Hepatobiliary, pancreas and spleen

Intraluminal gallbladder lesions

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

Gallbladder wall thickening

>3 mm in a well-distended gallbladder.

Diffuse

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.
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.

Focal

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

Biliary dilatation

CBD: >6 mm up to the age of 60 years, adding 1 mm for every decade thereafter. Postcholecystectomy: CBD >10 mm.

Intrahepatic ducts: >2 mm or >40% of the adjacent portal vein diameter.

On CT, beware of portal vein thrombosis mimicking intrahepatic biliary dilatation—with biliary dilatation, patent portal veins should be visible paralleling the dilated ducts. On MRCP, beware of pitfalls that can mimic a ductal lesion:

Intraductal gas bubbles—antidependent signal voids (more common in left lobe), form gas–fluid levels in larger ducts.
Biliary flow voids—located centrally within the duct (calculi sit dependently).
Normal cystic duct folds—spiral valves of Heister.
Extrinsic vascular impression of hepatic artery on CHD—common, no clinical significance.
Susceptibility artefact from cholecystectomy clips.

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

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 (see earlier).
3.
Primary sclerosing cholangitis (PSC) —autoimmune disease usually associated with IBD (UC > Crohn's). Results in multifocal short intra- and extrahepatic strictures, giving a ‘beaded’ or discontinuous appearance to the ducts. Biliary dilatation is often only mild. Acute episodes of cholangitis can cause diffuse mural thickening and enhancement involving a longer ductal segment. Extrahepatic strictures may also be long. Eventually progresses to cirrhosis, often with peripheral atrophy and marked caudate hypertrophy. Increased risk of cholangiocarcinoma—a dominant stricture or progressive biliary dilatation is worrying.
4.
Iatrogenic stricture —e.g. post biliary intervention, postsurgical anastomotic stricture, postcholecystectomy injury to bile duct (especially if there is variant anatomy, e.g. aberrant insertion of segment 6 duct close to the cystic duct), post radiotherapy.
5.
IgG4-related sclerosing cholangitis —typically causes long strictures with mural thickening and enhancement (cf. the shorter strictures in PSC); most common in the CBD but can involve any part of biliary tree. Look for other features of IgG4-related disease, especially autoimmune pancreatitis.
6.
Recurrent pyogenic cholangitis —endemic in Southeast Asia, related to parasitic (especially clonorchiasis) or bacterial infections. Recurrent cholangitis results in multifocal strictures and pigment stone formation in intra- and extrahepatic ducts (especially in the left lobe). Can be complicated by abscess formation, lobar atrophy or cholangiocarcinoma.
7.
Cystic fibrosis-related sclerosing cholangitis —similar appearance to PSC.
8.
Chemotherapy-induced sclerosing cholangitis —develops months after hepatic artery infusion chemotherapy or TACE. Typically involves the proximal CHD, hilum and central intrahepatic ducts ± GB and cystic duct; spares peripheral intrahepatic ducts and distal CBD. Mural thickening and enhancement on CT/MRI with mild upstream biliary dilatation.
9.
Ischaemic cholangiopathy —most commonly seen <6 months after liver transplant; other causes include vasculitis (polyarteritis nodosa, giant cell arteritis), sickle cell disease and long-term ICU admissions. Typically involves the proximal CHD, hilum and central intrahepatic ducts initially, but can progress to involve the entire biliary tree. Intraluminal filling defects (sloughed mucosa) and associated bilomas are highly suggestive of ischaemia.
10.
AIDS cholangiopathy —caused by opportunistic infections, e.g. Cryptosporidium , CMV, HSV. Multifocal strictures similar to PSC; also often causes papillary stenosis and can involve the GB.
11.
Eosinophilic cholangitis —rare; can be related to parasites, fungi or drugs.
12.
Sarcoidosis *—can rarely cause a granulomatous cholangitis leading to stricture formation, typically in the presence of disease elsewhere.
13.
Rare neoplasms —e.g. granular cell tumour, carcinoid, squamous cell carcinoma, heterotopia. These can present as single short strictures.

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.

Gas in the biliary tree

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 elderly.
2.
Spontaneous biliary fistula —typically due to a large GB calculus eroding through a chronically inflamed GB wall into the duodenum (± gallstone ileus) or less commonly the hepatic flexure. Rarely, a fistula may be caused by trauma, malignancy or a duodenal ulcer eroding into the CBD.
3.
Postoperative —e.g. hepaticojejunostomy for Whipple's procedure.

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).

Gas in the portal veins

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.

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.

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

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 rings.
2.
Simple cyst —wall calcification is uncommon but can occur following haemorrhage or infection. More common in polycystic liver disease.
3.
Chronic haematoma or abscess .
4.
Calcified (porcelain) gallbladder —possible association with GB carcinoma, especially if segmental rather than diffuse.
5.
Hepatic artery calcification —atherosclerosis or aneurysm.
6.
Portal vein calcification —chronic thrombus or portal hypertension.
7.
Schistosomiasis *—especially S. japonicum . Causes linear septal and capsular calcification creating a characteristic ‘turtleback’ appearance.

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 infiltrates.
3.
Gold therapy.
4.
Wilson's disease —though findings may be confounded by coexistent fatty infiltration.
5.
Glycogen storage diseases.
6.
Previous Thorotrast administration —old radiographic contrast agent. Deposited in liver, spleen and lymph nodes, creating marked diffuse or reticular hyperdensity (as dense as calcium). Associated with hepatic angiosarcoma and other malignancies.

Focal increased density (noncalcified)

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

Diffusely hypoechoic liver

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.

Diffusely hyperechoic liver

NB: liver echogenicity is normally similar to or slightly higher than that of a normal renal cortex.

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.
3.
Hepatitis —particularly chronic.
4.
Glycogen storage disease —associated with hepatic adenomas (often multiple).

Diffusely heterogeneous liver

This applies to US, CT and MRI.

1.
Cirrhosis —nodular liver contour ± signs of portal hypertension (splenomegaly, ascites, portosystemic shunts). The liver is often small with hypertrophy of the caudate and segments 2 and 3. It is usually difficult to ascertain the underlying cause on imaging, but some aetiologies can offer clues:
- (a)
  PSC —multifocal biliary strictures, peripheral distribution of fibrosis and volume loss, with hypertrophy of the caudate and central liver.
- (b)
  Primary biliary cirrhosis —typically in middle-aged women. Lace-like pattern of fibrosis ± characteristic periportal ‘halo’ of T2 hypointensity on MRI.
- (c)
  Haemochromatosis *—diffuse iron deposition causes T2 hypointensity and signal loss on the in-phase T1-weighted sequence.
- (d)
  Alpha-1 antitrypsin deficiency *—basal emphysema.
- (e)
  Cystic fibrosis *—bronchiectasis and fatty replacement of pancreas.
- (f)
  Cardiac cirrhosis —dilated hepatic veins and right atrium.
- (g)
  Congenital hepatic fibrosis —congenital ductal plate malformation (DPM) involving small ducts, resulting in fibrosis and cirrhosis usually by early adulthood. Associated with ARPKD and other hepatic DPMs: multiple biliary hamartomas (small ducts), polycystic liver disease (medium ducts) and Caroli disease (large ducts).
2.
Diffuse malignancy —primary (HCC, angiosarcoma) or metastatic (breast, small-cell lung cancer, lymphoma, leukaemia). The liver is typically enlarged ± a nodular contour, though breast cancer metastases can induce fibrosis and volume loss (‘pseudocirrhosis’).
3.
Fatty infiltration —can be very patchy or bizarre in distribution, mimicking metastatic disease on US/CT. Diagnosis confirmed on in-/opposed-phase MRI, with signal loss on the opposed phase.
4.
Abnormal perfusion —e.g. hepatic infarction (in severe shock, hypercoagulable states, sickle cell crisis or HELLP syndrome), hepatic artery occlusion (e.g. following TACE or liver transplant) or portal vein thrombosis. Also seen in:
- (a)
  Venous congestion —due to right heart failure, acute Budd-Chiari syndrome or venoocclusive disease; see Section 8.6 . 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.

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Hepatobiliary, pancreas and spleen

Intraluminal gallbladder lesions

Further reading

Gallbladder wall thickening

Diffuse

Focal

Further reading

Biliary dilatation

Luminal causes (and nonobstructive dilatation)

Mural causes (strictures)

Extrinsic causes (arranged from distal to proximal)

Further reading

Gas in the biliary tree

Within the bile ducts

Within the gallbladder

Gas in the portal veins

Further reading

Hepatomegaly without discrete lesions

Acute hepatitis

Cardiovascular

Neoplastic

Infiltrative/depositional

Storage disorders

Myeloproliferative disorders

Congenital

Further reading

Hepatic calcification and increased density

Small and punctate calcification

Curvilinear calcification

Calcification within a mass

Diffusely increased density

Focal increased density (noncalcified)

Further reading

Diffusely hypoechoic liver

Diffusely hyperechoic liver

Diffusely heterogeneous liver

You're Reading a Preview

Intraluminal gallbladder lesions

Further reading

Gallbladder wall thickening

Diffuse

Focal

Further reading

Biliary dilatation

Luminal causes (and nonobstructive dilatation)

Mural causes (strictures)

Extrinsic causes (arranged from distal to proximal)

Further reading

Gas in the biliary tree

Within the bile ducts

Within the gallbladder

Gas in the portal veins

Further reading

Hepatomegaly without discrete lesions

Acute hepatitis

Cardiovascular

Neoplastic

Infiltrative/depositional

Storage disorders

Myeloproliferative disorders

Congenital

Further reading

Hepatic calcification and increased density

Small and punctate calcification

Curvilinear calcification

Calcification within a mass

Diffusely increased density

Focal increased density (noncalcified)

Further reading

Diffusely hypoechoic liver

Diffusely hyperechoic liver

Diffusely heterogeneous liver

You're Reading a Preview

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