissue and later a fibrous wall. During maturation, the density of the contents may decrease as blood and debris liquefy. May remain within the pancreatic capsule, but is more common in extrapancreatic locations such as the peritoneal cavity, retroperitoneum, or even mediastinum. Observed in about 10% of patients with pancreatitis. Nearly 50% resolve spontaneously within 6 weeks; the rest require drainage.

May simulate a necrotic or cystic tumor, pseudoaneurysm, or abscess.

Cystic fibrosis (CF)

Abnormal glandular function with lipomatous hypertrophy of the pancreas.

Scan recommendation:

Biphasic CT (nonenhanced CT, PP).

Nonenhanced CT: Hypodense aspect of whole pancreas with or without several nodular cysts and calcifications.

PP: Inhomogeneous, predominantly low-density attenuation (fatty infiltration) of the pancreas.

Diagnostic pearls: Fatty degeneration of the pancreas with multiple nodular cyst and scattered calcifications.

CF is a recessively inherited multiorgan disease affecting particularly the lung, exocrine glands, and gut. Disorders of the pancreas are observed in > 80% of patients.

CF is the major reason for an insufficient exocrine pancreatic function during childhood.

Treatment through oral replacement of pancreas enzymes.

Benign neoplasms

Serous cystadenoma (or microcystic) tumor

Fig. 22.12 a, b

Cystic neoplasm, either macrocystic (cysts > 5 cm) or microcystic (cysts < 5 mm).

Scan recommendation:

Biphasic CT (nonenhanced CT, PP).

Nonenhanced CT: Hypodense cysts. Calcifications may occur within a central scar.

PP: Honeycomb pattern of microcystic adenoma with septal and capsular contrast enhancement. Macrocystic adenoma remains hypodense without enhancement.

Diagnostic pearls: Well-defined, spongelike cystic mass in the head of the pancreas with distinct capsular/septal enhancement and normal width of main pancreatic duct (MPD).

Rare (~1% of pancreatic neoplasms). Histologically, a glycogen-rich mucinous tumor arising from centroacinar cells.

Preferred location is the pancreas head, but it may occur in any part of the pancreas.

Simple cysts of the pancreas may be multiple (e.g., von Hippel–Lindau disease, polycystic disease) but typically have no internal architecture.

Differential diagnoses: IPMN, cystic islet cell tumor, and cystadenocarcinoma.

Serous cystadenoma has no malignant potential, but differentiation from these other cystic neoplasms based on imaging alone is often impossible.

Pancreatic cyst

Usually congenital true cysts that are caused neither by neoplastic nor by inflammatory disease.

Scan recommendation:

Biphasic CT (nonenhanced CT, PP).

Nonenhanced CT: Well-defined, round to oval, hypoattenuating cysts.

PP: Lesions remain hypodense without enhancement.

Histologic true cysts with epithelial lining.

Typically associated with cystic disease of the liver and other organs, such as autosomal dominant polycystic kidney disease (ADPKD) or von Hippel–Lindau disease.

Solitary or multiple collection of near-water density is seen within the pancreas.

Malignant neoplasms

Cystadenocarcinoma, mucinous cystic pancreatic tumor

Fig. 22.13

Cystic neoplasm of varying size (3–10 cm) in the body or tail of the pancreas.

Scan recommendation:

Multiphasic CT (nonenhanced CT, portal venous phase [PVP], PP).

Nonenhanced CT: Hypodense unilocular cystic mass with or without calcifications.

PVP: Small tumors may be better delineated during an early contrast phase.

PP: Distinct septal/capsular contrast enhancement. Macrocystic adenoma remains hypodense without enhancement.

Diagnostic pearls: Unilocular cystic mass in the body or tail of the pancreas with hyperattenuation of thick, irregular wall on postcontrast scans.

Cystic malignant neoplasms represent < 10% of all malignant neoplasms. Cysts are typically located distal to the tumor, representing either pseudo- or retention cysts.

As compared with simple cysts or pseudocysts, malignant neoplasms usually show higher central attenuation values and have irregular, thicker walls. Carcinomas may be masked in the presence of chronic inflammation. Ductal dilation often is the only abnormality on CT scans. In > 50% of patients, pancreatic duct (5–10 mm) and biliary tract dilation is observed. Stranding of peripancreatic fat is indicative of lymphangiosis and thus suspicious for extraglandular tumor growth. Mesenteric lymph nodes may be < 10 mm but still be infiltrated.

Ductal pancreas carcinoma

Fig. 22.14a, b

Pancreas carcinoma arising from ductal epithelium of exocrine pancreas.

Scan recommendation:

Biphasic CT (nonenhanced CT, PP).

Nonenhanced CT: Hypo-/isodense to normal pancreas tissue.

PP: Heterogeneous, often poor enhancement.

Diagnostic pearls: Heterogeneous, poorly enhancing irregular mass in the pancreas head with dilated common bile duct (CBD) and MPD (double duct sign).

Ductal pancreas carcinoma represents 95% of all pancreatic neoplasms. Histologically, presents as mainly mucinous adenocarcinomas.

Sixty percent in the head, 20% in the body, 5% in the tail, and 15% diffuse.

Grading into three stages:

I: confined to pancreas

II: stage I and regional lymph node metastases

III: stage II and distant metastases

Islet cell tumor

Fig. 22.15a, b

Neuroendocrine tumors arising from endocrine pancreatic cells (islet cells of Langerhans).

Scan recommendation:

Multiphasic CT (nonenhanced CT, arterial phase [AP], PVP). Nonenhanced CT: Small or large lesion, isodense to normal pancreatic tissue. Calcifications may be present.

AP: Small islet cell tumors enhance usually strong and homogeneously.

Large tumors may show ring enhancement with central necrotic low-density area.

PVP: Tumors quickly become isodense (masked) to normal pancreas.

Diagnostic pearls: A small hypervascular pancreatic mass with several liver lesions, showing a similar enhancement pattern.

Islet cell tumors are either secretory (functioning) or nonfunctioning. Secretory tumors are detected earlier due to clinical symptoms. Nonfunctioning tumors are usually large at the time of detection. Sixty to 75% of secretory islet cell tumors secrete insulin (insulinomas), and 20% are gastrin-secreting alpha-1 islet cell tumors (gastrinomas), causing Zollinger–Ellison syndrome.

Rare islet cell tumors include those producing glucagon (alpha-2 cell), vasoactive intestinal peptide (VIPoma, non-beta cells), and somatostatin (somatostatinoma [delta cells]). Amine precursor uptake and decarboxylation cell tumors (APUDomas) are occasionally encountered in the pancreas. They produce adrenocorticotropic hormone (ACTH), antidiuretic hormone (ADH), and vasoactive intestinal polypeptide (VIP).

Liver metastases are often detected before diagnosis of the primary islet cell tumor.

Papillary cystic carcinoma, solid and papillary tumor of the pancreas

Fig. 22.16

Well-defined large (> 2 cm) heterogeneous mass in tail or body of the pancreas.

Scan recommendation:

Biphasic CT (nonenhanced CT, PVP).

Nonenhanced CT: Well-defined, centrally hypodense mass, depending on hemorrhage/necrosis ratio. Calcifications may be present.

PVP: Lesion remains centrally hypoattenuating with thick and strongly enhancing wall.

Diagnostic pearls: Well-defined large (> 2–20 cm) tumor in the body or tail of the pancreas with coexistence of solid and cystic components.

Rare. Histologic solid and pseudopapillary structures surrounded by areas of necrosis and hemorrhage. Typically occurs in young (< 40 y) patients.

Surgery is the treatment of choice.

Rarely recurs after excision; thus, overall prognosis is good.

Intraductal papillary mucinous neoplasm (IPMN)

Fig. 22.17a, b

Mucin-producing neoplasm arising from the epithelial lining of the MPD and/or branch pancreatic ducts (BPD type).

Scan recommendation:

Biphasic CT (nonenhanced CT, PVP).

Nonenhanced CT: Dilated and tortuous main duct in MPD type. Rarely calcifications.

Nonenhanced CT: Dilated and tortuous main duct in MPD type. Rarely calcifications.

Grapelike cluster of multiple small hypodense cysts in BPD type.

PVP: Subtle, irregular enhancement of cyst wall lining.

Diagnostic pearls: Grapelike, hypoattenuating cluster of micronodular cysts within the uncinate process and emptying into a dilated MPD.

MPD IPMN usually located in body or tail, BPD type usually in the pancreatic head and uncinate process. Thirty percent of tumors transform into malignant variant.

Usually diagnosed in patients older than 60 y. Symptomatic IPMN may cause pain, recurrent pancreatitis, diabetes mellitus, diarrhea, and weight loss.

Treatment of choice is continuous monitoring in old and asymptomatic patients and surgical resection in young and symptomatic patients.

Pancreatic metastases

Pancreatic lesions without obstruction of the MPD.

Scan recommendation:

Biphasic CT (nonenhanced CT, PVP).

Nonenhanced CT: Usually isodense to normal pancreas (melanoma: hyperdense).

PVP: Variable; may resemble primary pancreas tumor.

Diagnostic pearls: Intrapancreatic lesion (s) with concomitant intra-abdominal metastases (lymph nodes, adrenal glands, kidneys, liver).

Most often metastases are from melanoma, lung cancer, breast cancer, and ovarian cancer. Carcinoma of the stomach, gallbladder, and liver may directly invade pancreatic tissue.

Lesions of the left adrenal gland and kidney initially displace the tail of the pancreas, subsequently invade peripancreatic fat, and may finally occlude the splenic vein.


Fig. 22.18a, b

Either a large, homogeneous, solid intraparenchymal mass or enlarged peripancreatic lymph nodes.

Scan recommendation:

Biphasic CT (nonenhanced CT, PVP).

Nonenhanced CT: Diffuse pancreas enlargement with stranding of perihepatic fat, enlarged peripancreatic lymph nodes.

PVP: Usually isoattenuating to pancreas; sometimes subtle enhancement of tumor.

Diagnostic pearls: Enlarged peripancreatic lymph nodes or diffusely enlarged pancreas in a patient with known lymphoma.

Primary lymphoma represents < 1% of all pancreatic neoplasms. Secondary lymphomas are more common. Most common subtype is non–Hodgkin lymphoma. Treatment of choice usually is chemotherapy.

Fig. 22.6 Pancreatic abscess. Well-defined cystic mass without intracystic gas in a patient with a known history of pancreatitis.
Fig. 22.7a, b Chronic pancreatitis due to a pancreas divisum. Typical signs of chronic pancreatitis such as an irregularly dilated main pancreatic duct, glandular atrophy of the tail, pseudocysts in the head, and tissue calcifications in the body (a). Pancreas divisum is clearly shown on magnetic resonance cholangiopancreatography showing nonfusion of dorsal and ventral pancreatic buds (b). CT shows a large edematous pancreatic head—due to acute inflammation—with two separate orifices: the long duct dorsally, ill-defined due to edema, and the short duct ventrally, well-defined and round.
Fig. 22.8a, b Annular pancreas. Encasement of the descending duodenum through ringlike pancreatic tissue on the axial scan (a), corresponding to the thin, linear soft tissue structure lateral to the descending duodenum on the coronal scan (b).
Fig. 22.9a, b Traumatic laceration of the pancreas in a patient involved in a severe car accident. There is marked hypodense fluid in the region of the pancreas head, which is completely destroyed and thus not visible. The pancreas body is displaced to the left and appears as a heart-shaped hyperattenuating structure ventrally to the left kidney (arrow) (a). Note the distinct exenteration of parts of the colon and small intestine to the left. The coronal multiplanar reconstruction reveals that the duodenum is cut proximally at the inferior part and displaced to the left (b). The displaced pancreas body is the triangular hyperattenuating structure cranial to it (arrow).
Fig. 22.10a–c Three stages of acute pancreatitis. Edematous with diffuse swelling of the complete organ (a). Exudative with distinct peripancreatic fluid (b). Hypoattenuating tail on postcontrast scan indicative of focal necrosis (c). Note the thickened and collapsed inferior gastric wall anterior (b), both signs of concomitant mural inflammation.
Fig. 22.11 Pancreatic pseudocyst. Fibrous, encapsulated, rim-enhancing, low-attenuating fluid collection between the pancreas head and the medial liver margin.
Fig. 22.12a, b Serous cystadenoma (or microcystic) tumor. Well-defined, spongelike cystic mass in the head of the pancreas with distinct capsular/septal enhancement (a) and only slightly dilated, main pancreatic duct (b).
Fig. 22.13 Cystadenocarcinoma. Cystic mass in the body or tail of the pancreas with hyperattenuation of a thick, irregular wall on postcontrast scans.
Fig. 22.14a, b Ductal pancreas carcinoma. Heterogeneous, poorly enhancing irregular mass in the pancreas head with stent in the (previously dilated) common bile duct (CBD) and MPD (double duct sign).
Fig. 22.15a, b Islet cell tumors. Two hyperattenuating lesions on hepatic arterial phase (HAP) scans in the pancreas head (arrow) (with central necrosis) (a) and tail (small, round nodule) (arrow) (b).
Fig. 22.16 Papillary cystic carcinoma. Irregular but well-defined large tumor in the tail of the pancreas with partly thickened hyperattenuating margins.
Fig. 22.17a, b Intraductal papillary mucinous neoplasm (IPMN). Grapelike hypoattenuating cluster of micronodular cysts within the pancreas head with clear emptying into a dilated MPD (a,b).
Fig. 22.18a, b Pancreas lymphoma. Diffusely enlarged pancreas in a patient with known non–Hodgkin lymphoma (a). Note the concomitant involvement of the spleen (b).

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Jul 6, 2020 | Posted by in GENERAL RADIOLOGY | Comments Off on 22 Pancreas

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