HEPATOBILIARY, SPLEEN AND PANCREAS Flashcards
INTRALUMINAL GALLBLADDER LESIONS
- 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. - Sludge—often forms mobile ‘balls’ of nonshadowing avascular
echogenic material. May fill GB. - 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. - Gallbladder empyema—distended thick-walled tender GB filled
with echogenic material, in a patient with sepsis. - 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. - 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. - Limy bile—milk of calcium in GB; very dense on CT.
- Gallbladder parasites—e.g. clonorchiasis, opisthorchiasis,
fascioliasis, ascariasis. Endemic in Southeast Asia. Floating
echogenic foci in the GB/bile ducts that may move
spontaneously.
GALLBLADDER WALL THICKENING
Diffuse
- 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). - 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 - 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. - 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. - 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. - 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. - Gallbladder volvulus—rare; markedly distended and thick-walled
GB extending beyond fossa + reduced mural enhancement. - 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. - Lymphoma*—rare, can diffusely infiltrate GB wall
GALLBLADDER WALL THICKENING
Focal
8
- 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. - 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. - Xanthogranulomatous cholecystitis—can sometimes be
focal. - Gallbladder metastases—via direct invasion (from liver tumours),
haematogenous (e.g. melanoma) or peritoneal spread (e.g.
gastric). - Lymphoma*—rare, usually in the presence of disease elsewhere.
- Intramural haematoma—due to trauma, liver biopsy, cystic artery
aneurysm, coagulopathy. Hyperattenuating on unenhanced CT. - Gallbladder varices—due to portal hypertension. Serpiginous
collateral veins. - Cystic artery aneurysm—usually due to severe or recurrent
cholecystitis
BILIARY DILATATION
Luminal causes (and nonobstructive dilatation)
8
- 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. - Small bowel obstruction—duodenal dilatation can impair biliary
drainage. - 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. - 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). - Choledochocoele—focal cystic dilatation of the distal CBD within
the ampulla, bulging into the duodenum. - 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. - 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. - Other rare polypoid neoplasms—e.g. bile duct adenoma,
inflammatory polyp, neurofibroma, primary melanoma
BILIARY DILATATION
Mural causes (strictures)
13
- 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. - 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 - 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. - 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. - 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. - 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. - Cystic fibrosis-related sclerosing cholangitis—similar
appearance to PSC. - 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. - 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. - 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. - Eosinophilic cholangitis—rare; can be related to parasites, fungi
or drugs. - Sarcoidosis*—can rarely cause a granulomatous cholangitis
leading to stricture formation, typically in the presence of disease
elsewhere. - Rare neoplasms—e.g. granular cell tumour, carcinoid, squamous
cell carcinoma, heterotopia. These can present as single short
strictures
BILIARY DILATATION Extrinsic causes (arranged from distal to proximal)
- 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. - Lemmel’s syndrome—rare; extrinsic compression of the distal
CBD by a periampullary duodenal diverticulum. - 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). - Pancreatitis—acute, chronic or autoimmune. Usually a smooth
tapered CBD narrowing ± PD dilatation/calculi. Associated
pseudocysts can also compress the CBD. - Periportal lymphadenopathy—compressing extrahepatic ducts.
- Cavernous transformation of portal vein—following portal vein
thrombosis. Venous collaterals around extrahepatic ducts can
cause mild dilatation (portal biliopathy). - 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. - Mirizzi syndrome—extrinsic compression of the CHD by a large
stone impacted in the GB neck. The stone may erode into the
common duct. - Hepatic masses—primary or metastatic tumours, abscesses.
Compress intrahepatic ducts causing focal or asymmetrical
intrahepatic biliary dilatation. - Hepatic hydatid cyst—may rupture contents into the biliary tree,
obstructing the lumen
GAS IN THE BILIARY TREE
Within the bile ducts
- Incompetent sphincter of Oddi—e.g. following sphincterotomy
or gallstone passage. A patulous sphincter can also be seen in the
elderly. - 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. - Postoperative—e.g. hepaticojejunostomy for Whipple’s procedure
GAS IN THE BILIARY TREE
Within the gallbladder
- All of the above.
- Gallstone containing gas—often has a
‘Mercedes-Benz’ morphology. - 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)
GAS IN THE PORTAL VEINS
- Bowel infarction—high mortality.
- Any other cause of bowel pneumatosis—see Section 7.25.
- Acute gastric dilatation—may resolve following decompression.
- Intraabdominal sepsis—e.g. diverticulitis, appendicitis,
pancreatitis, cholecystitis. - Following liver transplant.
HEPATOMEGALY WITHOUT
DISCRETE LESIONS
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.
HEPATIC CALCIFICATION AND
INCREASED DENSITY
Small and punctate calcification
- Healed granulomas—TB, histoplasmosis; less commonly
brucellosis or coccidioidomycosis. Small, punctate, usually multiple
± calcified granulomas elsewhere (lungs, nodes, spleen). - Intrahepatic ductal calculi—can be seen in PSC, Caroli disease
and recurrent pyogenic cholangitis. - Amyloidosis*—rare, can be numerous.
HEPATIC CALCIFICATION AND
INCREASED DENSITY
Curvilinear calcification
7
- 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. - Simple cyst—wall calcification is uncommon but can occur
following haemorrhage or infection. More common in polycystic
liver disease. - Chronic haematoma or abscess.
- Calcified (porcelain) gallbladder—possible association with GB
carcinoma, especially if segmental rather than diffuse. - Hepatic artery calcification—atherosclerosis or aneurysm.
- Portal vein calcification—chronic thrombus or portal
hypertension. - Schistosomiasis*—especially S. japonicum. Causes linear septal and
capsular calcification creating a characteristic ‘turtleback’ appearance.
HEPATIC CALCIFICATION AND
INCREASED DENSITY
Calcification within a mass
- Metastases—especially from mucinous primaries, e.g. colorectal
and gastric; rarely from osteosarcoma or teratoma. Metastases can
also calcify following radiotherapy or chemotherapy. - Fibrolamellar HCC—located within stellate central scar.
- Lipiodol—component of TACE therapy, deposits in the treated
tumour (e.g. HCC). Very dense on CT. - Haemangioma—cavernous and sclerosing subtypes may contain
central foci of calcification, especially if large. - 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)
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
- 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. - Amiodarone therapy—due to iodine content of the drug; ± lung
infiltrates. - Gold therapy.
- Wilson’s disease—though findings may be confounded by
coexistent fatty infiltration. - Glycogen storage diseases.
- 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
HEPATIC CALCIFICATION AND INCREASED DENSITY
Focal increased density (noncalcified)
2
- Haematoma—including haemorrhagic lesions such as adenoma,
HCC and angiomyolipoma. - Siderotic regenerative/dysplastic nodule—seen in cirrhosis.
DIFFUSELY HYPOECHOIC LIVER
- Acute hepatitis—with prominent periportal echogenicity giving a
‘starry-sky’ appearance. Mild hepatitis has a normal echo pattern. - Diffuse malignant infiltration—e.g. leukaemia
DIFFUSELY HYPERECHOIC LIVER
- 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. - Cirrhosis—irregular contour ± signs of portal hypertension.Hepatobiliary, pancreas and spleen 195
8 - Hepatitis—particularly chronic.
- Glycogen storage disease—associated with hepatic adenomas
DIFFUSELY HETEROGENEOUS LIVER
10
- 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). - 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’). - 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.
- 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. - Acute fulminant hepatitis—most commonly due to viral hepatitis or drugs/toxins (e.g. paracetamol overdose). Heterogeneous liver due to patchy necrosis.
- 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.
- 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.
- Schistosomiasis*—periportal fibrosis with a network of linear septal fibrosis and calcification giving a ‘turtleback’ appearance. Echogenic on US, dense on CT.
- 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).
- Amyloidosis*—enlarged heterogeneous liver, hypoattenuating on
CT ± calcifications.
FOCAL HYPERECHOIC LIVER LESION
With posterior acoustic shadowing
- Calcified lesions—see Section 8.7.
- Pneumobilia—linear, periportal; see Section 8.4.
- Gas within an abscess.
- Portal venous gas—linear, usually peripheral; see Section 8.5.Hepatobiliary, pancreas and spleen 197
8 - Biliary hamartomas—small, numerous; cause posterior ‘comet-tail’
artefact rather than shadowing
FOCAL HYPERECHOIC LIVER LESION
Nonshadowing
- 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. - Haemangioma—well-defined homogeneously hyperechoic lesion
without a hypoechoic halo. May be heterogeneous if large. - Metastases—from GI tract (especially colon), ovary, pancreas,
urogenital tract, thyroid, melanoma, NET, choriocarcinoma. Often
multiple + hypoechoic halo. - HCC—especially if fatty. Usually well-defined + hypoechoic halo.
Look for signs of cirrhosis. - Hepatic adenoma—especially if fatty or haemorrhagic, ±
hypoechoic halo. - Mass-forming cholangiocarcinoma—especially if large. Usually
ill-defined, no hypoechoic halo. Look for peripheral biliary
dilatation and capsular retraction. - Debris within a lesion—e.g. abscess, haematoma, hydatid cyst
(hydatid ‘sand’). - Rare lesions containing fat—e.g. angiomyolipoma, lipoma.
- Other lesions with variable echogenicity—e.g. FNH,
inflammatory pseudotumour, haemangioendothelioma
FOCAL HYPOECHOIC LIVER LESION
- Focal fatty sparing—typically adjacent to GB or porta, with
background steatosis. No distortion of vessels or liver contour. - Metastasis—including cystic or mucinous metastases (e.g. from GI
tract, pancreas, NET, ovary). - HCC—most commonly hypoechoic ± internal vascularity. Look for
signs of cirrhosis. - Abscess—± hyperechoic wall due to fibrosis, ± surrounding
hypoechoic rim due to oedema. Look for echogenic foci of gas. - Haemorrhagic or infected cyst—contains internal floating echoes
± septations. No internal vascularity. - Mass-forming cholangiocarcinoma—especially if small.
- Lymphoma*—may be markedly hypoechoic. Look for
splenomegaly and adenopathy. - Hydatid cyst—can contain hydatid ‘sand’ or solid material.198 Aids to Radiological Differential Diagnosis
- Other lesions with variable echogenicity—e.g. FNH, adenoma,
atypical haemangioma, haematoma.
PERIPORTAL HYPERECHOGENICITY
- Pneumobilia—with posterior acoustic shadowing; see Section 8.4.
- Portal venous gas—see Section 8.5.
- Periportal fibrosis—e.g. in cystic fibrosis, schistosomiasis infection
(± ‘turtleback’ appearance) or vinyl chloride workers. - Hepatic artery calcification—e.g. diabetes, chronic renal failure.
- Intrahepatic duct calculi—e.g. in PSC or recurrent pyogenic
cholangitis. - Inflammatory bowel disease*—echo-rich periportal cuffing can
rarely be seen. - Stents, drains and surgical clips.
- Langerhans cell histiocytosis*—in children; periportal
xanthomatous (fatty) deposits.
PERIPORTAL OEDEMA
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.
PERIPORTAL OEDEMA
Extrahepatic causes
- Raised central venous pressure/cardiac failure.
- Hypoproteinaemia.
- Systemic inflammation—e.g. sepsis, trauma, acute pancreatitis.
- Lymphatic obstruction—e.g. by malignant periportal adenopathy
PERIPORTAL LESIONS
Vascular
- 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. - Cavernous transformation of portal vein—a tangle of periportal
venous collaterals that develop after PV thrombosis. - 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)
PERIPORTAL LESIONS
Biliary
5
- Cholangiocarcinoma—periductal infiltrating or intraductal forms.
Both cause severe biliary dilatation ± PV narrowing or occlusion. - Cholangitis/strictures.
- Bile duct stones.
- Choledochal cyst.
- Biliary cystadenoma—can rarely arise from extrahepatic ducts
PERIPORTAL LESIONS
Haematological/lymphatic
- 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. - Metastatic lymphadenopathy—e.g. from HPB/GI malignancies.
- 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. - Extramedullary haematopoiesis—mimics lymphoma. Look for
features of bone marrow failure.
PERIPORTAL LESIONS
Others
- Focal fatty infiltration/sparing—can occur in periportal region.
Geographic appearance, no mass effect. - 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 - Fluid collections—following trauma/surgery or tracking from
cholecystitis or pancreatitis. - 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. - Schwannoma—well-defined rounded mass ± internal cystic
change or calcification. - Sarcomas—e.g. Kaposi sarcoma (typically causes enhancing
periportal nodules + hypervascular nodes), leiomyosarcoma,
MPNST
CYSTIC LIVER LESIONS
Unilocular and thin-walled
- Simple cyst—solitary or multiple, variable size. Usually unilocular
with an imperceptible wall. May contain thin nonenhancing septa.
Can become haemorrhagic or infected. - 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. - 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. - 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. - Focal bile duct dilatation—e.g. due to a stricture, biliary IPMN or
intrahepatic choledochal cyst. See Section 8.3. - Cystic metastases—can occasionally mimic simple cysts (see later).
- Hydatid cyst—CL and CE1 types (see later).
- 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. - Intrahepatic gallbladder—congenital anomaly. Often small and
located close to an empty GB fossa
CYSTIC LIVER LESIONS
Multilocular or thick-walled
- 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. - 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. - 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. - 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. - 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. - 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. - Inflammatory pseudotumour—can occasionally present as a
complex cystic mass with thick enhancing septa. - Multicystic biliary hamartoma—rare, benign. Tubulocystic
honeycomb-like mass with mural and septal enhancement,
typically in a peripheral location. - Biliary adenofibroma—rare benign tumour with some malignant
potential; complex multicystic mass + enhancing solid
components, indistinguishable from biliary cystadenocarcinoma. - Lymphangioma—intrahepatic location is rare.
- Glomus tumour—very rare. Complex cystic mass with arterially
enhancing mural nodules that persist into the delayed phase. - Mesenchymal hamartoma and embryonal sarcoma—typically
in children; very rare in adults. Both appear as complex
multilocular cystic masses
FAT-CONTAINING LIVER LESIONS
Macroscopic fat
- 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. - 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. - HCC/adenoma—can occasionally contain macroscopic fat.
- Lipoma—rare. Purely fatty.
- Surgical omentopexy—flap of omentum is placed on the liver
surface, e.g. after hydatid cyst surgery. - Hydatid cyst—can rarely contain droplets of fat.
- Hepatic adrenal rest tumour—rare; contains a mixture of soft
tissue and fat, mimicking AML. - Fatty metastasis—e.g. from teratoma or liposarcoma; rare.
Primary hepatic teratoma or liposarcoma is even rarer. - Lipopeliosis—rare; can occur in a transplanted liver after an
ischaemic insult. - Extramedullary haematopoiesis—the rare focal intrahepatic
form can contain fat. - Langerhans cell histiocytosis*—in children; periportal
xanthomatous deposits
FAT-CONTAINING LIVER LESIONS
Microscopic fat
- 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. - HCC—often contains fat. Hypervascular on arterial phase +
washout on later phases. Mainly seen in cirrhotic livers. - Hepatic adenoma—often contain fat. Hypervascular ± washout.
Most common in young women taking oral contraceptives. - Regenerative nodules—occasionally contain fat; usually multiple.
No enhancement (cf. HCC). Seen in cirrhotic livers. - FNH—uncommonly contains foci of intracellular fat, especially if
the background liver is fatty. - Angiomyolipoma—if fat-poor.
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
- 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. - Vascular malformation/shunt—has dilated feeding and draining vessels. May be arterioportal, arteriovenous or portosystemic. T2 dark (flow void).
- 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.
- Treated metastasis—can show persistent enhancement.
- Angiomyolipoma—typically contains macroscopic fat. Vascular
components enhance. - 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.
- 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.
- 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. - Leiomyoma—rare; usually hypervascular with persistent enhancement in the delayed phase
HYPERVASCULAR LIVER LESIONS
Arterial enhancement equilibrating on the delayed phase
6
- 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. - 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. - 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. - 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).
- Large regenerative nodules—seen in chronic Budd-Chiari
syndrome; often multiple. Imaging features are identical to FNH. - Intrahepatic splenosis—post splenectomy. Subcapsular deposits of
splenic tissue; heterogeneous arterial enhancement, becoming
homogeneous in the portal phase.
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.
- HCC—usually in cirrhotic livers. Characteristically shows arterial
enhancement followed by washout, ± internal fat ± enhancing
capsule ± venous invasion (tumour thrombus). May be multiple. - 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. - Hepatic adenoma—can show washout (especially the HNF1αmutated subtype).
- Fibrolamellar HCC—can show washout
Rare hypervascular hepatic tumours with nonspecific appearances
6
- Inflammatory pseudotumour—variable appearance; may be
hypervascular ± washout. - Solitary fibrous tumour—rare; solitary large well-defined mass
with heterogeneous arterial enhancement and areas of both high
and low T2 signal. - 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. - 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. - Intrahepatic bile duct adenoma—very rare; usually small (<2 cm)
and subcapsular. Heterogeneous arterial enhancement that may
persist or wash out, ± cystic change. - Adenomatoid tumour—very rare; solid or solid-cystic
hypervascular mass
LIVER LESIONS WITH GRADUAL DELAYED
ENHANCEMENT
Gradual delayed enhancement usually suggests a fibrotic lesion.
- Mass-forming cholangiocarcinoma—classically shows gradual
delayed enhancement, especially centrally. Usually causes capsular
retraction ± peripheral biliary dilatation ± vascular occlusion ±
restricted diffusion. - 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. - Haemangioma—some are late-filling (complete or partial),
especially the sclerosing subtype. - Treated metastasis/HCC—treatment results in fibrosis.
- Solid organizing abscess—this is a partially healed abscess that
contains late-enhancing fibrosis/granulation tissue. - Inflammatory pseudotumour—variable appearance, may show
delayed enhancement. - Solitary fibrous tumour—rare; often contains both hypervascular
areas and fibrotic late-enhancing areas.
HYPOVASCULAR LIVER LESIONS
12
- Metastases—e.g. from GI tract, pancreas, lung, breast, etc. Most
metastases tend to be hypovascular due to central necrosis ±
mild peripheral arterial enhancement. - Cholangiocarcinoma—may show minimal enhancement.
- 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. - 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. - 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. - Sclerosing haemangioma—may be completely hypovascular
with only mild T2 hyperintensity ± capsular retraction, mimicking
malignancy. May have calcification or a wedge-like morphology. - Previously treated HCC/metastasis—e.g. ablation, TACE,
chemotherapy. - 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 - Inflammatory pseudotumour—variable appearance, can be
hypovascular. - 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. - 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. - Other rare lesions—e.g. Langerhans cell histiocytosis,
amyloidoma, Rosai-Dorfman disease.
LIVER LESIONS WITH A CENTRAL SCAR
Scars often show delayed enhancement, and do not have to be
exactly central
8
- Focal nodular hyperplasia—the scar is typically T2 hyperintense
and noncalcified. - Cavernous haemangioma—especially if large.
- Fibrolamellar HCC—the scar is typically T2 hypointense and often
calcified. Conventional HCCs can also occasionally contain a
central scar. - Large regenerative nodules—seen in chronic Budd-Chiari
syndrome. Identical appearance to FNH. - 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). - Hepatic adenoma—occasionally.
- Metastases—can contain a central fibrotic component.
- Epithelioid haemangioendothelioma—rare; peripheral vascular
component + central fibrosis often giving a ‘target’ appearance.
HEPATIC CAPSULAR RETRACTION
- Metastases—especially after treatment or with fibrotic/necrotic
tumours, e.g. breast, carcinoid, lung, colorectal. Can create a
‘pseudocirrhosis’ appearance. - Mass-forming cholangiocarcinoma—classically shows capsular
retraction. - Confluent hepatic fibrosis—seen in cirrhosis; capsular retraction is
characteristic (see Section 8.25). - Sclerosing haemangioma—can cause adjacent capsular
retraction. - Post trauma—including iatrogenic, e.g. biliary drainage, biopsy.
- HCC—following ablation or TACE. Can also be seen with
fibrolamellar HCCs. - Epithelioid haemangioendothelioma—classically shows capsular
retraction. See Section 8.18. - Inflammatory pseudotumour—variable appearance; can mimic
cholangiocarcinoma. - Pseudomyxoma peritonei (mimic)—scalloping of liver surface
may resemble capsular retraction
T1 HYPERINTENSE LIVER LESIONS
- Fat—see Section 8.17.
- 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). - 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 - Melanoma metastases.
- Intrahepatic ductal calculi—pigment type, seen in PSC,
recurrent pyogenic cholangitis and Caroli disease. - Proteinaceous material—may be seen dependently in abscesses.
Can also be seen in the rare ciliated hepatic foregut cyst. - Calcification—can occasionally be T1 hyperintense.
- Chemical—gadolinium, lipiodol (contains fat).
- ‘Relative’—i.e. normal-signal liver surrounded by low-signal liver,
e.g. iron deposition (haemochromatosis/siderosis), oedema. - 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
T2 HYPOINTENSE LIVER LESIONS
11
- 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. - Gas—e.g. pneumobilia or gas within an abscess. Rises to the
antidependent surface. - 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. - Calcification—see Section 8.7.
- Vascular malformation/shunt—flow voids.
- Sarcoidosis*—numerous T2 hypointense nodules in liver and
spleen. - 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. - Liver ablation—e.g. for HCC/metastasis. Causes T2 hypointense
coagulative necrosis. - Thick mucin—e.g. within mucinous metastases.
- Leiomyoma—often T2 hypointense and hypervascular. Rare.
- Melanoma metastases—occasionally T2 hypointense.
LESIONS IN CHRONIC LIVER DISEASE
6
- 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).
- 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.
- 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.
- 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.
- 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.
- Large regenerative nodules—seen in chronic Budd-Chiari syndrome. Identical appearance to FNH
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
- 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. - 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). - 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. - 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. - 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:
- FNH—uptake > background liver is a characteristic feature. The
central scar is often hypointense. - Regenerative and dysplastic nodules—in cirrhosis.
- Lesions communicating with the biliary tree—e.g. choledochal
cyst, Caroli disease, biloma (if there is an ongoing bile leak). - Large regenerative nodules—seen in chronic Budd-Chiari
syndrome. Identical imaging features to FNH. - Focal fatty infiltration—uptake may be less than background liver.
- THID—see Section 8.18.
- Hepatic adenoma—inflammatory subtype can show peripheral
uptake. - Well-differentiated HCC—can show uptake
Pitfalls of using hepatocyte-specific contrast agents include: 2
- Assessing arterial enhancement—usually less intense than with
extracellular contrast agents, therefore hypervascular lesions (e.g.
haemangioma, HCC) may be less appreciable. - 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
SPLENOMEGALY
Huge spleen
- Chronic myeloid leukaemia.
- Myelofibrosis—look for bone sclerosis.
- Malaria*.
- Gaucher disease*—look for bone infarcts, e.g. in femoral heads.
- Lymphoma*.
- Visceral leishmaniasis (kala-azar)
Moderately large spleen
- All of the above.
- Haemolytic anaemias—including haemoglobinopathies.
- Portal hypertension—e.g. cirrhosis, splenic/portal vein occlusion,
right heart failure. - Leukaemias.
- Polycythaemia vera.
- Systemic mastocytosis—look for bone sclerosis.
- Glycogen storage diseases
Slightly large spleen
- All of the above.
- 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. - Sarcoidosis*.
- Rheumatoid arthritis*—Felty’s syndrome.
- Amyloidosis*.
- Systemic lupus erythematosus (SLE)*.
SPLENIC CALCIFICATION
Curvilinear
2
- Splenic artery atherosclerosis—especially splenic artery aneurysm.
- Cyst—any chronic cyst, including hydatid or posttraumatic.
SPLENIC CALCIFICATION
Multiple small nodular/punctate
- Phleboliths—± small central lucencies. Can be seen in
haemangiomas. - TB*—usually few in number + calcified intrathoracic nodes and
lung granulomas. - Histoplasmosis—calcifications are often larger than in TB or
other fungal infections, e.g. candidiasis; with calcified
intrathoracic nodes and lung granulomas. - Gamna-Gandy bodies—siderotic splenic nodules usually due to
portal hypertension. - Sickle cell anaemia.
- Pneumocystis jiroveci—e.g. in AIDS, ± hepatic, renal, adrenal and
nodal calcification. - Toxoplasmosis.
- Sarcoidosis*.
- SLE.
- Amyloidosis*—often with hepatic calcification
SPLENIC CALCIFICATION
Diffuse homogeneous
- Sickle cell anaemia—spleen is shrunken and diffusely calcified.
- Previous Thorotrast administration—with liver and nodal
calcification
SPLENIC CALCIFICATION
Solitary >1 cm
4
Healed
- Healed infarct or haematoma.
- Healed abscess.
- Healed granuloma—e.g. TB, histoplasmosis.
- Brucellosis—pathognomonic large ‘snowflake’ calcification within a chronic brucellar abscess; calcification persists after healing
CYSTIC SPLENIC LESIONS
- 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). - Epithelial cyst—thin-walled unilocular cyst ± septations, no
enhancement. - 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. - Hydatid cyst—usually in the presence of liver involvement; see
Section 8.16. - Lymphangioma—often multilocular with thin enhancing septa, no
solid components. - Cystic metastasis—e.g. from melanoma or mucinous primaries. Rare
SOLID SPLENIC LESIONS
Nonneoplastic 8
- 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). - Haematoma—usually traumatic; can also occur due to coagulopathy or splenomegaly. Hyperattenuating on unenhanced CT, no internal enhancement unless there is active bleeding.
- 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. - Sarcoidosis*—numerous small hypovascular T2 hypointense
nodules, usually with hepatic, nodal and thoracic involvement. - 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. - Extramedullary haematopoiesis—usually causes diffuse splenomegaly but can rarely present as a focal hypovascular mass ± internal fat.
- 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.
- Amyloidosis*—usually diffuse, causing strikingly poor arterial enhancement of the spleen and T2 hypointensity on MRI. Focal hypovascular amyloidomas are rare.
SOLID SPLENIC LESIONS
Benign neoplasms and hamartomas
- 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. - 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. - 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. - 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. - 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)
SOLID SPLENIC LESIONS
Malignant neoplasms
- 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. - Metastases—e.g. from melanoma, lung, breast, GI tract. Nearly
always with disseminated metastases elsewhere. Pancreatic tail
tumours can also directly invade the spleen. - 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. - Haemangioendothelioma—rare; usually seen in young adults, less
aggressive than angiosarcoma. Large, well-defined, heterogeneous
mass ± necrotic, haemorrhagic or calcified areas. - Other rare sarcomas—e.g. leiomyosarcoma, undifferentiated
pleomorphic sarcoma. Large, heterogeneous, nonspecific mass.
PANCREATIC CALCIFICATION
- 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. - Vascular calcification—e.g. splenic or gastroduodenal artery.
Typically linear; may mimic parenchymal calcification. - Pseudocyst—can rim calcify or contain milk of calcium.
- 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. - 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. - Cystic fibrosis*—typically causes diffuse fatty replacement of the
pancreas, but fine granular calcification can occur late in the
disease. - Shwachman-Diamond syndrome—also causes diffuse fatty
replacement of the pancreas; calcification is rarer than in CF. - Dystrophic calcification—e.g. following trauma, infection or
infarction. - Other mimics—distal CBD stone, oral contrast within a duodenal
diverticulum
PANCREATIC DUCT DILATATION
- 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.
- Obstructing PD calculi—due to chronic pancreatitis.
- 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.
- Ampullary tumour/gallstone—CBD dilatation > PD dilatation.
- 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.
- Necrotizing pancreatitis—often results in PD disruption and pancreatic collections, and can cause PD obstruction ± fistula.
- Pancreas divisum—dorsal duct drains into the minor ampulla which may drain poorly, resulting in mild PD dilatation
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
- 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. - 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 - 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. - 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. - 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. - 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. - 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. - Pancreatic adenocarcinoma—can rarely be markedly necrotic or
mucinous, appearing cystic. Look for associated duct obstruction
and vascular occlusion. - Cystic metastases—e.g. from RCC, melanoma or lung. Rare.
- 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. - 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. - 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 - 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). - 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
SOLID PANCREATIC LESIONS
Hypovascular 11
- 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. - 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). - Cholangiocarcinoma of the intrapancreatic CBD—centered on and obstructs the CBD but does not usually obstruct the PD (cf. pancreatic ductal adenocarcinoma).
- 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.
- Lymphoma*—usually in the presence of nodal disease elsewhere.
Homogeneous hypovascular mass which encases vessels without causing narrowing or CBD/PD obstruction. - Solid pseudopapillary tumour—; can be completely solid.
- 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.
- Hamartoma—well-defined solid mass ± fat or cystic change.
- TB*—can rarely involve the pancreas creating a hypovascular mass ± cystic change, usually in the presence of TB elsewhere (e.g. necrotic nodes).
- Sarcoidosis*—very rare, typically in the presence of disease
elsewhere. Single or multiple hypovascular masses. - Other rare tumours—e.g. granular cell tumour, inflammatory pseudotumour. Nonspecific appearances
SOLID PANCREATIC LESIONS
Hypervascular
- 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. - Metastasis—especially from RCC. May be an isolated finding
many years after initial diagnosis, mimicking a NET. - 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. - Vascular anomalies—e.g. gastroduodenal/splenic artery
aneurysms, intrapancreatic venous shunts due to portal venous
system thrombosis. - Serous cystadenoma—can appear solid and hypervascular on CT;
MRI better demonstrates microcystic nature (see Section 8.34). - Haemangioma—peripheral nodular enhancement with centripetal
filling ± phleboliths.226 Aids to Radiological Differential Diagnosis - Schwannoma—rare; mildly hypervascular ± necrosis/cystic change
± calcification. - Castleman disease—pancreatic involvement is very rare.
Well-defined hypervascular mass ± cystic change ± calcification. - Other rare tumours—e.g. solitary fibrous tumour,
leiomyosarcoma, other sarcomas. These are usually large masses
with heterogeneous enhancement ± necrosis/cystic change ±
calcification