HEPATOBILIARY, SPLEEN AND PANCREAS

Question 1

INTRALUMINAL GALLBLADDER LESIONS

Answer 1

1. Gallstones—single or multiple, small or large. ~80% are
   radiolucent on plain film, but ~80% are visible on CT. Often
   calcified, may contain central fat or gas. Typically mobile, but can
   be adherent to the GB wall. Typically show posterior acoustic
   shadowing, but calculi <5 mm may be nonshadowing and mimic a
   cholesterol polyp. Microlithiasis = multiple 1–3 mm calculi. A GB
   packed with calculi can mimic bowel gas on US (though gas
   shadows tend to be ‘dirtier’). Two main types of calculi (NB: most
   contain a mixture):
   (a) Cholesterol stones—most common in middle-aged obese
   women. Variable size and number. Pure cholesterol stones are
   often invisible on CT. Typically T1 and T2 hypointense on MRI,
   but can be heterogeneous.
   (b) Pigment stones—usually seen in chronic liver disease and
   chronic haemolysis. Typically small, numerous and calcified.
   Often T1 hyperintense and T2 hypointense on MRI.
2. Sludge—often forms mobile ‘balls’ of nonshadowing avascular
   echogenic material. May fill GB.
3. Gallbladder polyps—polyps measuring 6–9 mm require follow-up;
   surgery is suggested for polyps ≥10 mm. In patients with PSC,
   polyps of any size should be followed up or considered for
   cholecystectomy.
   (a) Cholesterol polyps—usually small (<10 mm), multiple and
   avascular. Nonmobile, nonshadowing. Mildly enhancing,
   intermediate T1 and T2 signal on MRI. Numerous small
   cholesterol polyps = cholesterolosis. No malignant potential.
   (b) Adenoma—usually solitary, often >10 mm and sessile with
   internal vascularity on US. Associated with PSC and polyposis
   syndromes. Risk of progression to adenocarcinoma.
   (c) Inflammatory polyps—usually small (<10 mm) and multiple,
   seen in chronically inflamed GBs. No malignant potential.
   8184 Aids to Radiological Differential Diagnosis
   (d) Rare polypoid lesions—e.g. leiomyoma, lipoma (fatty on
   CT/MR), fibroma, neurofibroma (usually in NF1),
   haemangioma, granular cell tumour, carcinoid tumour,
   and heterotopic gastric, hepatic or pancreatic tissue.
4. Gallbladder empyema—distended thick-walled tender GB filled
   with echogenic material, in a patient with sepsis.
5. Haematoma—due to trauma, surgery, biliary intervention,
   coagulopathy or cystic artery aneurysm (usually postinflammatory).
   Heterogeneous and avascular on US, hyperattenuating on
   unenhanced CT. Look for active contrast extravasation. Blood may
   fill and obstruct CBD or enter the duodenum, presenting with
   melaena.
6. Gallbladder carcinoma—may present as a solitary polypoid mass
   similar to an adenoma. Features suggesting malignancy: large size,
   wide polyp base, focal GB wall thickening adjacent to polyp, polyp
   enhancement > GB wall.
7. Limy bile—milk of calcium in GB; very dense on CT.
8. Gallbladder parasites—e.g. clonorchiasis, opisthorchiasis,
   fascioliasis, ascariasis. Endemic in Southeast Asia. Floating
   echogenic foci in the GB/bile ducts that may move
   spontaneously.

Question 2

GALLBLADDER WALL THICKENING

Diffuse

Answer 2

1. Acute calculous cholecystitis—caused by an obstructing gallstone
   in the GB neck or cystic duct. Distended thick-walled GB with
   adjacent fluid ± mucosal hyperenhancement on CT. Irregular or
   absent mucosal enhancement suggests gangrenous cholecystitis
   that may perforate, resulting in pericholecystic or intrahepatic
   collections. Intramural gas = emphysematous cholecystitis (usually
   in diabetics).
2. Chronic cholecystitis—thick-walled contracted GB containing
   gallstones, no adjacent fluid. Chronic cystic duct obstruction can
   also result in a grossly distended GB (hydrops). A chronically
   inflamed GB can become adherent to the duodenum or hepatic
   flexure ± erosion of calculi directly into the duodenum or colon,
   forming a fistula.Hepatobiliary, pancreas and spleen 185
   8
3. Passive mural oedema—seen in acute hepatitis, cirrhosis, portal
   hypertension, right heart failure, renal failure, fluid overload and
   hypoalbuminaemia. Diffuse mural oedema throughout GB with
   normal smooth mucosal enhancement, usually with periportal
   oedema and ascites. Reactive GB oedema can also be seen due to
   adjacent duodenitis or pancreatitis.
4. Acute acalculous cholecystitis—usually seen in critically ill patients
   due to hypoperfusion and ischaemia; the GB is usually distended
   (atonic) with sludge but no discrete calculi. Can also be caused by
   infectious mononucleosis and AIDS-related opportunistic infections,
   e.g. CMV, Cryptosporidium.
5. Diffuse adenomyomatosis—contracted, mildly thick-walled GB
   with echogenic intramural foci + comet-tail artefacts on US.
   Smooth mucosal hyperenhancement on CT with tiny enhancing
   foci extending into the thickened wall, representing
   Rokitansky-Aschoff sinuses—on MRI these appear as a string of
   small intramural cystic spaces.
6. Xanthogranulomatous cholecystitis (XGC)—chronic
   inflammatory disorder causing marked diffuse GB wall thickening
   with multiple intramural hypoattenuating nodules on CT,
   representing xanthogranulomas (mildly T2 hyperintense
   on MRI) or abscesses (T2 bright). Associated GB perforation or
   hepatic infiltration may be seen, mimicking adenocarcinoma;
   preservation of smooth mucosal enhancement suggests XGC.
7. Gallbladder volvulus—rare; markedly distended and thick-walled
   GB extending beyond fossa + reduced mural enhancement.
8. Gallbladder carcinoma—the rare signet ring variant can cause
   diffuse wall thickening similar to linitis plastica, mimicking benign
   thickening. Look for infiltration into adjacent structures.
9. Lymphoma*—rare, can diffusely infiltrate GB wall

Question 3

GALLBLADDER WALL THICKENING
Focal
8

Answer 3

1. Adenomyomatosis—can be focal (typically at GB fundus) or
   segmental (causing circumferential thickening of the GB body,
   giving it an hourglass shape). Characterized by intramural
   Rokitansky-Aschoff sinuses which appear on US as echogenic
   foci + ‘comet-tail’ artefact, and on CT/MRI as a string/cluster of
   small intramural cystic spaces. The sinuses may contain foci of
   calcification on CT.
2. Gallbladder carcinoma—most commonly presents as focal
   irregular thickening of the GB wall ± extension into the lumen or
   into adjacent structures (e.g. liver), ± lymphadenopathy or
   metastases. Risk factors include gallstones, polyposis, PSC and
   segmental GB wall calcification.
3. Xanthogranulomatous cholecystitis—can sometimes be
   focal.
4. Gallbladder metastases—via direct invasion (from liver tumours),
   haematogenous (e.g. melanoma) or peritoneal spread (e.g.
   gastric).
5. Lymphoma*—rare, usually in the presence of disease elsewhere.
6. Intramural haematoma—due to trauma, liver biopsy, cystic artery
   aneurysm, coagulopathy. Hyperattenuating on unenhanced CT.
7. Gallbladder varices—due to portal hypertension. Serpiginous
   collateral veins.
8. Cystic artery aneurysm—usually due to severe or recurrent
   cholecystitis

Question 4

BILIARY DILATATION
Luminal causes (and nonobstructive dilatation)
8

Answer 4

1. Obstructing ductal filling defect—e.g. stone (most common,
   may be multiple), sludge (less discrete than a stone), blood clot
   (look for GB haematoma) or parasites (ascariasis, clonorchiasis,
   fascioliasis, opisthorchiasis). Obstruction leads to infection and
   cholangitis—diffuse smooth mural thickening and enhancement of
   extrahepatic ducts.
2. Small bowel obstruction—duodenal dilatation can impair biliary
   drainage.
3. Choledochal cyst—focal or diffuse dilatation of common
   duct ± central intrahepatic ducts, caused by an anomalous
   pancreaticobiliary junction—CBD and PD form a long common
   channel upstream of the sphincter of Oddi, resulting in reflux
   of pancreatic juices into the CBD, degenerating the bile
   duct wall. Can be complicated by stone formation or cholangiocarcinoma.
4. Caroli disease—congenital DPM affecting the larger bile ducts,
   resulting in multifocal saccular dilatation of intrahepatic bile ducts,
   often containing a central ‘dot’ representing portal radicals. May
   be diffuse or segmental. Intraductal calculi are often seen. May be
   associated with congenital hepatic fibrosis (DPM affecting smaller
   ducts).
5. Choledochocoele—focal cystic dilatation of the distal CBD within
   the ampulla, bulging into the duodenum.
6. Bile duct diverticulum—solitary and saccular; usually extrahepatic
   but can also be intrahepatic (e.g. in PSC). May mimic a GB
   diverticulum or accessory GB if large.
7. Intraductal papillary mucinous neoplasm (biliary IPMN)—
   most common in Southeast Asia; usually arises from intrahepatic
   bile ducts. Results in marked segmental intrahepatic biliary
   dilatation (due to mucin hypersecretion) without a downstream
   obstructing stone or stricture. Slowly progressive premalignant
   lesion; causes lobar atrophy over time. Mural nodularity within
   the dilated ducts may be seen and suggests malignancy.
8. Other rare polypoid neoplasms—e.g. bile duct adenoma,
   inflammatory polyp, neurofibroma, primary melanoma

Question 5

BILIARY DILATATION
Mural causes (strictures)
13

Answer 5

1. Papillary stenosis/sphincter of Oddi dysfunction—recurrent
   passage of small stones through the ampulla can cause papillary
   stenosis due to fibrosis—small nonobstructing calculi may also be
   seen within the dilated CBD. Sphincter of Oddi dysfunction is
   caused by functional dyskinesia/spasm and can be seen
   postcholecystectomy or due to opioids.
2. Cholangiocarcinoma—risk factors include gallstones, PSC,
   cirrhosis, recurrent pyogenic cholangitis, Caroli disease,
   choledochal cyst. Three main types:
   (a) Mass-forming—typically arise from peripheral ducts in the liver.
   (b) Periductal infiltrating—subtle enhancing stricture with
   upstream biliary dilatation; infiltrates along ducts, usually
   without a significant soft tissue mass. Most common at the
   hilum (Klatskin tumour), where it causes complex stricturing with separation of intrahepatic ducts.
   (c) Intraductal—rare, polypoid intraluminal mass; usually arises from biliary IPMN
3. Primary sclerosing cholangitis (PSC)—autoimmune disease
   usually associated with IBD (UC > Crohn’s). Results in multifocal
   short intra- and extrahepatic strictures, giving a ‘beaded’ or
   discontinuous appearance to the ducts. Biliary dilatation is often
   only mild. Acute episodes of cholangitis can cause diffuse mural
   thickening and enhancement involving a longer ductal segment.
   Extrahepatic strictures may also be long. Eventually progresses to
   cirrhosis, often with peripheral atrophy and marked caudate
   hypertrophy. Increased risk of cholangiocarcinoma—a dominant
   stricture or progressive biliary dilatation is worrying.
4. Iatrogenic stricture—e.g. post biliary intervention, postsurgical
   anastomotic stricture, postcholecystectomy injury to bile duct
   (especially if there is variant anatomy, e.g. aberrant insertion of
   segment 6 duct close to the cystic duct), post radiotherapy.
5. IgG4-related sclerosing cholangitis—typically causes long
   strictures with mural thickening and enhancement (cf. the shorter
   strictures in PSC); most common in the CBD but can involve
   any part of biliary tree. Look for other features of IgG4-related
   disease, especially autoimmune pancreatitis.
6. Recurrent pyogenic cholangitis—endemic in Southeast Asia,
   related to parasitic (especially clonorchiasis) or bacterial
   infections. Recurrent cholangitis results in multifocal strictures and
   pigment stone formation in intra- and extrahepatic ducts
   (especially in the left lobe). Can be complicated by abscess
   formation, lobar atrophy or cholangiocarcinoma.
7. Cystic fibrosis-related sclerosing cholangitis—similar
   appearance to PSC.
8. Chemotherapy-induced sclerosing cholangitis—develops
   months after hepatic artery infusion chemotherapy or TACE.
   Typically involves the proximal CHD, hilum and central
   intrahepatic ducts ± GB and cystic duct; spares peripheral
   intrahepatic ducts and distal CBD. Mural thickening and
   enhancement on CT/MRI with mild upstream biliary dilatation.
9. Ischaemic cholangiopathy—most commonly seen <6 months
   after liver transplant; other causes include vasculitis (polyarteritis
   nodosa, giant cell arteritis), sickle cell disease and long-term ICU
   admissions. Typically involves the proximal CHD, hilum and
   central intrahepatic ducts initially, but can progress to involve the
   entire biliary tree. Intraluminal filling defects (sloughed mucosa)
   and associated bilomas are highly suggestive of ischaemia.
10. AIDS cholangiopathy—caused by opportunistic infections, e.g.
    Cryptosporidium, CMV, HSV. Multifocal strictures similar to PSC;
    also often causes papillary stenosis and can involve the GB.
11. Eosinophilic cholangitis—rare; can be related to parasites, fungi
    or drugs.
12. Sarcoidosis*—can rarely cause a granulomatous cholangitis
    leading to stricture formation, typically in the presence of disease
    elsewhere.
13. Rare neoplasms—e.g. granular cell tumour, carcinoid, squamous
    cell carcinoma, heterotopia. These can present as single short
    strictures

Question 6

BILIARY DILATATION
Extrinsic causes (arranged from distal to proximal)

Answer 6

1. Ampullary tumours—e.g. adenoma, carcinoma, carcinoid.
   Obstructs CBD ± PD. Often small and hard to see on imaging if
   the duodenum is not well-distended; ampullary soft tissue >1 cm
   in diameter is abnormal and warrants endoscopy.
2. Lemmel’s syndrome—rare; extrinsic compression of the distal
   CBD by a periampullary duodenal diverticulum.
3. Pancreatic head tumour—especially adenocarcinoma. Abrupt
   CBD narrowing at the level of the tumour, usually with
   upstream PD dilatation and atrophy (cf. cholangiocarcinoma
   of distal CBD).
4. Pancreatitis—acute, chronic or autoimmune. Usually a smooth
   tapered CBD narrowing ± PD dilatation/calculi. Associated
   pseudocysts can also compress the CBD.
5. Periportal lymphadenopathy—compressing extrahepatic ducts.
6. Cavernous transformation of portal vein—following portal vein
   thrombosis. Venous collaterals around extrahepatic ducts can
   cause mild dilatation (portal biliopathy).
7. Bile duct metastasis—via direct invasion (e.g. from GB),
   haematogenous (e.g. melanoma) or peritoneal spread (e.g.
   gastric). Usually involves hilum or proximal common duct.
8. Mirizzi syndrome—extrinsic compression of the CHD by a large
   stone impacted in the GB neck. The stone may erode into the
   common duct.
9. Hepatic masses—primary or metastatic tumours, abscesses.
   Compress intrahepatic ducts causing focal or asymmetrical
   intrahepatic biliary dilatation.
10. Hepatic hydatid cyst—may rupture contents into the biliary tree,
    obstructing the lumen

Question 7

GAS IN THE BILIARY TREE

Within the bile ducts

Answer 7

1. Incompetent sphincter of Oddi—e.g. following sphincterotomy
   or gallstone passage. A patulous sphincter can also be seen in the
   elderly.
2. Spontaneous biliary fistula—typically due to a large GB calculus
   eroding through a chronically inflamed GB wall into the
   duodenum (± gallstone ileus) or less commonly the hepatic
   flexure. Rarely, a fistula may be caused by trauma, malignancy or a
   duodenal ulcer eroding into the CBD.
3. Postoperative—e.g. hepaticojejunostomy for Whipple’s procedure

Question 8

GAS IN THE BILIARY TREE

Within the gallbladder

Answer 8

1. All of the above.
2. Gallstone containing gas—often has a
   ‘Mercedes-Benz’ morphology.
3. Emphysematous cholecystitis—due to
   gas-forming organisms, often in elderly
   diabetics. Intramural and intraluminal gas, usually without gas in
   the bile ducts (due to cystic duct obstruction)

Question 9

GAS IN THE PORTAL VEINS

Answer 9

1. Bowel infarction—high mortality.
2. Any other cause of bowel pneumatosis—see Section 7.25.
3. Acute gastric dilatation—may resolve following decompression.
4. Intraabdominal sepsis—e.g. diverticulitis, appendicitis,
   pancreatitis, cholecystitis.
5. Following liver transplant.

Question 10

HEPATOMEGALY WITHOUT

DISCRETE LESIONS

Answer 10

Acute hepatitis
The liver is enlarged and often hypoechoic on US. Periportal
oedema and GB oedema are often seen on CT/MR ± reactive
periportal nodes.
1. Infective.
(a) Viral—hepatitis, infectious mononucleosis.
(b) Protozoal—malaria, African trypanosomiasis, visceral
leishmaniasis.
2. Alcoholic.
3. Drug-induced—e.g. paracetamol overdose.
4. Autoimmune—can rarely present acutely.
5. Sickle cell crisis—look for other features of the disease.
Cardiovascular
These can all cause venous congestion in the liver, creating a
mottled ‘nutmeg’ appearance on postcontrast CT/MR and signs of
(postsinusoidal) portal hypertension.
1. Right heart failure—e.g. due to congestive cardiac failure,
constrictive pericarditis or tricuspid valve disease. Distended
hepatic veins and IVC ± ascites.
2. Acute Budd-Chiari syndrome—thrombosed hepatic veins.
3. Hepatic venoocclusive disease—seen following bone marrow
transplant/chemotherapy. Small calibre but patent hepatic veins.
Neoplastic
Diffuse malignant infiltration can cause parenchymal
heterogeneity without discrete lesions. The liver surface can be
irregular, mimicking cirrhosis. The portal and hepatic veins may
appear distorted.
1. Diffuse lymphoma—with lymphadenopathy and splenomegaly.
Also seen in leukaemia.
2. Diffuse metastases—especially from breast or small-cell lung
cancer.
3. Infiltrative HCC—can blend in with background cirrhosis.
4. Angiosarcoma—rare; often diffusely infiltrative.192 Aids to Radiological Differential Diagnosis
Infiltrative/depositional
1. Steatosis—fat infiltration. Hyperechoic on US (relative to normal
renal cortex), hypoattenuating on unenhanced CT (>10 HU less
than spleen). On MRI, shows signal loss on opposed-phase
T1-weighted sequence, in keeping with microscopic fat content.
May be diffuse or geographic.
2. Haemochromatosis—iron deposition. Liver may appear
hyperattenuating on unenhanced CT. T2 hypointense on MRI
(especially on gradient echo sequences that are more prone to
susceptibility effects), with signal loss on in-phase T1-weighted
sequence (cf. steatosis).
3. Wilson’s disease—copper deposition, often with coexisting
steatosis.
4. Sarcoidosis—usually with splenic and thoracic involvement.
5. Amyloidosis—hypoattenuating liver on CT ± calcifications.
Storage disorders
1. Glycogen storage diseases—hyperechoic on US, hyperattenuating
on CT; ± hepatic adenomas.
2. Gaucher disease.
3. Niemann-Pick disease—with interlobular septal thickening in the
lungs (type B) or CNS involvement (type C). Type A is fatal in early
childhood.
4. Mucopolysaccharidoses.
Myeloproliferative disorders
Usually accompanied by splenomegaly.
1. Extramedullary haematopoiesis—e.g. in myelofibrosis.
2. Polycythaemia vera.
3. Mastocytosis*.
Congenital
1. Riedel’s lobe—anatomical variant; tongue-like inferior extension of
right lobe that can mimic hepatomegaly. Often associated with an
accessory hepatic vein.

Question 11

HEPATIC CALCIFICATION AND
INCREASED DENSITY
Small and punctate calcification

Answer 11

1. Healed granulomas—TB, histoplasmosis; less commonly
   brucellosis or coccidioidomycosis. Small, punctate, usually multiple
   ± calcified granulomas elsewhere (lungs, nodes, spleen).
2. Intrahepatic ductal calculi—can be seen in PSC, Caroli disease
   and recurrent pyogenic cholangitis.
3. Amyloidosis*—rare, can be numerous.

Question 12

HEPATIC CALCIFICATION AND
INCREASED DENSITY
Curvilinear calcification
7

Answer 12

1. Hydatid cyst—calcification does not necessarily indicate death
   of the parasite, but extensive calcification favours an inactive
   cyst. Calcification of daughter cysts produces several calcified
   rings.
2. Simple cyst—wall calcification is uncommon but can occur
   following haemorrhage or infection. More common in polycystic
   liver disease.
3. Chronic haematoma or abscess.
4. Calcified (porcelain) gallbladder—possible association with GB
   carcinoma, especially if segmental rather than diffuse.
5. Hepatic artery calcification—atherosclerosis or aneurysm.
6. Portal vein calcification—chronic thrombus or portal
   hypertension.
7. Schistosomiasis*—especially S. japonicum. Causes linear septal and
   capsular calcification creating a characteristic ‘turtleback’ appearance.

Question 13

HEPATIC CALCIFICATION AND
INCREASED DENSITY
Calcification within a mass

Answer 13

1. Metastases—especially from mucinous primaries, e.g. colorectal
   and gastric; rarely from osteosarcoma or teratoma. Metastases can
   also calcify following radiotherapy or chemotherapy.
2. Fibrolamellar HCC—located within stellate central scar.
3. Lipiodol—component of TACE therapy, deposits in the treated
   tumour (e.g. HCC). Very dense on CT.
4. Haemangioma—cavernous and sclerosing subtypes may contain
   central foci of calcification, especially if large.
5. Other tumours—can occasionally contain calcification, e.g.
   adenoma and HCC (related to prior haemorrhage),
   cholangiocarcinoma, FNH (within central scar, rare), biliary
   cystadenoma/carcinoma (mural), epithelioid
   haemangioendothelioma, teratoma. Calcification is also common
   in certain paediatric liver tumours (hepatoblastoma, nested
   stromal–epithelial tumour)

Question 14

HEPATIC CALCIFICATION AND
INCREASED DENSITY
Diffusely increased density

Assess by comparing the liver with the spleen (normally up to 12
HU > spleen). Also, intrahepatic vessels stand out as low-density
against high-density background liver

Answer 14

1. Haemochromatosis*—due to iron deposition. Pancreas and heart
   may also be involved. NB: secondary haemosiderosis (due to
   chronic blood transfusions or iron therapy) usually affects the
   spleen and bone marrow more than the liver.
2. Amiodarone therapy—due to iodine content of the drug; ± lung
   infiltrates.
3. Gold therapy.
4. Wilson’s disease—though findings may be confounded by
   coexistent fatty infiltration.
5. Glycogen storage diseases.
6. Previous Thorotrast administration—old radiographic contrast
   agent. Deposited in liver, spleen and lymph nodes, creating
   marked diffuse or reticular hyperdensity (as dense as calcium).
   Associated with hepatic angiosarcoma and other malignancie

Question 15

HEPATIC CALCIFICATION AND INCREASED DENSITY
Focal increased density (noncalcified)
2

Answer 15

1. Haematoma—including haemorrhagic lesions such as adenoma,
   HCC and angiomyolipoma.
2. Siderotic regenerative/dysplastic nodule—seen in cirrhosis.

Question 16

DIFFUSELY HYPOECHOIC LIVER

Answer 16

1. Acute hepatitis—with prominent periportal echogenicity giving a
   ‘starry-sky’ appearance. Mild hepatitis has a normal echo pattern.
2. Diffuse malignant infiltration—e.g. leukaemia

Question 17

DIFFUSELY HYPERECHOIC LIVER

Answer 17

1. Fatty infiltration—attenuates the US beam when severe,
   obscuring the deep portions of the liver. May see focal hypoechoic
   fatty sparing in typical locations, e.g. adjacent to GB or porta.
2. Cirrhosis—irregular contour ± signs of portal hypertension.Hepatobiliary, pancreas and spleen 195
   8
3. Hepatitis—particularly chronic.
4. Glycogen storage disease—associated with hepatic adenomas

Question 18

DIFFUSELY HETEROGENEOUS LIVER

10

Answer 18

1. Cirrhosis—nodular liver contour ± signs of portal hypertension (splenomegaly, ascites, portosystemic shunts). The liver is often
   small with hypertrophy of the caudate and segments 2 and 3. It is usually difficult to ascertain the underlying cause on imaging, but some aetiologies can offer clues:
   (a) PSC—multifocal biliary strictures, peripheral distribution of
   fibrosis and volume loss, with hypertrophy of the caudate
   and central liver.
   (b) Primary biliary cirrhosis—typically in middle-aged women.
   Lace-like pattern of fibrosis ± characteristic periportal ‘halo’ of
   T2 hypointensity on MRI.
   (c) Haemochromatosis—diffuse iron deposition causes T2
   hypointensity and signal loss on the in-phase T1-weighted
   sequence.
   (d) Alpha-1 antitrypsin deficiency—basal emphysema.
   (e) Cystic fibrosis*—bronchiectasis and fatty replacement of
   pancreas.
   (f) Cardiac cirrhosis—dilated hepatic veins and right atrium.
   (g) Congenital hepatic fibrosis—congenital ductal plate malformation (DPM) involving small ducts, resulting in fibrosis and cirrhosis usually by early adulthood. Associated with ARPKD and other hepatic DPMs: multiple biliary
   hamartomas (small ducts), polycystic liver disease (medium ducts) and Caroli disease (large ducts).
2. Diffuse malignancy—primary (HCC, angiosarcoma) or metastatic
   (breast, small-cell lung cancer, lymphoma, leukaemia). The liver is
   typically enlarged ± a nodular contour, though breast cancer metastases can induce fibrosis and volume loss (‘pseudocirrhosis’).
3. Fatty infiltration—can be very patchy or bizarre in distribution, mimicking metastatic disease on US/CT. Diagnosis confirmed on in-/opposed-phase MRI, with signal loss on the opposed phase.
4. Abnormal perfusion—e.g. hepatic infarction (in severe shock, hypercoagulable states, sickle cell crisis or HELLP syndrome), hepatic artery occlusion (e.g. following TACE or liver transplant) or portal vein thrombosis. Also seen in:
   (a) Venous congestion—due to right heart failure, acute Budd-Chiari syndrome or venoocclusive disease; Chronic Budd-Chiari syndrome results in peripheral liver atrophy and marked caudate hypertrophy; the normal hepatic veins are obliterated and replaced by tortuous intrahepatic venous shunts; multiple large regenerative nodules may also be seen.
   (b) Hereditary haemorrhagic telangiectasia*—markedly heterogeneous enhancement throughout the liver, especially on arterial phase CT/MR, due to innumerable intrahepatic telangiectasias and AVMs. Tends to equilibrate on later phases. Hepatic arteries and veins are often dilated with early
   venous filling due to shunting. FNH-like lesions can also be seen. Look for lung AVMs to confirm diagnosis.
5. Acute fulminant hepatitis—most commonly due to viral hepatitis or drugs/toxins (e.g. paracetamol overdose). Heterogeneous liver due to patchy necrosis.
6. Sarcoidosis*—usually in the presence of disease elsewhere. Innumerable small (<1 cm) granulomas throughout the liver and spleen; hypovascular on CT/MR, usually T2 hypointense.
7. Hepatic microabscesses—in immunocompromised patients; most commonly due to candidiasis, but can be seen in other fungal infections and TB. Innumerable small abscesses (most <1 cm) throughout the liver ± spleen, T2 hyperintense on MRI with restricted diffusion.
8. Schistosomiasis*—periportal fibrosis with a network of linear septal fibrosis and calcification giving a ‘turtleback’ appearance. Echogenic on US, dense on CT.
9. Nodular regenerative hyperplasia—microscopic regenerative nodules without fibrosis (cf. cirrhosis). Associated with organ transplantation, immunosuppression, pulmonary hypertension, autoimmune diseases, myeloproliferative disorders and other malignancies. The liver may appear normal or heterogeneous on imaging with signs of portal hypertension. The individual nodules are invisible and the liver surface is usually smooth (cf. cirrhosis).
10. Amyloidosis*—enlarged heterogeneous liver, hypoattenuating on
    CT ± calcifications.

Question 19

FOCAL HYPERECHOIC LIVER LESION

With posterior acoustic shadowing

Answer 19

1. Calcified lesions—see Section 8.7.
2. Pneumobilia—linear, periportal; see Section 8.4.
3. Gas within an abscess.
4. Portal venous gas—linear, usually peripheral; see Section 8.5.Hepatobiliary, pancreas and spleen 197
   8
5. Biliary hamartomas—small, numerous; cause posterior ‘comet-tail’
   artefact rather than shadowing

Question 20

FOCAL HYPERECHOIC LIVER LESION

Nonshadowing

Answer 20

1. Focal fatty infiltration—most common adjacent to falciform
   ligament but can occur anywhere. Geographic margins, no
   distortion of vessels or liver contour. Can be multifocal.
2. Haemangioma—well-defined homogeneously hyperechoic lesion
   without a hypoechoic halo. May be heterogeneous if large.
3. Metastases—from GI tract (especially colon), ovary, pancreas,
   urogenital tract, thyroid, melanoma, NET, choriocarcinoma. Often
   multiple + hypoechoic halo.
4. HCC—especially if fatty. Usually well-defined + hypoechoic halo.
   Look for signs of cirrhosis.
5. Hepatic adenoma—especially if fatty or haemorrhagic, ±
   hypoechoic halo.
6. Mass-forming cholangiocarcinoma—especially if large. Usually
   ill-defined, no hypoechoic halo. Look for peripheral biliary
   dilatation and capsular retraction.
7. Debris within a lesion—e.g. abscess, haematoma, hydatid cyst
   (hydatid ‘sand’).
8. Rare lesions containing fat—e.g. angiomyolipoma, lipoma.
9. Other lesions with variable echogenicity—e.g. FNH,
   inflammatory pseudotumour, haemangioendothelioma

Question 21

FOCAL HYPOECHOIC LIVER LESION

Answer 21

1. Focal fatty sparing—typically adjacent to GB or porta, with
   background steatosis. No distortion of vessels or liver contour.
2. Metastasis—including cystic or mucinous metastases (e.g. from GI
   tract, pancreas, NET, ovary).
3. HCC—most commonly hypoechoic ± internal vascularity. Look for
   signs of cirrhosis.
4. Abscess—± hyperechoic wall due to fibrosis, ± surrounding
   hypoechoic rim due to oedema. Look for echogenic foci of gas.
5. Haemorrhagic or infected cyst—contains internal floating echoes
   ± septations. No internal vascularity.
6. Mass-forming cholangiocarcinoma—especially if small.
7. Lymphoma*—may be markedly hypoechoic. Look for
   splenomegaly and adenopathy.
8. Hydatid cyst—can contain hydatid ‘sand’ or solid material.198 Aids to Radiological Differential Diagnosis
9. Other lesions with variable echogenicity—e.g. FNH, adenoma,
   atypical haemangioma, haematoma.

Question 22

PERIPORTAL HYPERECHOGENICITY

Answer 22

1. Pneumobilia—with posterior acoustic shadowing; see Section 8.4.
2. Portal venous gas—see Section 8.5.
3. Periportal fibrosis—e.g. in cystic fibrosis, schistosomiasis infection
   (± ‘turtleback’ appearance) or vinyl chloride workers.
4. Hepatic artery calcification—e.g. diabetes, chronic renal failure.
5. Intrahepatic duct calculi—e.g. in PSC or recurrent pyogenic
   cholangitis.
6. Inflammatory bowel disease*—echo-rich periportal cuffing can
   rarely be seen.
7. Stents, drains and surgical clips.
8. Langerhans cell histiocytosis*—in children; periportal
   xanthomatous (fatty) deposits.

Question 23

PERIPORTAL OEDEMA

Answer 23

Hepatic causes
1. Acute hepatitis/cholangitis—see Sections 8.3 and 8.6.
2. Cirrhosis.
3. Regional inflammation—e.g. cholecystitis, abscess, eosinophilic
gastroenteritis.
4. Following liver transplant—can reflect lymphoedema, biliary
necrosis or rejection.

Question 24

PERIPORTAL OEDEMA

Extrahepatic causes

Answer 24

1. Raised central venous pressure/cardiac failure.
2. Hypoproteinaemia.
3. Systemic inflammation—e.g. sepsis, trauma, acute pancreatitis.
4. Lymphatic obstruction—e.g. by malignant periportal adenopathy

Question 25

PERIPORTAL LESIONS

Vascular

Answer 25

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)

Question 26

PERIPORTAL LESIONS
Biliary
5

Answer 26

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

Question 27

PERIPORTAL LESIONS

Haematological/lymphatic

Answer 27

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.

Question 28

PERIPORTAL LESIONS

Others

Answer 28

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

Question 29

CYSTIC LIVER LESIONS

Unilocular and thin-walled

Answer 29

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

Question 30

CYSTIC LIVER LESIONS

Multilocular or thick-walled

Answer 30

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

Question 31

FAT-CONTAINING LIVER LESIONS

Macroscopic fat

Answer 31

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

Question 32

FAT-CONTAINING LIVER LESIONS

Microscopic fat

Answer 32

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.

Question 33

HYPERVASCULAR LIVER LESIONS
Arterial enhancement persisting on the delayed phase
The lesion continues to enhance more than the background liver on the delayed phase.
9

Answer 33

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

Question 34

HYPERVASCULAR LIVER LESIONS
Arterial enhancement equilibrating on the delayed phase
6

Answer 34

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.

Question 35

HYPERVASCULAR LIVER LESIONS
Arterial enhancement with washout on portal or delayed phase
The lesion enhances less than the background liver on the portal
or delayed phase.

Answer 35

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

Question 36

Rare hypervascular hepatic tumours with nonspecific appearances
6

Answer 36

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

Question 37

LIVER LESIONS WITH GRADUAL DELAYED
ENHANCEMENT
Gradual delayed enhancement usually suggests a fibrotic lesion.

Answer 37

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.

Question 38

HYPOVASCULAR LIVER LESIONS

12

Answer 38

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.

Question 39

LIVER LESIONS WITH A CENTRAL SCAR
Scars often show delayed enhancement, and do not have to be
exactly central
8

Answer 39

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.

Question 40

HEPATIC CAPSULAR RETRACTION

Answer 40

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

Question 41

T1 HYPERINTENSE LIVER LESIONS

Answer 41

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

Question 42

T2 HYPOINTENSE LIVER LESIONS

11

Answer 42

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.

Question 43

LESIONS IN CHRONIC LIVER DISEASE

6

Answer 43

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

Question 44

HEPATOCYTE-SPECIFIC MR
CONTRAST AGENTS
These agents (e.g. Primovist) are taken up by hepatocytes and
excreted in bile, contrary to extracellular MR contrast agents (e.g.
Gadovist), which stay in the extracellular space. This provides
the opportunity to obtain an extra ‘hepatobiliary’ phase
post contrast—in the case of Primovist this phase is seen at
~20 min. This can be used as a problem-solving tool in certain
circumstances

Uses
5

Answer 44

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.

Question 45

Lesions which take up hepatocyte-specific contrast agents in the
hepatobiliary phase include:

Answer 45

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

Question 46

Pitfalls of using hepatocyte-specific contrast agents include: 2

Answer 46

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

Question 47

SPLENOMEGALY

Huge spleen

Answer 47

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)

Question 48

Moderately large spleen

Answer 48

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

Question 49

Slightly large spleen

Answer 49

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)*.

Question 50

SPLENIC CALCIFICATION
Curvilinear
2

Answer 50

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

Question 51

SPLENIC CALCIFICATION

Multiple small nodular/punctate

Answer 51

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

Question 52

SPLENIC CALCIFICATION

Diffuse homogeneous

Answer 52

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

Question 53

SPLENIC CALCIFICATION
Solitary >1 cm
4
Healed

Answer 53

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

Question 54

CYSTIC SPLENIC LESIONS

Answer 54

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

Question 55

SOLID SPLENIC LESIONS

Nonneoplastic 8

Answer 55

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.

Question 56

SOLID SPLENIC LESIONS

Benign neoplasms and hamartomas

Answer 56

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)

Question 57

SOLID SPLENIC LESIONS

Malignant neoplasms

Answer 57

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.

Question 58

PANCREATIC CALCIFICATION

Answer 58

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

Question 59

PANCREATIC DUCT DILATATION

Answer 59

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

Question 60

CYSTIC PANCREATIC LESIONS

A high CEA level within the aspirated fluid
suggests a mucinous lesion (i.e. sidebranch IPMN or mucinous
cystadenoma), whereas a low CEA suggests either a pseudocyst
(high amylase) or serous cystadenoma (low amylase). Mucinous
lesions carry a risk of malignancy and are usually resected

Answer 60

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

Question 61

SOLID PANCREATIC LESIONS

Hypovascular 11

Answer 61

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

Question 62

SOLID PANCREATIC LESIONS

Hypervascular

Answer 62

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