Radiology differential diagnosis > HEPATOBILIARY, SPLEEN AND PANCREAS > Flashcards

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  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
    (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
  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



  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
  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


  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
  4. Gallbladder metastases—via direct invasion (from liver tumours),
    haematogenous (e.g. melanoma) or peritoneal spread (e.g.
  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

Luminal causes (and nonobstructive dilatation)

  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
  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
  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

Mural causes (strictures)

  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
  13. Rare neoplasms—e.g. granular cell tumour, carcinoid, squamous
    cell carcinoma, heterotopia. These can present as single short
Extrinsic causes (arranged from distal to proximal)
  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


Within the bile ducts

  1. Incompetent sphincter of Oddi—e.g. following sphincterotomy
    or gallstone passage. A patulous sphincter can also be seen in the
  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


Within the gallbladder

  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)


  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.




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
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.
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.
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
3. Infiltrative HCC—can blend in with background cirrhosis.
4. Angiosarcoma—rare; often diffusely infiltrative.192 Aids to Radiological Differential Diagnosis
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
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
4. Mucopolysaccharidoses
Myeloproliferative disorders
Usually accompanied by splenomegaly.
1. Extramedullary haematopoiesis—e.g. in myelofibrosis.
2. Polycythaemia vera.
3. Mastocytosis*.
1. Riedel’s lobe—anatomical variant; tongue-like inferior extension of
right lobe that can mimic hepatomegaly. Often associated with an
accessory hepatic vein.


Small and punctate calcification

  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.

Curvilinear calcification

  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
  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
  7. Schistosomiasis*—especially S. japonicum. Causes linear septal and
    capsular calcification creating a characteristic ‘turtleback’ appearance.

Calcification within a mass

  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)

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

  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
  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

Focal increased density (noncalcified)

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


  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


  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
  3. Hepatitis—particularly chronic.
  4. Glycogen storage disease—associated with hepatic adenomas



  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
    (d) Alpha-1 antitrypsin deficiency
    —basal emphysema.
    (e) Cystic fibrosis*—bronchiectasis and fatty replacement of
    (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.


With posterior acoustic shadowing

  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
  5. Biliary hamartomas—small, numerous; cause posterior ‘comet-tail’
    artefact rather than shadowing



  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


  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.


  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
  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.



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



Extrahepatic causes

  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



  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)


  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



  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
  4. Extramedullary haematopoiesis—mimics lymphoma. Look for
    features of bone marrow failure.



  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,


Unilocular and thin-walled

  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
    (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


Multilocular or thick-walled

  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
  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’
    (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


Macroscopic fat

  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


Microscopic fat

  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.

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

  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

Arterial enhancement equilibrating on the delayed phase

  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
    (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.

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

  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

Rare hypervascular hepatic tumours with nonspecific appearances

  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

Gradual delayed enhancement usually suggests a fibrotic lesion.

  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.



  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
    (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,
  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
  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.

Scars often show delayed enhancement, and do not have to be
exactly central

  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.


  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
  3. Confluent hepatic fibrosis—seen in cirrhosis; capsular retraction is
    characteristic (see Section 8.25).
  4. Sclerosing haemangioma—can cause adjacent capsular
  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
  9. Pseudomyxoma peritonei (mimic)—scalloping of liver surface
    may resemble capsular retraction


  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



  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
  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.



  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

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


  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.

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

  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
  8. Well-differentiated HCC—can show uptake

Pitfalls of using hepatocyte-specific contrast agents include: 2

  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


Huge spleen

  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)

Moderately large spleen

  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

Slightly large spleen

  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)*.


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


Multiple small nodular/punctate

  1. Phleboliths—± small central lucencies. Can be seen in
  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


Diffuse homogeneous

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

Solitary >1 cm

  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


  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,
  2. Epithelial cyst—thin-walled unilocular cyst ± septations, no
  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


Nonneoplastic 8

  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.


Benign neoplasms and hamartomas

  1. Haemangioma—most common incidental solid splenic lesion.
    Usually hyperechoic on US without vascularity on Doppler, ±Hepatobiliary, pancreas and spleen 219
    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 ±


Malignant neoplasms

  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
  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.


  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
  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
  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
  9. Other mimics—distal CBD stone, oral contrast within a duodenal


  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


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

  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
  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
  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


Hypovascular 11

  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



  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 ±