HEPATOBILIARY, SPLEEN AND PANCREAS Flashcards

Question

PERIPORTAL LESIONS | Vascular

Answer 1

1. Portal vein thrombosis—either bland thrombus (e.g. related to portal hypertension, local inflammation or hypercoagulable states) or tumour thrombus (most commonly due to direct extension from HCC). Tumour thrombus tends to expand the portal vein and may contain internal vascularity or enhancement. 2. Cavernous transformation of portal vein—a tangle of periportal venous collaterals that develop after PV thrombosis. 3. Aneurysm—arterial (e.g. due to trauma, surgery, atherosclerosis, polyarteritis nodosa, fibromuscular dysplasia, mycotic) or portal venous (e.g. congenital or due to portal hypertension, trauma, surgery or pancreatitis)

Answer 2

1. Cholangiocarcinoma—periductal infiltrating or intraductal forms. Both cause severe biliary dilatation ± PV narrowing or occlusion. 2. Cholangitis/strictures. 3. Bile duct stones. 4. Choledochal cyst. 5. Biliary cystadenoma—can rarely arise from extrahepatic ducts

Answer 3

1. Reactive/inflammatory lymphadenopathy—e.g. due to acute hepatitis, cirrhosis (especially Hep C, PBC and PSC), TB (necrotic), sarcoidosis. Nodes tend to be discrete, homogeneous (except TB) and small volume. 2. Metastatic lymphadenopathy—e.g. from HPB/GI malignancies. 3. Lymphoma*—confluent homogeneous periportal adenopathy. PTLD also commonly involves the periportal region, manifesting as a homogeneous soft tissue mass encasing but not occluding the portal vein, with only mild biliary dilatation (cf. cholangiocarcinoma). Leukaemia can also create a similar appearance. 4. Extramedullary haematopoiesis—mimics lymphoma. Look for features of bone marrow failure.

Answer 4

1. Focal fatty infiltration/sparing—can occur in periportal region. Geographic appearance, no mass effect. 2. Peritoneal malignancy—including direct periportal tumour extension (e.g. from GB, stomach or pancreas), peritoneal metastases, pseudomyxoma peritonei and primary peritoneal tumours, e.g. mesothelioma.200 Aids to Radiological Differential Diagnosis 3. Fluid collections—following trauma/surgery or tracking from cholecystitis or pancreatitis. 4. Neurofibroma—in NF1. Plexiform sheath-like mass encasing but not narrowing the portal vein or obstructing the bile ducts; low attenuation on CT (almost cystic), often extends into mesenteric root or retroperitoneum. 5. Schwannoma—well-defined rounded mass ± internal cystic change or calcification. 6. Sarcomas—e.g. Kaposi sarcoma (typically causes enhancing periportal nodules + hypervascular nodes), leiomyosarcoma, MPNST

Answer 5

1. Simple cyst—solitary or multiple, variable size. Usually unilocular with an imperceptible wall. May contain thin nonenhancing septa. Can become haemorrhagic or infected. 2. Fibropolycystic liver diseases—these are all caused by congenital ductal plate malformations; end result depends on the size of the ducts involved. The conditions can overlap with each other and with congenital hepatic fibrosis and polycystic kidney disease. (a) Multiple biliary hamartomas—small ducts. Numerous small cysts (most <1 cm) on CT/MR; can be hypo- or hyperechoic on US ± ‘comet-tail’ artefact. No communication with biliary tree. Usually nonenhancing, though some may contain enhancing fibrous stromal nodules. (b) Polycystic liver disease—medium ducts. Multiple cysts of varying size (can be large); no communication with biliary tree. Thin nonenhancing walls, unless complicated by haemorrhage or infection. Some of the cysts may coalesce, mimicking a multilocular cystic lesion, but the presence of cysts elsewhere aids diagnosis.Hepatobiliary, pancreas and spleen 201 8 (c) Caroli disease—large ducts. Multifocal saccular dilatations of intrahepatic bile ducts, often containing a central ‘dot’ representing portal radicals. May be diffuse or segmental. Intraductal calculi are often seen. Can be associated with medullary sponge kidney. 3. Peribiliary cysts—small (<2 cm) and multiple, seen in cirrhotic or polycystic livers. Located along portal tracts, usually close to the hilum. May mimic biliary dilatation if confluent. No enhancement or communication with the biliary tree. 4. Subcapsular fluid collections—e.g. subcapsular gallbladder rupture, postsurgical seroma or biloma, pancreatic pseudocyst, chronic haematoma; these cause scalloping of the liver margin. An intrahepatic biloma in a posttransplant patient suggests biliary necrosis due to hepatic artery occlusion. 5. Focal bile duct dilatation—e.g. due to a stricture, biliary IPMN or intrahepatic choledochal cyst. See Section 8.3. 6. Cystic metastases—can occasionally mimic simple cysts (see later). 7. Hydatid cyst—CL and CE1 types (see later). 8. Ciliated hepatic foregut cyst—rare; typically a thin-walled unilocular wedge-like cyst located in the periphery of segment 4. May contain mucinous material, increasing attenuation on CT and T1 signal on MRI. Small risk of malignancy—thick septations or solid components are worrying. 9. Intrahepatic gallbladder—congenital anomaly. Often small and located close to an empty GB fossa

Answer 6

1. Haemorrhagic or infected simple cyst—common in polycystic livers. T1 hyperintensity suggests haemorrhage; wall thickening and enhancement ± restricted diffusion suggests infection. NB: haemorrhage into a cyst almost excludes hydatid cyst from the differential. 2. Abscess—these typically show internal restricted diffusion on MRI, intense rim enhancement + surrounding oedema (‘double-target’ sign) ± associated venous thrombosis. Clinical and biochemical signs of infection are typically present. (a) Pyogenic—often multilocular or septated ± internal gas (especially with Klebsiella). Tend to form clusters when multiple. Klebsiella abscesses may also contain multiple discontinuous T2 hypointense enhancing septa (‘turquoise’ sign). (b) Amoebic—usually large, solitary, round and unilocular, with a thick wall and perilesional oedema. Usually no internal gas. Rupture of an abscess through the diaphragm suggests amoebic abscess. (c) Candidiasis—in immunocompromised patients; innumerable microabscesses (most <1 cm), usually involving both liver 202 Aids to Radiological Differential Diagnosis and spleen. Mycobacterial and other fungal infections can look identical. (d) Melioidosis—endemic in tropical Australasia. Single or multiple abscesses with a characteristic ‘honeycomb’ appearance, usually also with splenic involvement. (e) Fascioliasis—parasitic GI tract infection endemic in the tropics. The parasites burrow through the intestinal wall into the peritoneal space, where they migrate to and invade the liver, heading to the bile ducts. This results in a linear array of small subcapsular abscesses along the path of parasite migration through the liver parenchyma towards the hilum. Peripheral eosinophilia is usually present. (f) Visceral larva migrans—parasitic infection (most commonly Toxocara from dogs or cats) that can cause clustered or coalescent liver abscesses similar to pyogenic abscesses. The presence of peripheral eosinophilia is suggestive. (g) Aseptic abscesses—most commonly related to IBD (Crohn’s > UC); may precede the diagnosis. Usually multiple, variable size. More common in the spleen. 3. Cystic metastases—typically multiple. Do not usually exhibit the surrounding rim of oedema (‘double-target’ sign) or central restricted diffusion seen with abscesses. Three sources: (a) Mucinous tumours—e.g. from GI tract (intraparenchymal) or ovary (subcapsular). Often have irregular walls and septa. (b) Cystic degeneration of hypervascular metastases—e.g. NET, melanoma, sarcoma; usually show nodular rim enhancement. (c) Treatment-related cystic change—especially with GIST metastases; can mimic simple cysts. 4. Biliary cystadenoma—typically solitary, large and multilocular with septal vascularity and enhancement ± calcification. Usually in middle-aged women, most often in segment 4. Upstream biliary dilatation is common (rare with simple cysts). Mural or septal nodularity is worrying for malignant transformation to cystadenocarcinoma, although it is often not possible to reliably differentiate the two. 5. Hydatid cyst—caused by Echinococcus granulosus, usually seen in patients in close contact with sheep. Well-defined rounded margin; may be solitary or multiple ± involvement of other organs (most commonly lung, but can occur anywhere). Characteristic imaging appearance depending on stage of disease (NB: internal septa and solid components never show vascularity or enhancement—cf. other cystic lesions): (a) CL (active)—simple unilocular cyst, no internal echoes or visible wall. Mimics a simple hepatic cyst; upstream biliary dilatation may help differentiate (very rare with simple cysts). (b) CE1 (active)—same as CL but with internal echoes (hydatid sand) and a visible thin wall on (c) CE2 (active)—multilocular cyst due to filling of ‘mother’ cyst with several smaller ‘daughter’ cysts. No solid components. (d) CE3a (transitional)—cyst with detached internal membranes (‘water-lily’ sign). (e) CE3b (transitional)—similar to CE2 but with solid components between the daughter cysts. (f) CE4 (inactive)—cyst with heterogeneous solid contents (‘ball of wool’ sign). No daughter cysts. (g) CE5 (inactive)—cyst with solid contents and wall calcification. The entire lesion may become calcified. 6. Cystic HCC—rare form of HCC due to marked central necrosis; usually shows mural nodular enhancement + washout. Cystic necrosis within a solid HCC is more commonly seen after RFA/ TACE therapy. 7. Inflammatory pseudotumour—can occasionally present as a complex cystic mass with thick enhancing septa. 8. Multicystic biliary hamartoma—rare, benign. Tubulocystic honeycomb-like mass with mural and septal enhancement, typically in a peripheral location. 9. Biliary adenofibroma—rare benign tumour with some malignant potential; complex multicystic mass + enhancing solid components, indistinguishable from biliary cystadenocarcinoma. 10. Lymphangioma—intrahepatic location is rare. 11. Glomus tumour—very rare. Complex cystic mass with arterially enhancing mural nodules that persist into the delayed phase. 12. Mesenchymal hamartoma and embryonal sarcoma—typically in children; very rare in adults. Both appear as complex multilocular cystic masses

Answer 7

1. Pseudolipoma of Glisson’s capsule—small subcapsular fatty nodule, usually located on the liver dome. Represents a detached colonic epiploic appendage that attaches to the liver capsule. 2. Angiomyolipoma—rare; contains fat and enhancing soft tissue, similar to renal AMLs. Can be associated with tuberous sclerosis. Fat content varies; some are fat-poor. The presence of internal vessels is characteristic and aids differentiation from other lesions. 3. HCC/adenoma—can occasionally contain macroscopic fat. 4. Lipoma—rare. Purely fatty. 5. Surgical omentopexy—flap of omentum is placed on the liver surface, e.g. after hydatid cyst surgery. 6. Hydatid cyst—can rarely contain droplets of fat. 7. Hepatic adrenal rest tumour—rare; contains a mixture of soft tissue and fat, mimicking AML. 8. Fatty metastasis—e.g. from teratoma or liposarcoma; rare. Primary hepatic teratoma or liposarcoma is even rarer. 9. Lipopeliosis—rare; can occur in a transplanted liver after an ischaemic insult. 10. Extramedullary haematopoiesis—the rare focal intrahepatic form can contain fat. 11. Langerhans cell histiocytosis*—in children; periportal xanthomatous deposits

Answer 8

1. Focal fatty infiltration—most common adjacent to the falciform ligament or porta but can occur anywhere; often has a geographic morphology but can appear nodular (focal nodular steatosis). No mass effect, abnormal enhancement or restricted diffusion. 2. HCC—often contains fat. Hypervascular on arterial phase + washout on later phases. Mainly seen in cirrhotic livers. 3. Hepatic adenoma—often contain fat. Hypervascular ± washout. Most common in young women taking oral contraceptives. 4. Regenerative nodules—occasionally contain fat; usually multiple. No enhancement (cf. HCC). Seen in cirrhotic livers. 5. FNH—uncommonly contains foci of intracellular fat, especially if the background liver is fatty. 6. Angiomyolipoma—if fat-poor.

Answer 9

1. Haemangioma—classically shows peripheral nodular (discontinuous) enhancement on arterial phase with progressive centripetal filling on later phases. The enhancement follows the enhancement of the blood pool. Small capillary haemangiomas often ‘flash-fill’ homogeneously on the arterial phase. Large cavernous haemangiomas may not fill completely even on delayed phases due to central fibrosis. Haemangiomas are typically T2 bright on MRI (almost cyst-like)—most other hypervascular lesions are only mildly-moderately T2 hyperintense. Restricted diffusion may be present. 2. Vascular malformation/shunt—has dilated feeding and draining vessels. May be arterioportal, arteriovenous or portosystemic. T2 dark (flow void). 3. Mass-forming cholangiocarcinoma—can contain hypervascular areas, especially in the periphery, with central fibrosis that enhances in the delayed phase (± peripheral washout). Also note that mixed HCC-cholangiocarcinoma neoplasms can occur that exhibit imaging features of both tumours. 4. Treated metastasis—can show persistent enhancement. 5. Angiomyolipoma—typically contains macroscopic fat. Vascular components enhance. 6. Angiosarcoma—large aggressive infiltrative mass + satellite nodules; may diffusely infiltrate entire liver. Heterogeneous multifocal arterial enhancement ± partial filling on later phases. Areas of haemorrhage, necrosis and cystic change are common. Often metastatic at presentation. Most common in older men. 7. Epithelioid haemangioendothelioma—rare malignant vascular tumour, less aggressive than angiosarcoma. Typically, multifocal subcapsular masses that often coalesce + capsular retraction ± a T2 bright core (‘target’ sign). Often shows peripheral target-like arterial enhancement ± partial filling on later phases; may mimic haemangioma. 8. Peliosis hepatis—single or multiple blood-filled cystic spaces within the liver. Most common in immunocompromised patients (especially AIDS) due to Bartonella infection; can also be seen in various chronic illnesses (e.g. diabetes, coeliac disease, vasculitis, TB) and secondary to drugs (e.g. steroids, OCP). Peripheral (ring-like) or central arterial enhancement with centripetal or centrifugal filling on later phases. May rupture into peritoneal cavity. Usually regresses after removing the cause. 9. Leiomyoma—rare; usually hypervascular with persistent enhancement in the delayed phase

Answer 10

1. Transient hepatic attenuation/intensity difference (THAD/ THID)—region of increased arterial enhancement on CT (THAD) or MRI (THID) that equilibrates with the background liver on later phases, usually with no corresponding abnormality on other MRI sequences. Small peripheral wedge-shaped THADs/THIDs are common, especially in cirrhosis, and are of no consequence. Other causes include: (a) Hyperaemia adjacent to inflammation—e.g. liver abscess, peritonitis (Fitz-Hugh-Curtis syndrome), cholecystitis, duodenitis, colitis. Ill-defined region of arterial hyperenhancement + mild T2 hyperintensity (oedema). (b) Portal vein occlusion—e.g. due to thrombus or tumour. Causes a wedge of arterial hyperenhancement peripheral to the occluded portal vein. (c) Arterioportal/arteriovenous shunt—can be congenital (AVM—multiple in HHT) or secondary to cirrhosis, trauma or an underlying hypervascular mass. Focal arterial hyperenhancement around the shunt due to reduced vascular resistance. A dilated feeding artery and draining vein are often seen. (d) Biliary obstruction—causes arterial hyperenhancement in the surrounding liver due to elevated sinusoidal pressure. (e) SVC/IVC obstruction—collateral veins entering the liver cause hyperenhancement of the adjacent parenchyma. 2. FNH—focal hyperplastic response around a (central) vascular malformation; usually an incidental finding in young adults (F>M). Typically shows homogeneous arterial enhancement that equilibrates with the background liver on later phases. Often has a T2 hyperintense central scar which enhances in the delayed phase. May be multiple. 3. Hepatic adenoma—clinical and radiological features depend on subtype. Generally, adenomas are mildly T2 hyperintense and hypervascular ± washout ± fat content ± associated haemorrhage. Hepatocyte-specific MR contrast agents (e.g. Primovist) can aid differentiation from FNH. (a) Inflammatory— most common; usually in women on the OCP. Marked arterial enhancement (more than other subtypes) which may persist on the delayed phase. No/minimal fat content. Moderately T2 hyperintense; a peripheral T2 bright rim (‘atoll’ sign) is characteristic if present. Highest risk of associated haemorrhage. (b) HNF1α-mutated—almost exclusively in women, usually on the OCP. Diffuse microscopic fat content is characteristic. Often multiple. Least T2 hyperintense and least hypervascular subtype; tends to show washout on later phases. (c) β-catenin-mutated—more common in men, especially those on anabolic steroids. Also seen in glycogen storage disease (multiple) and FAP. No fat content. May contain a T2 hyperintense scar. Highest risk of malignant transformation. (d) Unclassified—no specific imaging features. 4. Fibrolamellar HCC—variant of HCC that occurs in noncirrhotic livers, usually in young adults. Mimics FNH on imaging but tends to be larger (>5 cm) with a T2 hypointense central scar and heterogeneous enhancement ± washout. Calcification is common (rare in FNH). 5. Large regenerative nodules—seen in chronic Budd-Chiari syndrome; often multiple. Imaging features are identical to FNH. 6. Intrahepatic splenosis—post splenectomy. Subcapsular deposits of splenic tissue; heterogeneous arterial enhancement, becoming homogeneous in the portal phase.

Answer 11

1. HCC—usually in cirrhotic livers. Characteristically shows arterial enhancement followed by washout, ± internal fat ± enhancing capsule ± venous invasion (tumour thrombus). May be multiple. 2. Hypervascular metastases—e.g. from NETs, RCC, thyroid, melanoma, breast, sarcoma (including Kaposi), choriocarcinoma. Usually multiple. Often T2 bright + restricted diffusion. Metastases from insulinoma may be surrounded by a halo of fatty infiltration. 3. Hepatic adenoma—can show washout (especially the HNF1αmutated subtype). 4. Fibrolamellar HCC—can show washout

Answer 12

1. Inflammatory pseudotumour—variable appearance; may be hypervascular ± washout. 2. Solitary fibrous tumour—rare; solitary large well-defined mass with heterogeneous arterial enhancement and areas of both high and low T2 signal. 3. Primary hepatic NET—e.g. carcinoid, gastrinoma, paraganglioma; very rare. Often large ± areas of cystic (T2 bright) or haemorrhagic (T1 hyperintense) change. Heterogeneous arterial enhancement that may persist or wash out. 4. Clear cell myomelanocytic tumour—rare tumour of perivascular epithelioid cells (PEComa) seen in children and young adults; usually arises from or adjacent to the falciform ligament. Usually large + heterogeneous arterial enhancement and areas of necrosis. 5. Intrahepatic bile duct adenoma—very rare; usually small (<2 cm) and subcapsular. Heterogeneous arterial enhancement that may persist or wash out, ± cystic change. 6. Adenomatoid tumour—very rare; solid or solid-cystic hypervascular mass

Answer 13

1. Mass-forming cholangiocarcinoma—classically shows gradual delayed enhancement, especially centrally. Usually causes capsular retraction ± peripheral biliary dilatation ± vascular occlusion ± restricted diffusion. 2. Confluent hepatic fibrosis—seen in cirrhosis; see Section 8.25. Can mimic cholangiocarcinoma but tends to be more wedge-like, with no restricted diffusion, biliary dilatation or vascular occlusion. 3. Haemangioma—some are late-filling (complete or partial), especially the sclerosing subtype. 4. Treated metastasis/HCC—treatment results in fibrosis. 5. Solid organizing abscess—this is a partially healed abscess that contains late-enhancing fibrosis/granulation tissue. 6. Inflammatory pseudotumour—variable appearance, may show delayed enhancement. 7. Solitary fibrous tumour—rare; often contains both hypervascular areas and fibrotic late-enhancing areas.

Answer 14

1. Metastases—e.g. from GI tract, pancreas, lung, breast, etc. Most metastases tend to be hypovascular due to central necrosis ± mild peripheral arterial enhancement. 2. Cholangiocarcinoma—may show minimal enhancement. 3. Granulomatous lesions—typically small and numerous. (a) Sarcoidosis*—numerous small hypovascular nodules, typically involving both liver and spleen and usually in the presence of nodal and thoracic disease. The nodules are typically T2 hypointense (cf. other granulomatous processes below). (b) TB*—numerous small hypovascular nodules, typically involving both liver and spleen. Usually in immunocompromised patients; can mimic fungal infection (e.g. candidiasis) but the presence of necrotic lymph nodes and lung involvement suggests TB. Nodules often calcify after healing. (c) Brucellosis—can present as a solitary abscess or multiple hypovascular granulomas ± calcification. (d) Cat-scratch disease—caused by Bartonella henselae. Usually involves lymph nodes but hepatic (± splenic) dissemination with multiple hypovascular necrotizing granulomas can occur. May mimic TB or fungal infection, but typically occurs in immunocompetent children or young adults. 4. Nodular steatosis—can mimic malignancy on CT, especially when multifocal. Diagnosis confirmed on in-/opposed-phase MRI. May have a pathognomonic rim of more marked fatty infiltration. 5. Haematoma—due to trauma, coagulopathy or underlying mass lesion. Hyperattenuating on unenhanced CT, no internal enhancement (unless there is active bleeding). Variable MRI signal depending on age. 6. Sclerosing haemangioma—may be completely hypovascular with only mild T2 hyperintensity ± capsular retraction, mimicking malignancy. May have calcification or a wedge-like morphology. 7. Previously treated HCC/metastasis—e.g. ablation, TACE, chemotherapy. 8. Lymphoma*—well-defined homogeneous mass, masses or micronodules that may have a periportal distribution. Leukaemia and extraosseous myeloma can have a similar appearance.210 Aids to Radiological Differential Diagnosis 9. Inflammatory pseudotumour—variable appearance, can be hypovascular. 10. Hydatid disease*—the two Echinococcus species have different imaging features, but neither shows internal enhancement as the contents are derived from the parasite, not the host. (a) Cystic echinococcosis—E. granulosus. Types CE4 and CE5 appear solid, the latter being calcified (see Section 8.16). (b) Alveolar echinococcosis—E. multilocularis. Irregular heterogeneous mass or masses, often with foci of calcification ± peripheral fibrosis showing mild delayed enhancement. No restricted diffusion. 11. Other rare primary tumours— e.g. leiomyosarcoma (associated with immunosuppression, may be centrally cystic), other sarcomas (e.g. carcinosarcoma, fibrosarcoma), epithelioid haemangioendothelioma (may be hypovascular), melanoma (may be T1 hyperintense and T2 hypointense), squamous cell carcinoma, GIST, PNET. These are often large nonspecific heterogeneous necrotic masses. 12. Other rare lesions—e.g. Langerhans cell histiocytosis, amyloidoma, Rosai-Dorfman disease.

Answer 15

1. Focal nodular hyperplasia—the scar is typically T2 hyperintense and noncalcified. 2. Cavernous haemangioma—especially if large. 3. Fibrolamellar HCC—the scar is typically T2 hypointense and often calcified. Conventional HCCs can also occasionally contain a central scar. 4. Large regenerative nodules—seen in chronic Budd-Chiari syndrome. Identical appearance to FNH. 5. Mass-forming cholangiocarcinoma—can have a peripheral hypervascular component and a central fibrous component, giving the appearance of a central scar. Look for associated biliary dilatation (rare with benign lesions). 6. Hepatic adenoma—occasionally. 7. Metastases—can contain a central fibrotic component. 8. Epithelioid haemangioendothelioma—rare; peripheral vascular component + central fibrosis often giving a ‘target’ appearance.

Answer 16

1. Metastases—especially after treatment or with fibrotic/necrotic tumours, e.g. breast, carcinoid, lung, colorectal. Can create a ‘pseudocirrhosis’ appearance. 2. Mass-forming cholangiocarcinoma—classically shows capsular retraction. 3. Confluent hepatic fibrosis—seen in cirrhosis; capsular retraction is characteristic (see Section 8.25). 4. Sclerosing haemangioma—can cause adjacent capsular retraction. 5. Post trauma—including iatrogenic, e.g. biliary drainage, biopsy. 6. HCC—following ablation or TACE. Can also be seen with fibrolamellar HCCs. 7. Epithelioid haemangioendothelioma—classically shows capsular retraction. See Section 8.18. 8. Inflammatory pseudotumour—variable appearance; can mimic cholangiocarcinoma. 9. Pseudomyxoma peritonei (mimic)—scalloping of liver surface may resemble capsular retraction

Answer 17

1. Fat—see Section 8.17. 2. Haemorrhage—in the subacute stage due to methaemoglobin. Haematomas do not show internal enhancement and can be either traumatic (e.g. post biopsy), spontaneous or related to an underlying mass, e.g. adenoma, HCC. Haemorrhagic cysts are also usually T1 hyperintense, either homogeneously or graduated (slightly higher intensity dependently). 3. Cirrhotic nodules—regenerative/dysplastic nodules and HCC can all be T1 hyperintense, even without fat (due to copper content). This can make it difficult to assess arterial enhancement— subtraction images may help.212 Aids to Radiological Differential Diagnosis 4. Melanoma metastases. 5. Intrahepatic ductal calculi—pigment type, seen in PSC, recurrent pyogenic cholangitis and Caroli disease. 6. Proteinaceous material—may be seen dependently in abscesses. Can also be seen in the rare ciliated hepatic foregut cyst. 7. Calcification—can occasionally be T1 hyperintense. 8. Chemical—gadolinium, lipiodol (contains fat). 9. ‘Relative’—i.e. normal-signal liver surrounded by low-signal liver, e.g. iron deposition (haemochromatosis/siderosis), oedema. 10. Artefact—pulsation artefact from abdominal aorta can produce a periodic ‘ghost’ artefact along the phase-encoded direction that can be hypo- or hyperintense depending on the phase

Answer 18

1. Siderotic nodules—in cirrhosis, regenerative and low-grade dysplastic nodules containing iron are typically T2 hypointense. Occasionally early HCCs can also appear T2 hypointense due to a combination of iron and copper content. 2. Gas—e.g. pneumobilia or gas within an abscess. Rises to the antidependent surface. 3. Haemorrhage—traumatic, spontaneous, within a cyst or related to a mass, e.g. adenoma, HCC, metastasis, AML, peliosis. T1 and T2 signals vary based on age of blood products. 4. Calcification—see Section 8.7. 5. Vascular malformation/shunt—flow voids. 6. Sarcoidosis*—numerous T2 hypointense nodules in liver and spleen. 7. Fibrous masses—often have T2 hypointense areas, e.g. fibrolamellar HCC (especially in central scar), cholangiocarcinoma, some metastases (e.g. from adenocarcinoma or posttreatment), solitary fibrous tumour, solid organizing abscess. 8. Liver ablation—e.g. for HCC/metastasis. Causes T2 hypointense coagulative necrosis. 9. Thick mucin—e.g. within mucinous metastases. 10. Leiomyoma—often T2 hypointense and hypervascular. Rare. 11. Melanoma metastases—occasionally T2 hypointense.

Answer 19

1. Regenerative nodules—typically numerous, small (<2 cm) and T2 iso/hypointense. Variable T1 signal. Variable attenuation on unenhanced CT—siderotic nodules are often dense. No hyperenhancement or restricted diffusion. May contain fat (tend to be multiple—a single fat-containing nodule is worrying). 2. Dysplastic nodules—usually small (<2 cm). Tend to be T2 hypointense (low-grade) or mildly T2 hyperintense (high-grade). Variable T1 signal and CT attenuation. No restricted diffusion. High-grade dysplastic nodules may show arterial enhancement, but do not wash out. 3. HCC—characteristically shows arterial enhancement followed by washout. NB: the arterial phase must be well-timed to detect the transient arterial enhancement—this may be missed if the phase is too early (no splenic enhancement) or too late (too much portal vein enhancement). Typically mildly T2 hyperintense. Variable T1 signal. May show restricted diffusion. May be well-defined and encapsulated or ill-defined and infiltrative; may also develop within a large dysplastic nodule (‘nodule-in-nodule’ appearance). Portal vein invasion is diagnostic if present. 4. Confluent hepatic fibrosis—peripheral well-defined wedge-like area of volume loss, T2 hyperintensity and capsular retraction which shows gradual delayed enhancement. No restricted diffusion or associated biliary dilatation or vascular occlusion. 5. Mass-forming cholangiocarcinoma—especially in PSC. Can mimic confluent hepatic fibrosis but tends to be more mass-like ±associated peripheral biliary dilatation, vascular occlusion and restricted diffusion. 6. Large regenerative nodules—seen in chronic Budd-Chiari syndrome. Identical appearance to FNH

Answer 20

1. Ascertaining the extent of liver metastases—the hepatobiliary phase has a high sensitivity for detecting even very small liver metastases (which appear hypointense as they do not contain hepatocytes), and aids decision-making when considering liver resection for colorectal liver metastases. 2. FNH vs hepatic adenoma—both lesions are hypervascular, mildly T2 hyperintense and most common in young adult women. In the absence of haemorrhage, washout or internal fat it can be difficult to differentiate the two on conventional imaging—this is important as FNH can be left alone whereas adenomas should be followed up or resected if large (due to risk of haemorrhage). With hepatocyte-specific contrast agents an FNH is characteristically iso- or hyperintense to background liver on the hepatobiliary phase. In contrast, adenomas are typically hypointense to background liver (though inflammatory adenomas may have a rim of hyperintensity). 3. Diagnosing bile leaks—on the hepatobiliary phase contrast should be visible in the biliary tree; in the case of a bile leak contrast extravasation into an adjacent fluid collection can be seen. 4. Aiding characterization of nodules in a cirrhotic liver— regenerative and dysplastic nodules are typically iso- or hyperintense on the hepatobiliary phase, whereas HCC is usually hypointense. NB: some well-differentiated HCCs may be iso-/hyperintense, and some high-grade dysplastic nodules may be hypointense, so this is not entirely reliable. 5. Other biliary applications—e.g. assessing variant anatomy, bile flow dynamics and obstruction, and differentiating peribiliary cysts from lesions communicating with the biliary tree.

Answer 21

1. FNH—uptake > background liver is a characteristic feature. The central scar is often hypointense. 2. Regenerative and dysplastic nodules—in cirrhosis. 3. Lesions communicating with the biliary tree—e.g. choledochal cyst, Caroli disease, biloma (if there is an ongoing bile leak). 4. Large regenerative nodules—seen in chronic Budd-Chiari syndrome. Identical imaging features to FNH. 5. Focal fatty infiltration—uptake may be less than background liver. 6. THID—see Section 8.18. 7. Hepatic adenoma—inflammatory subtype can show peripheral uptake. 8. Well-differentiated HCC—can show uptake

Answer 22

1. Assessing arterial enhancement—usually less intense than with extracellular contrast agents, therefore hypervascular lesions (e.g. haemangioma, HCC) may be less appreciable. 2. Assessing washout on the delayed phase—by this time hepatocytes have begun to take up the contrast, so lesions that normally do not wash out (e.g. haemangiomas) often show ‘pseudo-washout’, appearing less intense than the background liver

Answer 23

1. Chronic myeloid leukaemia. 2. Myelofibrosis—look for bone sclerosis. 3. Malaria*. 4. Gaucher disease*—look for bone infarcts, e.g. in femoral heads. 5. Lymphoma*. 6. Visceral leishmaniasis (kala-azar)

Answer 24

1. All of the above. 2. Haemolytic anaemias—including haemoglobinopathies. 3. Portal hypertension—e.g. cirrhosis, splenic/portal vein occlusion, right heart failure. 4. Leukaemias. 5. Polycythaemia vera. 6. Systemic mastocytosis—look for bone sclerosis. 7. Glycogen storage diseases

Answer 25

1. All of the above. 2. Infections. (a) Viral—infectious hepatitis, infectious mononucleosis, HIV. (b) Bacterial—septicaemia (e.g. intravenous drug user), brucellosis, typhoid, TB. (c) Rickettsial—typhus. (d) Fungal—histoplasmosis. 3. Sarcoidosis*. 4. Rheumatoid arthritis*—Felty’s syndrome. 5. Amyloidosis*. 6. Systemic lupus erythematosus (SLE)*.

Answer 26

1. Splenic artery atherosclerosis—especially splenic artery aneurysm. 2. Cyst—any chronic cyst, including hydatid or posttraumatic.

Answer 27

1. Phleboliths—± small central lucencies. Can be seen in haemangiomas. 2. TB*—usually few in number + calcified intrathoracic nodes and lung granulomas. 3. Histoplasmosis—calcifications are often larger than in TB or other fungal infections, e.g. candidiasis; with calcified intrathoracic nodes and lung granulomas. 4. Gamna-Gandy bodies—siderotic splenic nodules usually due to portal hypertension. 5. Sickle cell anaemia. 6. Pneumocystis jiroveci—e.g. in AIDS, ± hepatic, renal, adrenal and nodal calcification. 7. Toxoplasmosis. 8. Sarcoidosis*. 9. SLE. 10. Amyloidosis*—often with hepatic calcification

Answer 28

1. Sickle cell anaemia—spleen is shrunken and diffusely calcified. 2. Previous Thorotrast administration—with liver and nodal calcification

Answer 29

1. Healed infarct or haematoma. 2. Healed abscess. 3. Healed granuloma—e.g. TB, histoplasmosis. 4. Brucellosis—pathognomonic large ‘snowflake’ calcification within a chronic brucellar abscess; calcification persists after healing

Answer 30

1. Pseudocyst—accounts for most splenic cysts. Usually posttraumatic; can also be seen following infection, infarction or pancreatitis. Can be simple or complex (thick wall, septa, debris, calcification). 2. Epithelial cyst—thin-walled unilocular cyst ± septations, no enhancement. 3. Abscess—pyogenic, TB (may be T2 hypointense), fungal (microabscesses + liver involvement), aseptic (e.g. in IBD, see Section 8.16). Restricted diffusion, ± rim enhancement. A peripheral ‘necklace’ of small locules suggests melioidosis; a large ‘snowflake’ calcification suggests brucellosis. 4. Hydatid cyst—usually in the presence of liver involvement; see Section 8.16. 5. Lymphangioma—often multilocular with thin enhancing septa, no solid components. 6. Cystic metastasis—e.g. from melanoma or mucinous primaries. Rare

Answer 31

1. Infarct—peripheral wedge-shaped area of poor enhancement ± rim of capsular enhancement. Usually embolic (± infarcts elsewhere) or related to a haematological disorder (e.g. sickle cell disease, leukaemia, lymphoma). 2. Haematoma—usually traumatic; can also occur due to coagulopathy or splenomegaly. Hyperattenuating on unenhanced CT, no internal enhancement unless there is active bleeding. 3. Siderotic nodules—also known as Gamna-Gandy bodies, seen in portal hypertension. T1 and T2 dark on MRI; may be calcified. Typically, multiple within an enlarged spleen. 4. Sarcoidosis*—numerous small hypovascular T2 hypointense nodules, usually with hepatic, nodal and thoracic involvement. 5. Peliosis—rare; nearly always in the presence of hepatic peliosis and with a similar appearance. Is a rare benign vascular condition characterized by dilatation of sinusoidal blood-filled spaces within the liver. 6. Extramedullary haematopoiesis—usually causes diffuse splenomegaly but can rarely present as a focal hypovascular mass ± internal fat. 7. Gaucher disease*—marked splenomegaly ± numerous hypovascular nodules. Look for bone infarcts. is the most common lysosomal storage disorder in humans. It is an autosomal recessive, multisystem disease arising from a deficiency of glucocerebrosidase or beta-glucosidase activity, resulting in the accumulation of a glycolipid (glucocerebroside) within the lysosomes of macrophages, particularity in the bone marrow, spleen and liver. 8. Amyloidosis*—usually diffuse, causing strikingly poor arterial enhancement of the spleen and T2 hypointensity on MRI. Focal hypovascular amyloidomas are rare.

Answer 32

1. Haemangioma—most common incidental solid splenic lesion. Usually hyperechoic on US without vascularity on Doppler, ±Hepatobiliary, pancreas and spleen 219 8 calcifications (phleboliths). Hypoattenuating on unenhanced CT. Enhancement varies; may be homogeneous, heterogeneous or similar to hepatic haemangiomas (peripheral and nodular with progressive filling). T2 hyperintense on MRI. May be multiple or diffuse (haemangiomatosis) in Klippel-Trénaunay or BeckwithWiedemann syndromes. 2. Hamartoma—solitary well-defined mass with arterial enhancement persisting or equilibrating on the delayed phase, ± calcification ± fat content ± central scar. Usually hyperechoic on US and hypervascular on Doppler. Nearly isoattenuating to background spleen on unenhanced CT, and nearly T1/T2 isointense on MRI (cf. haemangioma). May be multiple in tuberous sclerosis or Wiskott-Aldrich syndrome. 3. Sclerosing angiomatoid nodular transformation—fibrosing variant of hamartoma. Solitary well-defined mass with centripetal delayed enhancement due to central fibrosis. Centrally T2 hypointense on MRI ± hypointense bands radiating to the edges. 4. Littoral cell angioma—usually numerous ill-defined hypovascular nodules which equilibrate with the background spleen on the delayed phase. Variable T2 signal on MRI depending on haemosiderin content. Splenomegaly is nearly always present. 5. Other rare lesions—inflammatory pseudotumour (usually large, variable appearance), lipoma (contains fat only), angiomyolipoma (fat + enhancing soft tissue, usually in tuberous sclerosis), solitary fibrous tumour (well-defined heterogeneous hypervascular mass ± calcification)

Answer 33

1. Lymphoma*—usually with splenomegaly and disease elsewhere. Can present as solitary or multiple homogeneous hypoechoic hypovascular masses, micronodules or diffuse splenomegaly without a discrete lesion. May invade adjacent organs. Leukaemia and extraosseous myeloma can appear similar. 2. Metastases—e.g. from melanoma, lung, breast, GI tract. Nearly always with disseminated metastases elsewhere. Pancreatic tail tumours can also directly invade the spleen. 3. Angiosarcoma—rare overall, but the most common primary nonhaematolymphoid splenic malignancy; usually seen in older adults. Solitary or multiple ill-defined heterogeneously enhancing masses ± calcification ± haemorrhage. Often metastatic at presentation. 4. Haemangioendothelioma—rare; usually seen in young adults, less aggressive than angiosarcoma. Large, well-defined, heterogeneous mass ± necrotic, haemorrhagic or calcified areas. 5. Other rare sarcomas—e.g. leiomyosarcoma, undifferentiated pleomorphic sarcoma. Large, heterogeneous, nonspecific mass.

Answer 34

1. Chronic pancreatitis—especially due to alcohol (numerous, various sizes); can also be seen in chronic gallstone pancreatitis (smaller and fewer), hereditary pancreatitis (children and young adults) and tropical calcific pancreatitis (large ductal calculi in young patients in tropical developing countries). Rare in autoimmune pancreatitis. Calcification may be ductal or parenchymal. 2. Vascular calcification—e.g. splenic or gastroduodenal artery. Typically linear; may mimic parenchymal calcification. 3. Pseudocyst—can rim calcify or contain milk of calcium. 4. Calcification within a tumour—e.g. NET (coarse and irregular), serous cystadenoma (in central scar), mucinous cystadenoma (in wall or septa), IPMN, solid pseudopapillary neoplasm (peripheral and punctate), acinar cell carcinoma (variable pattern), haemangioma (phleboliths), pancreatoblastoma (children), mucinous metastasis (e.g. from GI tract). Calcification is almost never seen in primary adenocarcinoma. 5. Hyperparathyroidism*—due to a combination of metastatic calcification (directly due to hypercalcaemia) and recurrent hypercalcaemia-induced pancreatitis. Most have nephrocalcinosis or urolithiasis, suggesting the diagnosis. 6. Cystic fibrosis*—typically causes diffuse fatty replacement of the pancreas, but fine granular calcification can occur late in the disease. 7. Shwachman-Diamond syndrome—also causes diffuse fatty replacement of the pancreas; calcification is rarer than in CF. 8. Dystrophic calcification—e.g. following trauma, infection or infarction. 9. Other mimics—distal CBD stone, oral contrast within a duodenal diverticulum

Answer 35

1. Pancreatic ductal adenocarcinoma—focal PD dilatation with an abrupt transition point should always be considered suspicious for an underlying adenocarcinoma, as these can be isoattenuating on CT. Look for focal splenic vein/portal confluence narrowing, upstream pancreatic atrophy and CBD dilatation. Endoscopic ultrasound (EUS) may be necessary for further assessment. PD obstruction is much less common with other pancreatic tumours. 2. Obstructing PD calculi—due to chronic pancreatitis. 3. Benign stricture—e.g. due to recurrent/chronic pancreatitis (strictures are often multifocal), trauma or surgery (e.g. pancreaticojejunostomy). Benign strictures tend to be shorter and smoother than malignant strictures. 4. Ampullary tumour/gallstone—CBD dilatation > PD dilatation. 5. Main duct IPMN—markedly dilated PD filled with mucin, usually extending to ampulla (which may bulge into duodenum) with dilated sidebranches ± intraluminal soft tissue. No focal strictures. High risk of malignancy. 6. Necrotizing pancreatitis—often results in PD disruption and pancreatic collections, and can cause PD obstruction ± fistula. 7. Pancreas divisum—dorsal duct drains into the minor ampulla which may drain poorly, resulting in mild PD dilatation

Answer 36

1. Pseudocyst—most common cystic pancreatic lesion. Usually unilocular with a mildly thick fibrous wall, ± internal debris ± fistula with PD. No enhancing solid components. Other signs of chronic pancreatitis are usually present, e.g. atrophy, calcification, PD irregularity, ectatic sidebranches. May become infected. 2. Ectatic PD sidebranch—common and early finding in chronic pancreatitis. Benign stricture at insertion of sidebranch onto the main PD causes focal sidebranch dilatation that can mimic a small (<1 cm) unilocular sidebranch IPMN. Often multiple.222 Aids to Radiological Differential Diagnosis 3. Sidebranch IPMN—most common in older men (‘grandfather’). Uni-/multilocular cyst communicating with PD (best seen on MRCP). Lower risk of malignancy versus main duct IPMN; enhancing solid components, size >3 cm and extension into the main PD (causing dilatation) are worrying features. Can be multiple. 4. Serous cystadenoma—usually in older women (‘grandmother’), most common in the head. Typically multilocular and microcystic with innumerable tiny locules giving a honeycomb or sponge-like appearance. May have a characteristic central scar ± calcification. The cysts may be so small that the lesion appears solid and hypervascular on CT (microcysts are better appreciated on MRI). Occasionally macrocystic, mimicking a mucinous cystadenoma. No communication with PD. No malignant potential. Can be multiple in vHL disease. 5. Mucinous cystadenoma—almost exclusively in women (contains ovarian stroma), usually middle-aged (‘mother’). Typically in the body/tail. Typically uni-/multilocular and macrocystic with large locules (>2 cm). No communication with PD. Mural nodularity, septal thickening or calcification are worrying for malignant transformation to mucinous cystadenocarcinoma. 6. Solid pseudopapillary tumour—almost exclusively in young adult women (‘daughter’), especially Afro-Caribbeans. Large well-defined encapsulated mixed solid-cystic mass ± calcification, with peripheral irregular soft tissue and central cystic change, haemorrhage and necrosis. Usually benign. 7. Neuroendocrine tumour—can occasionally undergo marked cystic change (suggests malignant degeneration). Peripheral irregular/nodular arterial enhancement is usually present, differentiating this from other cystic lesions. 8. Pancreatic adenocarcinoma—can rarely be markedly necrotic or mucinous, appearing cystic. Look for associated duct obstruction and vascular occlusion. 9. Cystic metastases—e.g. from RCC, melanoma or lung. Rare. 10. Epithelial (true) cyst—rare; usually seen in autosomal dominant polycystic kidney disease, vHL disease and cystic fibrosis, where they are usually multiple. Thin-walled, unilocular, no solid components, no communication with PD. 11. Lymphoepithelial cyst—rare, benign; usually macrocystic, located in the body/tail. Similar appearance to mucinous cystadenoma except usually seen in men. May contain microscopic fat on in-/opposed-phase MRI ± T2 hypointensity and restricted diffusion due to keratin content. 12. Acinar cystic transformation—rare, benign. Solitary or multiple cysts in a clustered, segmental or diffuse distribution ± calcification. No communication with PD (cf. IPMN).Hepatobiliary, pancreas and spleen 223 8 13. Other rare cystic lesions—cystic teratoma (+ fat and calcification), lymphangioma (multiloculated and thin-walled), endometrioma (blood products on MRI), hydatid cyst (characteristic appearance; see Section 8.16), pancreatoblastoma (nearly always in children). 14. Mimics—a fluid-filled duodenal diverticulum, duplication cyst, cystic dystrophy of the duodenal wall (due to paraduodenal pancreatitis) or CBD diverticulum may mimic a pancreatic cyst

Answer 37

1. Ductal adenocarcinoma—ill-defined infiltrative hypovascular mass, usually causing PD obstruction, upstream atrophy and narrowing/occlusion of the splenic vein, superior mesenteric vein or portal confluence ± encasement of the superior mesenteric artery or coeliac axis. Tumours in the head tend to present earlier due to CBD obstruction and painless jaundice; tumours in the tail tend to present late with metastases. No calcification. The mass may be isoattenuating and very subtle—the secondary signs above may be the only indication of an underlying tumour. 2. Focal pancreatitis—can mimic carcinoma, or both may coexist. Associated nodular fat necrosis can mimic metastatic disease. Acute inflammation tends to cause more ill-defined fat stranding, usually without CBD/PD dilatation. Portal or splenic vein thrombosis can be seen but narrowing does not usually occur acutely unless compressed by a collection. Other inflammatory mimics of pancreatic cancer include: (a) Chronic pancreatitis—can create a focal fibroinflammatory mass, typically with calcification, most common in the head ± upstream PD dilatation due to obstructing ductal calculi.Mild CBD dilatation and splenic vein occlusion may also be seen. A narrow CBD/PD may be seen to traverse the mass (‘duct-penetrating’ sign; not seen with carcinoma). (b) Paraduodenal pancreatitis—focal inflammation in the pancreaticoduodenal groove ± ill-defined sheet-like fibrous mass ± mild CBD/PD dilatation ± duodenal stricture. Cystic change is common (not usually seen with carcinoma). Tends to displace the pancreatic head and distal CBD away from the duodenum. Chronic calcific pancreatitis often coexists. (c) Autoimmune pancreatitis—typically causes diffuse ‘sausage-like’ swelling of the pancreas with a thin discrete halo of fat stranding but can occasionally be focal, mimicking a mass. Common manifestation of IgG4-related disease. An associated stricture of the distal CBD can also be seen ± IgG4-cholangitis upstream. PD dilatation and vascular occlusion are typically absent (useful discriminating feature). 3. Cholangiocarcinoma of the intrapancreatic CBD—centered on and obstructs the CBD but does not usually obstruct the PD (cf. pancreatic ductal adenocarcinoma). 4. Metastasis—e.g. from lung (especially small-cell carcinoma), breast, melanoma, GI tract. Usually well-defined, often multiple, with disseminated metastases elsewhere. Duct obstruction and venous occlusion are much less common than with primary ductal adenocarcinoma. 5. Lymphoma*—usually in the presence of nodal disease elsewhere. Homogeneous hypovascular mass which encases vessels without causing narrowing or CBD/PD obstruction. 6. Solid pseudopapillary tumour—; can be completely solid. 7. Acinar cell carcinoma—well-defined heterogeneous mass ±necrosis/cystic change ± calcification, usually without CBD/PD dilatation. Can cause ectopic fat necrosis and bone infarcts due to lipase secretion. 8. Hamartoma—well-defined solid mass ± fat or cystic change. 9. TB*—can rarely involve the pancreas creating a hypovascular mass ± cystic change, usually in the presence of TB elsewhere (e.g. necrotic nodes). 10. Sarcoidosis*—very rare, typically in the presence of disease elsewhere. Single or multiple hypovascular masses. 11. Other rare tumours—e.g. granular cell tumour, inflammatory pseudotumour. Nonspecific appearances

Answer 38

1. Neuroendocrine tumour (NET)—most are hyperfunctioning, presenting as a small hypervascular mass with a characteristic clinical syndrome. Nonfunctioning tumours are more likely to be malignant and present as a larger heterogeneously enhancing mass ± cystic change ± calcification ± tumour thrombus in the splenic/portal vein. NETs are associated with MEN1 (especially nonfunctioning and gastrinomas, typically multiple), vHL (nonfunctioning, often multiple), NF1 (especially periampullary somatostatinoma) and tuberous sclerosis (especially insulinoma). (a) Insulinoma—presents with episodes of hypoglycaemia. Usually benign, solitary and <2 cm in diameter. Even distribution throughout the pancreas. (b) Gastrinoma—presents with multiple peptic ulcers (Zollinger-Ellison syndrome)—look for diffuse gastric fold thickening. The majority are malignant. Typically located in the ‘gastrinoma triangle’ which includes the pancreatic head and neck. Variable size. (c) Glucagonoma—presents with 4D syndrome (dermatitis, diabetes, DVT, depression), weight loss and diarrhoea. Most are malignant. Typically >2 cm, usually in the body/tail. (d) VIPoma—presents with WDHA syndrome (profuse watery diarrhoea, hypokalaemia, achlorhydria)—look for multiple fluid-filled loops of bowel. Most are malignant. Typically >2 cm, most common in the tail. (e) Somatostatinoma—presents with diabetes, gallstones and steatorrhoea. Most are malignant. Typically >2 cm, most common in the head. 2. Metastasis—especially from RCC. May be an isolated finding many years after initial diagnosis, mimicking a NET. 3. Intrapancreatic splenunculus—typically small and in the tail. Enhances similarly to spleen (heterogeneous in arterial phase, homogeneous in portal phase). Identical signal characteristics to spleen on MRI. 4. Vascular anomalies—e.g. gastroduodenal/splenic artery aneurysms, intrapancreatic venous shunts due to portal venous system thrombosis. 5. Serous cystadenoma—can appear solid and hypervascular on CT; MRI better demonstrates microcystic nature (see Section 8.34). 6. Haemangioma—peripheral nodular enhancement with centripetal filling ± phleboliths.226 Aids to Radiological Differential Diagnosis 7. Schwannoma—rare; mildly hypervascular ± necrosis/cystic change ± calcification. 8. Castleman disease—pancreatic involvement is very rare. Well-defined hypervascular mass ± cystic change ± calcification. 9. Other rare tumours—e.g. solitary fibrous tumour, leiomyosarcoma, other sarcomas. These are usually large masses with heterogeneous enhancement ± necrosis/cystic change ± calcification

HEPATOBILIARY, SPLEEN AND PANCREAS Flashcards

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