Hepatobiliary System

The hepatic lobule is 1-2mm, hexagonal with central hepatic vein and peripheral portal triads (hence hepatocytes are centrilobular or periportal). Hepatocytes are arranged in triangular acini with vascularised bases at penetrating septal venules (from portal veins), blood travels through fenestrated sinusoids to the less vascularised apices at the terminal hepatic venules. Scattered Kupffer cells (mononuclear phagocyte system) lie adjacent to the endothelial cells. The space of Disse is between endothelial cells and hepatocytes, which contains protruding microvilli of hepatocytes and fat-containing hepatic stellate cells (HSCs).

Changes in perfusion between portal veins and hepatic arteries explain enhancement abnormalities and altered patterns of diffuse liver disease. Portal venous flow is altered by obstruction (thrombus, tumour), extrinsic compression (ribs, diaphragmatic slips, tumour on liver capsule), ‘third inflow’ from systemic veins (pericholecystic, parabiliary, epigastric-paraumbilical). Hepatic artery flow is increased by focal hypervascular lesions, inflammation of adjacent organs (cholecystitis, pancreatitis), aberrant hepatic aa.

Density of liver should be >/= spleen on unenhanced, </= spleen on arterial and >/= on portal venous phases. Liver slightly > T1 and </= T2 to spleen. Echogenicity is slightly >/= kidney, < pancreas.

Bilirubin is end product of heme degradation; 85% from breakdown of senescent red cells by the mononuclear phagocytic system (spleen, liver and bone marrow), 15% from turnover of hepatic heme/hemoproteins (eg cytochrome P-450) and destruction of bone marrow precursors. This unconjugated/indirect bilirubin is tightly bound to serum albumin (insolube in water, cannot be excreted in urine, neurotoxic), taken up by the liver and conjugated into (direct) bilirubin glucuronides (soluble, nontoxic, can be excreted in urine) before excretion into bile. Gut bacteria deconjugate the bilirubin into urobilinogens of which 80% is excreted in faeces, 20% reabsorbed and re-excreted into bile, small amount excreted in urine. 2/3 of the organic materials in bile is bile salts (bile acids with taurine and gycine), which are used for detergents to solubilise water-insoluble lipids; 95% is reabsorbed from the gut lumen (enterohepatic circulation). 1L of bile is secreted by the liver per day, stored in the GB between meals where it is concentrated.

Jaudice occurs when serum bilirubin (normal 0.3-1.2mg/dL) raises above 2.0-2.5mg/dL. Unconjugated birirubinemia is from excessive extrahepatic production (haemolytic anaemia, resorption of internal haemorrhage, ineffective erythropoiesis), reduced hepatic uptake (drug interference), impaired bilirubin conjugation (physiologic jaundice of the newborn, diffuse hepatocellular disease, hereditary hyperbilirubinemia including Gilbert syndrome). Conjugated hyperbilirubinaemia is from reduced hepatocellular excretion or impaired bile flow. Cholestasis (impaired bile formation or bile flow, raised ALP, GGT, conjugated bilirubin) may be obstructive (extrahepatic or intrahepatic) or non-obstructive (defective hepatocyte secretion). There is accumulation of bile pigments within hepatocytes and Kupffer cells, distended bile ducts/ductules, portal triad oedema, apoptotic hepatocytes. Biliary obstruction may be from hepatitis (swollen hepatocytes block biliary capillaries) or surgical (extrahepatic) obstruction. Multiple branching tubular/round/oval ducts coursing to the porta, intrahepatic ducts >40% of adjacent portal vein (or >2mm centrally, >1.8mm peripherally), CBD >6-7mm (internal diameter, larger with age due to elastic tissue degeneration at 1mm/decade after 60yo, appear larger on contrast cholangiography due to distension and magnification), GB hydrops >50mm. Causes include:

  • Benign (75%)
    • Biliary stone (20%) – Crescent of bile around stone.
    • Stricture (40-45%) – Gradual tapering. From surgery/instrumentation, trauma, stone passage, pancreatitis, cholangitis, choledochal cyst, radiotherapy. Wall enhances minimally (cf hyperenhancement with malignancy).
    • Parasite.
    • Liver cyst.
  • Malignancy (25%) – Abrupt termination. Includes pancreatic, ampullary/duodenal carcinoma, cholangiocarcinoma, metastases.

Mickey Mouse configuration of the hepatic porta with head PV, R ear CBD and L ear HA.

Echogenic bile from sludge, blood, pus or parasites. Bile duct filling defects include:

  • Biliary stones
  • Air bubbles
  • Blood clot
  • Neoplasm – Cholangiocarcinoma, ampullary carcinoma, granular cell myoblastoma, mesenchymal tumour.
  • Parasites – Ascaris lumbricoides, liver fluke.

Portal venous gas is branching extending to capsule (ie peripheral), often also seen in mesenteric/portal vv. From bowel ischaemia, NEC, recent colonoscopy, enema, gastrostomy, abdominal trauma, IBD, perforated gastric ulcer, necrotising pancreatitis, diverticulitis, abdominal abscess.

Biliary tree gas is central and doesn’t extend into peripheral 20mm. Causes include:

  • Postsurgical – Sphincterotomy, choledochoduodenostomy, choledochojejunostomy.
  • Biliray-enteric fistula:
    • Cholecystoduodenal fistula – Gallstone eroding into duodenum.
    • Choledochoduodenal fistula – Penetrating peptic ulcer.
    • Surgery/trauma.
    • Tumour erosion.
  • Infection – Emphysematous cholecystitis, pyogenic cholangitis.

Gallbladder wall thickening >3mm (between lumen and liver parenchyma) from:

  • Contracted GB
  • Acute/chronic cholecystitis
  • Adenomyomatosis
  • GB carcinoma
  • AIDS cholangiopathy
  • Sclerosing cholangitis
  • Oedema – Hypoproteinemia, CHF, cirrhosis, portal hypertension, portal LN obstruction.
  • Hepatitis – Reduced bile flow and GB volume.

Gallbladder is normally well-distended after a 4hr fast. Hydropic when >50mm diameter, contracted when <20mm.

Diffuse Liver Disease

Hepatomegaly causes a rounded inferior border (should be sharp), extension of right lobe inferior to right kidney, length at midclavicular line >155mm. DDx Reidel lobe (esp women) where L lobe should be correspondingly smaller. Causes include:

  • Vascular congestion – CHF, hepatic vein thrombosis, constrictive pericarditis. Associated with distended IVC and hepatic veins, pulsatile/bidirectional portal venous flow from RA activity through congested sinusoids, ascites, pleural and pericardial effusions.
  • Fatty infiltration – Alcohol, drugs/chemotherapy, hepatic toxins, Gaucher disease, lipidoses.
  • Carbohydrate infiltration – Glycogen storage disease, diabetes.
  • Iron infiltration – Haemochromatosis.
  • Amyloid infiltration – Amyloidosis.
  • Cellular infiltration – Metastases, diffuse HCC, lymphoma, extramedullary haematopoiesis, systemic mastocytosis.
  • Cysts – Polycystic disease.
  • Inflammation/infection – Hepatitis, sarcoidosis, TB, malaria.

Hepatic failure occurs after 80-90% of functional capacity is lost. From acute massive injury (fulminant hepatic failure from drugs, toxins, hepatitis A/B), end stage progressive chronic liver damage (more common, from cirrhosis), or hepatic dysfunction without overt necrosis (eg tetracycline toxicity, acute fatty liver of pregnancy). Jaundice, hypoalbuminaemia, hyperammonemia, fetor hepaticus (musty body odor), portosystemic shunting, hyperestrogenemia (palmar erythema, spider angiomas of skin, hypogonadism, gynaecomastia), coagulopathy. Grave complications include hepatic encephalopathy (disorder of neurotransmission in CNS from elevated hyperammonemia), hepatorenal syndrome (renal failure from reduced renal perfusion and reduced GFR, prognosis 2/52-6/12), hepatopulmonary syndrome (hypoxaemia, intra-pulmonary vascular dilatations).

Fatty Infiltration

(Hepatic steatosis). Common, nonspecific hepatocyte response to injury and toxins, becoming filled with cholesterol and triglycerids within 3/52 of insult, may resolve within 6 days. From alcoholism, obesity, malnutrition, hyperalimentation, steroids, diabetes, pancreatitis, glycogen storage disease, chemotherapy, radiotherapy.

  • Diffuse fatty infiltration – Most common, might not be uniform.
  • Focal fatty infiltration – Geographic or fan-shaped, commonly adjacent to falciform ligament, GB, porta hepatis (DDx ‘third inflow’ artifact).
  • Focal sparing – Diffuse infiltration with spared areas, usually segment IV, perilesional sparing.

Hypodense (< spleen on unenhanced), echogenic (> kidneys, ‘flip-flop’ phenomenon with CT/US, difficult to distinguish portal triads), coarsened echotexture, poor US penetration (difficult to see deep portions and diaphragm). Loss of signal on out-of phase (cf in-phase, most sensitive sign) as fat signal nulls out water signal, most marked when ratio is 50:50. Lack of mass effect (lack of bulging contour and displaced intrahepatic vessels) with geometric boundaries between involved and uninvolved areas, vessels continue to traverse through the lesion. May be multifocal.

Parafalcine fat/perfusion – Hypodensity adjacent to the falciform is usually perfusional from persistent paraumbilical venous drainage (veins of Sappey), not seen on NECT or MRI. May occasionally be exacerbated by focal fatty infiltration.

Alcoholic Liver Disease

Forms of disease include:

  • Hepatic steatosis (fatty liver disease) – From shunting of catabolism to lipid biosynthesis, impaired assembly and secretion of lipoproteins and increased peripheral catabolism. Microvesicular lipid droplets then macrovesicular globules within hepatocytes displacing the nucleus peripherally. Mild reversible steatosis may occur after only several days. Liver is enlarged, soft, yellow and greasy. Fatty change is completely reversibe with alcohol abstenance. Continued abuse leads to fibrosis around hepatic veins, extending into sinusoids.
  • Alcoholic hepatitis/steatohepatitis – From acetaldehyde (intermediate alcohol metabolite), cytochrome P-450 metabolism producing ROS, impaired hepatic metabolism, malnutrition, release of bacterial endotoxin from the gut into portal circulation. Usually follows a bout of heavy drinking, causing variable hepatic failure and 10-20% mortality. Hepatocyte swelling and necrosis, cholestasis, mallory bodies (eosinophilic cytoplasmic clumps in hepatocytes), neutrophil infiltration, fibrosis (activation of stellate cells and portal tract fibroblasts with sinusoidal and perivenular fibrosis).
  • Cirrhosis – Over years liver becomes brown, shrunken, nonfatty. Develops in 10-15% of alcoholics, increased risk with females, African-Americans, FHx, iron overload, HBV/HCV. Initially uniform micronodular. Later mixed with macronodular as parenchymal islands are engulfed by wider bands of fibrosis, bile staining identical to other causes of cirrhosis.


Irreversible diffuse parenchymal destruction with bridging fibrous septa (scars linking portal tracts and hepatic veins), parenchymal nodules (hepatocytes encircled by fibrosis from cycles of regeneration and scarring), diffuse architectural disruption. There is death of hepatocytes, activation of Kupffer cells (releasing cytokines and chemokines), collagen deposition in the space of Disse (transformation of stellate cells into myofibroblasts with loss of sinusoidal fenestrations), and vascular reorganisation with new vessels bridging portal and termial hepatic veins. Surviving hepatocytes are stimulated to regenerate and proliferate into spherical nodules. Reduced delivery of blood to hepatocytes and reduced ability to secrete substances into the plasma leads to progressive liver failure, portal hypertension, increased risk of HCC (from chronic inflammation rather than cirrhosis itself). Risk of HCC and portal HTN remains, despite ‘reversal’ of cirrhosis with resorption of the fibrous tissue. Causes include toxins (alcohol, drugs), infection (esp hepatitis B/C), biliary obstruction, hereditary (Wilson disease, haemochromatosis). Western most commonly alcohol; Asia/Africa most commonly infection.

Early hepatomegaly and late hepatic atrophy, coarsened heterogeneous texture, reduced visualisation of portal triad structures, fine or coarse irregular/nodular surface (characterstic), areas of fatty infiltration, atrophy of R lobe with hypertrophy of L and caudate lobes (typical of alcoholic cirrhosis), regenerating nodules, fibrosis (high T2), heterogeneous delayed enhancement (pooling of contrast in extracellular spaces). Architectural distortion with irregular vessels. Atrophy with widening of the falciform notch, widened porta (>10mm on Ax). Portal hypertension, splenomegaly, ascities. Flattened hepatic venous Dopper (normally triphasic) from relative venous outflow obstruction (seen with fatty infiltration, cirrhosis, metastatic infiltration; DDx valsalva). Focal lesions in chirrhosis include:

  • Cirrhosis-associated nodules – histological spectrum from regenerative/cirrhotic nodules (RN/CNs), low-grade dysplastic nodules (LGDNs), high-grade dysplastic nodules (HGDNs) to HCC.
    • Regenerative/cirrhotic nodules (RN, most common) – Hepatocytes surrounded by coarse fibrous septations, <10mm, numerous small nodules cause micronodular pattern (alcoholic cirrhosis). Siderotic nodules with iron deposits have higher HU and lower MR signal. May be adenomatous hyperplastic. Usually homogeneous, uniform in size, may be variable T1, no early arterial enhancement (cf HCC), hypo-(siderotic) or iso-T2 (not hyper-T2). Enhancement same as normal liver (including hepatobiliary phase, except siderotic which may be low due to susceptibility). Macro-regenerative nodules often seen in PSC cirrhosis, usually more T1 intense, normal vessels traverse through.
    • Dysplastic nodules (DN) – Proliferative, precancerous, in 20% of cirrhotic livers. >10mm, similar characteristics to RNs. Usually high T1, iso-T2. May have microscopic fat. No washout. High T2 indicates cellular atypia or malignancy.
    • HCC – Variable signal, >10mm, characterstically hyper-T2, hypodense, diffuse homogeneous hyperenhancing with rapid washout, intralesional fat, blood products, ‘capsule’ appearance, mosaic architecture, tumour in vein. Rapid growth. Lesions >30mm usually have distinct capsule with ring enhancement. Poor US sensitivity.
  • Cholangiocarcinoma – 2nd most common hepatic malignancy in cirrhosis. Features that favour CCA over HCC include peripheral hyper-enhancement, peripheral washout, progressive central enhancement, target appearance on hepatobiliary phase or DWI, lobulated shape, disproportionate biliary dilatation, capsular retraction, elevated CA19-9/CEA. CCA never has intralesional fat/T1 hyperintensity. Ratio of HCC to CCA is 50:1, so appearances suggesting CCA still more likely an atypical HCC than CCA. However, due to very different treatment of these lesions biopsy should be performed.
  • Confluent fibrosis – Advanced cirrhosis, wedge-shaped/triangular/geographical change extending to hilum or radiating hypodense on NECT, enhances, volume loss of affected portion, hypo-T1, hyper-T2 scar.
  • Sclerosing haemangioma – less T2 hyperintensity than a typical haemangioma, mimicking HCC, however there is associate capsular retraction. Eventually completely scleroses and involutes.
  • Haemangioma, cyst, focal fatty infiltration/sparing, vascular anomoly.
  • Metastases – Extremely rare, may occur with breast cancer. Pseudocirrhosis – necrosis of metastases with scarring after chemotherapy.
  • No FNH or adenomas – These do not exist in cirrhosis.

LI-RADs can be used to categorize observations (lesions) in the setting of a liver at high risk of HCC (eg cirrhosis, chronic hepatitis). Maximal diameter should be performed from outer edge to outer edge in the sequence and plane than shows the observation with the most circumscribed margin (avoiding arterial phase if possible, due to corona/AP shunting). Assign LI-RADS as per flowchart then if required use ancillary features to upgrade (max to LR-4) or downgrade, then if required tie-breaking rules (category of lower degree of certainty, ie closer to LR-3). Ancillary features include mild/mod high T2, DWI, corona, mosaic architecture, nodule-in-nodule, fat, iron/fat sparing, blood, increase in size, distinct rim, low hepatobiliary phase (of lesion or rim). Negative ancillary features include undistorted vessels, parallels blood pool, reduction in size or stability >/=2yr, hepatobiliary phase iso-intense.

  • LR-1 – Definitely benign
  • LR-2 – Probably benign. An LR-2 cirrhosis-associated nodule is <20mm, homogeneous, iso-enhancing to background cirrhotic nodules on all phases, and differs from background nodules in at least one of: larger, mild/mod hyperdense, mild/mod high T1, mild-marked low T2/T2*.
  • LR-3 – Indetemediate probability for HCC. Moderate probability of both HCC and benign entitiy
  • LR-4 – Probably HCC
  • LR-5 – Definitely HCC
  • LR-5V – Definitely HCC with tumour in vein
  • LR-M – Probably malignant, but features not specific for HCC, eg features suggestive of cholangiocarcinoma. Needs biopsy.
  • LR-Treated – Locoregionally treated observation. Currently there are no criteria for assessing response.


Tx transjugular intrahepatic portosystemic shunt (TIPS) for portal hypertension and oesophageal variceal bleeding, liver transplant.

Metabolic Liver Disease

Acquired or inherited.

  • Nonalcoholic steatohepatitis (NASH, nonalcoholic fatty liver disease NAFLD) – Inflammatory response associated with obesity, type 2 DM, hyperlipidemia, anorexia nervosa. Steatosis with parenchymal inflammation and fibrosis. Two-hit model of hepatocyte damage induced by fat accumulation and oxidative stress causing release of ROS. Elevated AST and ALT (AST:ALT <1 cf alcoholic >2). May progress to cirrhosis. Rarely causes acute fulminant hepatic failure.
  • Wilson disease – AR mutation of ATP7B gene on chromosome 13, failure to incorporate copper into ceruloplasmin (low serum levels) leading to accumulation of copper in the liver, brain, eyes (almost all have green-brown Kayser-Fleischer rings in the cornea). Hepatic steatosis, acute hepatitis, chronic hepatitis, cirrhosis. Atrophy and cavitation of the basal ganglia esp putamen, Parkinson disease-like syndrome.
  • Haemochromatosis:
    • Hereditary/primary haemochromatosis (HH) – AR, most mutation of HFE gene on chromosome 6 (others transferrin receptor). M>F (physiologic iron loss in females). Deposition of haemosiderin in liver (chocolate brown, periportal then rest of lobule), pancreas, myocardium, pituitary, adrenals, thyroid, parathyroids, synovial lining of joints (leads to CPPD), skin. Stains blue with Prussion blue stain. Causes micronodular cirrhosis, pancreatic fibrosis with diabetes mellitis (in 75-80%), skin pigmentation (75-80%), atrophic testes (from derranged hypothalamic-pituitary axis). Iron accumulation is lifelong, injury is slow and progressive with Sx starting 40s-50s. Superparamagnetic with diffuse marked low T2, moderately low T1 in liver and spleen. If severe liver is hyperdense at 75-130HU. Increased risk of HCC.
    • Haemosiderosis (secondary/aquired haemochromatosis) – Tissue iron deposition from repetitive transfusions for treatment of ineffective erythropoiesis (thalassemia and myelodysplastic syndromes).
  • Alpha-1-antitrypsin deficiency – AR on chromosome 14. α1-antitrypsin is syntehsized in the liver, inhibits proteases (esp neutrophil elastase, proteinase) normally released from neutrophils at sites of inflammation. Deficiency leads to emphysema, liver disease, cutaneous panniculitis, aneurysms, bronchiectasis, Wegener’s granulomatosis. The abnormal malformed polypeptide causes hepatocyte damage and apoptosis. Cytoplasmic globular inclusions, periodic acid-Schiff (PAS) positive. Hepatitis, cirrhosis. Increased risk of HCC.
  • Neonatal cholestasis – Prolonged conjugated hyperbilirubinaemia. From primary biliary atresia (20%), neonatal hepatitis (multiple causes including idiopathic neonatal hepatitis in 50%, α1-antitrypsin in 15%).

Liver Disease in Pregnancy

In pregnant women with or without pre-existing chronic liver disease. Viral hepatitis is the most common cause of jaundice in pregnancy.

  • HELLP syndrome (haemolysis, elevated liver enzymes and low platelets) – In setting of preeclampsia. Periportal coagulative necrosis with haemorrhage into the space of Disse (may dissect under capsule and rupture into abdomen).
  • Acute fatty liver of pregnancy (AFLP) – Usually 3rd trimester with variable hepatic failure. Unkonwn aetiology ?mitochondrial dysfunction.
  • Intrahepatic cholestasis of pregnancy – Usually 3rd trimester with elevated conjugated bilirubin. Altered hormonal state causes defect in secretion of bile salts. Usually benign, but increased risk of gallstones and malabsorption.

Post Transplant Appearances

Peritransplant fluid is common, if simple anechoic may represent ascites, bile or lymph; echogenic debris may be pus or blood. Complications include hepatic aa thrombosis, stenosis, pseudoaneurysms (uncommon in portal vein or IVC); bile leaks, bile duct anastomotic strictures, necrosis of bile ducts, stones. Posttransplant lymphoproliferative disorder at 4-12/12 – focal solid hypoechoic masses in or adjacent to liver. Increased risk of HCC.

Infection and Inflammation


Sytemic viruses that cause hepatitis include infectious mononucleaosis (EBV, mild), CMV (esp newborn, immunosuppressed), yellow fever virus (severe, tropical countries). Extrahepatic infections/sepsis can induce mild hepatic inflammation and cholestasis due to cytokines released by Kupffer cells. Viral hepatitis usually refers to hepatotropic viruses. All are RNA viruses except hepatitis B (DNA virus).

  • Hepatitis A virus (HAV) – Usually mild, self-limited, doesn’t cause chronic hepatitis, rarely fulminant hepatitis. Faecal-oral transmission.
  • Hepatitis B virus (HBV) – May cause acute hepatitis with clearance, nonprogressive chronic hepatitis (uncommon), progressive leading to cirrhosis, fulminant hepatitis (rare) with massive necrosis, or asymptomatic carrier state. 70% have mild or no symptoms, 30% nonspecific constitutional symptoms; rarely does chronic disease occur in non-endemic areas. 1/3 of world population has been infected, most are carriers in Asia (esp perinatal infection). In high prevalence regions perinatal transmission predominates; intermediate prevalence via haematogenous or mucous membrane contact with horizontal spread; in low prevalence areas most transmission is via sexual contact and IVDU. HBsAg (surface antigen), HbeAg (precore antigen), HBV-DNA and DNA polymerase appear before onset of symptoms, peaks during disease and disappears by 3-6/12; persistence indicants persisting active viral replication (probable progression to chronic hepatitis). Anti-HBs (surface antibody) rises weeks-months after dissapearance of HBsAg, may persist for life (indicating immunity). Anti-HBe implies acute infection has peaked and the disease is on the wane; persistence indicates carrier state. IgM anti-HBc (core antibody) is detected shortly before symptoms; IgM declines with persisting total anti-HBc (indicationg replacement with IgG anti-HBc) after the acute illness. Raised anti-HBs (>/=10mIU/mL) with negative anti-HBc indicates immunity due to vaccination; both are raised (with negative HBsAg) in natural immunity.
  • Hepatitis C virus (HCV) – Most common cause of chronic liver disease. 80-85% of have persistent infection and chronic hepatitis (despite being asymptomatic), with cirrhosis in 20-30%. Risk factors include IVDU, mutiple sexual partners, recent surgery, needlestick injury (risk 6x higher than HIV), multiple HCV contacts. Infection persists despite presence of antibodies. HCV RNA testing is used to assess viral replication and infection. Episodic elevation in aminotransferases with intervening normal/near-normal periods. Fulminant hepatic failure is rare.
  • Hepatitis D virus (HDV) – Dependent on HBV infection (HbsAg). Common in Africa (uncomon in Asia).
  • Hepatitis E (HEV) – Endemic in Asia and India. High mortality in pregnancy. Most self-limited, doesn’t cause chronic hepatitis.

Clinicopathologic syndromes:

  • Acute hepatitis – Symptomatic or asymptomatic, not usually detected with imaging. Heterogeneous enhancement, diffuse oedema reducing echogenicity and causing bright portal venules (‘starry sky’, DDx leukaemic or lymphoma infiltrates, toxic shock syndrome, diffusely reduced liver glycogen stores). There is diffuse hepatocyte swelling, inconstant cholestasis, hypertrophy and hyperplasia or Kupfer cells. Portal tracts are infiltrated with inflammatory cells and oedema. Free fluid, gallbladder thickening. Periportal lymph nodes.
  • Acute fulminant hepatitis – Hepatic encephalopathy within 2-3/52 without chronic liver disease. From drug induced injury (most common, esp paracetamol), viral hepatitis (HBV or HAV), or unknown cause. There is massive diffuse or random areas of necrosis with muddy red/mushy areas with haemorrhage (hypodense) leaving a collapsed framework and preserved portal tracts. Very high mortality, Tx transplantation.
  • Carrier state – Individual who carries the virus, but has no liver disease or assymptomatic non-progressive liver damage. Typically positive anti-HBe but no HBeAg, normal aminotransferases, low or undetectable serum HBV DNA.
  • Chronic hepatitis – Persisting/relapsing disease for >6/12. Common in HCV, uncommon HBV. Higher risk with younger age at infection. High risk of permanent liver damage, even with normal transaminases. In milder forms inflammation is limited to portal tracts, bridging necrosis between portal tracts and hepatic veins, fibrosis (initially portal tracts then periportal septal then bridging firbosis). Persisting loss of hepatocytes and fibrosis leads to cirrhosis (typically large irregular nodules = post-necrotic cirrhosis). Subtle coarsened echogenicity, minimal fatty infiltration. Liver usually not enlarged.

Autoimmune hepatitis is chronic and progressive of unknown aetiology. Commonly associated with coelic diseae, SLE, RA, thyroiditis, Sjogren sydnrome, UC. F>M. Untreated mortality up to 40%, cirrhosis in 40%.

Liver Abscess

Bacterial infections include S.aureus (toxic shock syndrome), Salmonella typhi (typhoid fever), T.pallidum (tertiary syphilis) or enteric bacteria (portal venous spread, ascending cholangitis). Parasitic infections are common worldwide, including malaria, schistosomiasis, strongyloidiasis, cryptosporidiosis, leishmaniasis, echinococcosis, liver flukes. Liver abscess in developed contries are uncommon, most commonly bacterial infection from portal venous spread (appendicitis/diverticulitis/colitis), haematogenous spread (lines, SBE), ascending cholangitis, direct/contiguous invasion or penetrating injury. In developing countries infection is usually echinococcal or amoebic. Haematogenous spread tends to cause multiple small abscesses (microabscesses in immunocompromised from fungal or parasitic septicaemia); direct extension solitary large abscess. Rupture of subcapsular abscesses may cause peritonitis. Fever and pain. Destruction of liver with solitary cavity or group of loculated abscesses. Peripheral rim enhancement. Surrounding hypodense oedema. Gas in 20%. Commonly calcifies when healed.

  • Amoebic abscess – Usually more acutely ill with travel to endemic areas (India, Africa, East Asia, Central/South America). Usually solitary, thick nodular walls, R lobe. May elevate R hemidiaphragm, rupture into pleural space. Fluid is often proteinaceaous. The more calcium, the more likely the organism is dead.


Cholelithiasis in 15% of 40-60yo, F:M 4:1. Increased risk with haemolytic anaemia, ileal disease, cirrhosis, DM. >80% remain silent and asymptomatic, become symptomatic at 1-4% per year. Increased risk of gallbladder carcinoma (0.5% after >20yrs). 15% of cholesterol stones and 50-75% of pigment stones contain enough calcium carbonate/bilirubinate to be radiopaque on XR, usually laminated with lucent centre. May contain nitrogen gas with branching linar ‘crow’s-feet’ lucency. Facets from multiple stones. 95% seen on US, 80% on CT. If they are echogenic, shadowing and mobile then 100% specific. If not shadowing, then use high-frequency probe with focal point at stone to demostrate shadow. Usually low T1/T2/FIESTA, occasionally high T1 from cholesterol/protein/calcium. Wall-echo-shadow (WES) sign – GB completely filled with stones, clear dark shadow cf dirty brighter shadow with air-filled loop of bowel. Double arc shadow sign – thin layer of bile separating wall from stones.

  • Cholesterol stones (85%, yellow) – Form when concentration exceeds solubilising capacity of bile (supersaturation). Increased risk with age, F:M 2:1, oestrogen (OCP, pregnancy), obesity and rapid weight loss, gallbladder stasis, hyperlipidemia.
  • Pigment stones (15%, black/brown) – Form from elevated unconjugated bilirubin in bile due to haemolytic syndromes, severe ileal dysfunction, biliary tree infection (E.coli, Ascaris lumbricoides, fiver fluke O.sinesis), any form of cirrhosis.

Choledocholithiasis – Stones in the biliary tree. Occasional stones are formed primarily in the biliary tree (usually pigmented, esp Asia). US sensitivity 75%, CT 70% with target/cresent sign (stone partially surrounded by hypodense bile), MRCP 95-99% (more sensitive than ERCP). May cause obstruction, pancreatitis, cholangitis, hepatic abscess, secondary biliary cirrhosis or acute calculous cholecystitis.

GB sludge is thick particular matter (precipitated calcium bilirubinate, cholesterol crystals) in concentrated bile from prolonged biliary stasis (lack of oral intake, hyperalimentation, biliary obstruction). Hyerechoic, hyperdense, high T1 bile. May be seen in a fasting but otherwise normal patient. DDx pus, blood, milk of calcium.

DDx and MRCP pitfalls:

  • Sludge balls – From biliary stasis, thickening forming mobile masses. No shadowing.
  • Floating cholesterol crystals or gas – Short comet-tail artifacts.
  • Pneumobilia – Non-dependent, fluid-air levels, meniscus.
  • Arterial pulsation artefact – Signal void with straight edges immediately adjacent to right hepatic artery.
  • Cholesterol polyp – Benign triglycerides and cholesterol in macrophages of wall of no clinical significance.
  • Adenomyomatosis
  • Adenomatous polyp (small, usually flat), carcinoma (most >10mm).

Acute Cholecystitis

95% from gallstones obstructing the GB neck or cystic duct. Cholelithiasis, oedematous GB wall thickening (>3mm), sonographic Murphy’s positive (90% predictive), GB distension (>50mm), pericholecystic fluid with C sign (fluid between liver and diaphragm/abdominal wall), wall hyperaemia on power Doppler, high density bile, intraluminal sloughed membranes, blurring of GB/liver interface, prominent hyperenhancement of liver adjacent to GB.

Acalculous cholecystitis (10%) – Inflammation from ischaemia (most, cystic artery is an end artery), infection, or less commonly obstruction (adenomyomatosis, polyps, neoplasm). Increased risk in sepsis with hypotension and multisystem failure, immunosuppression, major trauma/burns, diabetes, infections. Distended GB, thickened wall without stones, most too ill to reliable elicit sonographic Murphy sign.

Complications in 40% include:

  • Gangrenous cholecystitis – Older men, cardiovascular disease. Obstruction -> high pressure -> GB distension -> ischaemic necrosis of wall with intramural haemorrhage or abscess. GB wall shows striated assymetric thickening, irregular/disrupted enhancement of wall, ulceration (concave high T2), heterogeneous high T2/T1 (haemorrhage/necrosis/microabscess), multiple lucent layers. Risk of perforation.
  • Perforation – Mortality 25%. Free into peritoneal cavity, adjacent to liver forming pericholecystic fluid collection/abscess, or cholecystoenteric fistula. Usually fundus (reduced perfusion). Pericholecystic fluid >10mm is suggestive. GB wall is irregularly thickened, heterogeneous high T2/T1, disruption (better seen on enhanced MR), GB gas (fistula, signal void), loculated ascites. Gallstone ileus – stone obstructs distal ileum: Tx enterolithotomy, GB usually left alone (tissue very friable). Bouveret’s syndrome – GB stuck to stomach with stone eroding into stomach and impacting in pylorus or D1 causing gastric outlet osbtruction.
  • Emphysematous cholecystitis – Usually from ischaemia associated with gas-forming clostridium perfinges, E.Coli or Klebsiella. 50-70yo, diabetic, peripheral vascular disease. Intraluminal or intramural gas, other findings as per gangrenous cholecystitis. High mortality.
  • Mirizzi syndrome – Stone in cystic duct obstructing common hepatic duct.
  • Empyema/suppurative cholecystitis – Diabetics. Gallbladder filled with virtually pure pus, appears like sludge but lower T2 signal.
  • Haemorrhagic cholecystitis (rare) – From atherosclerotic GB wall, neoplasm, vascular abnormality (eg aneurysm), trauma, anticoagulation, ectopic pancreatic or gastric mucosa. High T1/low T2 in wall or lumen from metHb, dependent layer under bile.

Chronic Cholecystitis

From repeated bouts of acute cholecystitis or apparent absence of attacks. Gallstones in 90%, thickened GB wall, contracted GB lumen, poor GB contractility. Supersaturation of bile predisposes to chronic inflammation and stone formation. E.coli and enterococci cultured in 1/3. Prominent Rokitansky-Aschoff sinuses (mucosal outpouchings).

  • Milk of calcium bile (limy bile) – Presipitated calcium, dense on XR/CT, dependent layering, extremely echogenic.
  • Hydrops of the gallbladder – Atrophic, chronically obstructed gallbladder containing only clear secretions.
  • Porcelain gallbladder (rare) – Dystrophic calcification in wall. 10-20% risk of GB carcinoma.
  • Xanthogranulomatous cholecystitis (rare) – Nodular lipid-laden macrophage deposits in GB wall, proliferative fibrosis. Marked GB wall thickening >20mm, fat density nodules, narrowing of lumen. DDx GB carcinoma.


Infected bile in 10% of those with complete obstruction, 60% of partial/intermittent obstruction. From choledocholithiasis, biliary strictures, indwelling stents/catheters, tumours, acute pancreatitis. Bacteria enter through the sphincter of Oddi, usually enteric G-neg aerobes (E.coli, Klebsiella, Enterococcus, Enterobacter), Clostridium, Bacteroides. Ascending cholangitis is infection spreading into intrahepatic ducts. High pressure may cause hepatico-venous reflux -> sepsis. Suppurative cholangitis (empyema) – purulent bile distends bile ducts. Intraductal low T2, intermediate T1. Periportal inflammation (high T2 along portal vein and ducts).

AIDS-associated cholangitis – Opportunistic infections (CMV, cryptosporidium, HIV) causing inflammation and oedema with thickening of walls of ducts and GB, stenosis (esp ampulla), proximal dilatation, ulcers in CBD, inflammation in duodenum. Sludge is common, stones uncommon. Echogenic nodule at papilla from oedema.

Recurrent pyogenic cholangitis (oriental cholangiohepatitis) – Opisthorchis sinensis infection endemic in Southeast Asia. Recurrent jaundice, pain, fever, chills. Associated with parasitic infestation (clonarchiasis, ascariasis) and nutritional deficiency. Severe IHBD and EHBD dilatation with soft pigmented stones and pus (‘biliary mud’), focal strictures, straightening and rigidity of intrahepatic ducts. Cx liver abscess, bilioma, pancreatitis, cholangiocarcinoma.

Biliary Ascariasis

Worms are moving tubular echogenic structures with lucent core in biliary tree and GB. May cause cholangitis, cholecystitis or pancreatitis. High mortality.

Other Biliary Tract Diseases

  • Secondary biliary cirrhosis – Prolonged extrahepatic biliary obstruction causing cholestasis (reversible) and secondary inflammation with periportal fibrosis, cirrhosis. Subtotal obstruction may lead to bacterial infection with ascending cholangitis with enteric organisms (coliforms, enterococci). Distended small and large bile ducts with inspissated pigmented material, bile lakes.
  • Primary biliary cirrhosis (PBC) – Autoimmune disease affecting medium-sized intrahepatic ducts with portal inflammation, scarring -> uniform micronodular cirrhosis (after many years) and liver failure. F:M 6:1, peak 40-50yo. Increased risk with FHx, associated with other autoimmune diseases. Hepatomegaly, eyelid xanthelasmas (cholesterol-rich macrophages), skin hyperpigmentation (melanin), inflammatory arthropathy. Elevated ALP and cholesterol, late hyperbilirubinaemia. Antimitochondrial antibodies (AMA) in 90-95%. Upstream biliary duct proliferation, parenchymal cholestasis, bile staining of the liver. Increased risk of HCC.
  • Primary sclerosing cholangitis (PSC) – Unknown aetiology. Inflammation and obliterative fibrosis of intrahepatic and extrahepatic ducts with dilatation of preserved segments. 60% associated with IBD esp UC (PSC in 5% of patients with UC). M>F, 20s-40s. Concentric periductal fibrosis (onion-skin fibrosis). Beaded pattern of ducts, small saccular outpouchings (duct diverticula, pathognomonic). Biliary cirrhosis develops in 50%, cholangiocarcinoma in 7%, increased risk of chronic pancreatitis and HCC.
  • IgG4 disease – Identical to PSC. May be associated with autoimmune pancreatitis, pseudotumours in other organs (esp kidneys). Very responsive to steroids.

Liver Tumours

Most hepatic tumours derive blood from hepatic arteries. Most lesions are low T1, high T2. Lesions with high T1 from fat (focal fat, HCC, lipoma, AML, adenoma), blood (haematoma, haemorrahge into tumour), protein (in cysts, necrosis in tumour, abscess), copper (HCC), melanin (melanoma metastases), contrast (Gad, lipiodol), ghosting artifact (flow in adjacent vessels), or relatively high due to surrounding liver low-T1 (oedema, iron). Low T2 from fibrosis in capsule (HCC, adenoma, rarely FNH) or central scar (fibrolamellar HCC, FNH). Wash-in/hypervascular lesions are relatively hyperdense on arterial phase. Wash-out lesions are relatively hypodense on PV phase (after being hyper/iso-dense on the arterial phase).

Hepatocyte specifc contrast agents (HSCA) include gadoxetate disodium (Gd-EOB-DTPA eg Eovist, Primovist) and gadobenate dimeglumine (Gd-BOPTA including MultiHance); are actively transported into hepatocytes and excreted into bile canaliculi. Hepatocellular/hepatobiliary phase peaks at 10-20min for EOB-DTPA, at 2 hours for BOPTA, with enhancement in normal liver parenchyma and bile ducts. Transition phase occurs after the PV phase, when contrast is seen within the extracellar compartments and starting to accumulate intracellularly.

Liver and splenic granulomas are calcified healed foci (TB, histoplasmosis), multiple, small and dense.

Tiny hypodense lesions too small to characterise <10mm, usually only sen on PV phase (hence not seen on NECT or US to biopsy) – Cyst, haemangioma or metastases. Most are benign even with a history of malignancy. Multiple small <10mm lesions include:

  • Metastases (breast, lung, ovarian, gastric, melanoma, prostate)
  • Regenerative nodules (cirrhosis)
  • Multinodular HCC
  • Lymphoma
  • Histoplasmosis
  • Abscesses in immunocompromised, bacterial
  • Sarcoid
  • Kaposi sarcoma in AIDS
  • Gamma-Gandy bodies in portal HTN

Fat-cointaining lesions include HCC, adenoma, dysplastic cirrhotic nodule and angiomyolipoma. Central scars (not very useful) seen in FNH, fibrolamellar HCC, haemangioma, metastases. Capsular retration seen in treated metastases/lesions, CCA, confluent hepatic fibrosis, sclerosed haemangioma, epithelioid haemangioendothelioma.

Cavernous Haemangioma

Misnomer, not a true haemangioma (neoplasm), but rather a vascular malformation. 5% of population, F>M, multiple in 10%. Congenital benign large thin-walled vascular spaces separated by fibrous septa with slow-flow, forming red-blue nodules. Thrombosis may cause central fibrosis, calcification. Sclerosing haemangioma can occur in the setting of cirrhosis.

Most <50mm, generally directly underneath the capsule. Large >60mm lesions may cause mass effect, haemorrhage, AV shunting. Most stable in size over time (2% enlarge, in which case reassess). Well-defined, homogeneously hyperechoic (in 80%), acoustic enhancement; may be relatively hypoechoic in setting of a hyperechoic steatotic liver; most show no colour Doppler flow. Lobulated, hypodense similar to other vessels, nodular peripheral enhancement (may be flame-shaped) -> progressive in-filling with persistance at 20-30min due to slow-flow, large lesions may never fill in completely. Tc99-labelled RBC shows prolonged intense activity on delayed. MR hypo/iso-T1, very high-T2 (light-bulb) apart from ares of fibrosis (DDx cyst, abscess, hypervascular metastasis), enhancement pattern as per CT. Calcium and fat are very rare. Biopsy can be done if </=20G.

High-flow haemangiomas are an uncommon subgroup, usually small (<20mm), fill rapidly (often completely in arterial phase). May have adhacent wedge-shaped transient hepatic intensity/attenuation difference (THID/THAD) due to perfusion changes.

Focal Nodular Hyperplasia (FNH)

Benign, abnormally arranged hepatocytes, bile ducts and Kupffer cells. More common with anabolic hormones or contraceptives. F>M. Most <50mm, solitary, isodense NECT, isoechoic (may have hypoechoic halo), slight hypo/iso-T1 and slight hyper/iso-T2 (normal parenchymal components), lobulated, well-circumscribed but lacks capsule. Hypervascular with intense brief (~1min) uniform arterial enhancement, iso- in PV phase (follows arteries). Central vascular scar with radiating septa in 60% characteristic (low-T1/high-T2), containnig thick-walled vessels (usually arteries) that enhance on delayed. Haemorrhage, necrosis and infarction are extremely rare. Most show normal/increased Tc sulfur colloid liver-spleen activity due to Kupffer cells (specific, but DDx occasionally adenoma). Hyperintense or isointense on hepatocellular phase (HSCA) due to functioning hepatocytes (very specific, DDx CCA from extracellular pooling).

Hepatic Adenoma

(Hepatocellular adenoma). Rare, more common in women on long-term COCP (usually regress with termination), androgen steroids, glycogen storage disease. Benign pale yellow-tan neoplasm of hepatocytes. May cause catastrophic haemorrhage (poor connective tissue support), especially if subcapsular (particularly under oestrogen stimulation with pregnancy); rarely malignant degeneration (esp in glycogen storage diseases). Sheets and cords of hepatocytes without acinar architexture, occasionally abundant fat, some have nonfunctional Kupffer cells. Most solitary, smooth, encapsulated, up to 300mm. Commonly areas of necrosis, haemorrhage, fibrosis -> hyperechoic, hypodense. Calcification in 15%. Intense homogeneous hypervascularity, isodense with liver on PV and delayed. High heterogeneous T1 (steatosis/haemorrhage), most high T2 (more than FNH). Usually cold on Tc sulfur colloid scan. Hypointense on hepatocellular phase (HSCA) due to lack of functioning hepatocytes (cf FNH, which can otherwise be indistinguishable). When small, are indistinguishable from HCC.

Hepatic adenomatosis – Multiple adenomas in otherwise normal liver.

Nodular Regenerative Hyperplasia

Liver entirely transformed into spherical nodules in absence of fibrosis. Associated with altered intrahepatic flow including solid organ transplant (esp renal), bone marrow transplant, vasculitis, HIV. May lead to portal hypertension.


See Paediatric Abdomen section.

Hepatocellular Carcinoma (HCC)

(Hepatoma, hepatocarcinoma). Most common primary malignancy, increased risk with cirrhosis (esp Western), chronic hepatitis (esp Asia), chronic alcoholism, NASH, carcinogens (sex hormones, aflatoxin from Aspergillus flavus in contaminated peanuts/grains, Thorotrast), glycogen storage disease, haemochromatosis, alpha-1-antitrypsin, tyrosinaemia (40% have HCC), M>F. Elevated serum alpha-fetoprotein in 50%.

Patterns include diffuse infiltrative (difficult to detect), unifocal/solitary massive or multinodular/multifocal. Tumour usually paler than normal liver, bile-stained with composed of hepatocytes capable of secreting bile. Encapsulated HCC in 25% (variant of solitary form), more common in Asia, better prognosis.

Common intratumour haemorrhage and necrosis (lack of stroma). Calcification in 10% (punctate, stippled or rimlike). May be hyperechoic with fat, to hypoechoic with necrosis. Low on hepatocellular phase due to imapired HSCA transporter expression. Metastases to LN (perihilar, peripancreatic, para-aortic), lungs, adrenals, bone. Poor prognosis for large tumours, most die within 2yrs. Tx liver transplant (curative), surgical resection (<30mm, may not be curative once progressed with arterial enhancement due to tendency for early hepatic metastases), radiofrequency ablation (local control), chemoembolisation. Incurable lesions (and hence not surgical candidates) have extrahepatic disease or invasion of the portal veins, hepatic veins or bile ducts. Characteristic features include:

  • Arterial hyper-enhancement – increased arterial supply resulting in increased density/signal than normal liver. Best seen in late arterial phase (PV slightly enhanced).
  • Washout – hypodense/hypointense cf liver parenchyma. With HSCA can only use PV phase to determine washout, as on later transitional phase surrounding normal hepatocellular uptake can create relative hypodensity.
  • Vascular invasion – Tumour thrombus into portal > hepatic veins in 50%, very specific. Low density in expanded vein, enhancing, may have arterial Doppler trace.
  • Capsule appearance – refers to smooth marginated enhancement better seen on portal venous or delayed phases, thicker or more conspicuous than background cirrhotic nodules, may be low T1/T2, hypoechoic. Do not use the term capsule for early peripheral enhancement. This may represent a pseudocapsule, and does not always represent a true tumour capsule.
  • Corona enhancement – marginal rim enhancement in late arterial phase ~10 sec after enhancement of the primary lesion, which later reduces. This represents early drainage of contrast into sinusoids, with the region prone to metastases (hence should be resected with the primary).
  • Arterioportal shunting – Early/prolonged enhancement of portal vein or wedge of parenchymal enhancement adjacent to the tumour (THID/THAD). Enhancement occurs at the same time as the tumour. May represent a micrometastasis to an adjacent PV venule.
  • Hypointense on hepatobiliary phase – However, 5% of HCC can have OATB transporter, but should still have peripheral hypointensity (cf FNH).
  • Satellite nodules (metastases) common
  • Fatty metamorphosis – Areas of fat density or chemical shift artifact.
  • Mosaic architecture
  • Nodule-in-nodule appearance
  • Excessive copper accumulation – From abundant copper-binding protein in cancer cells making it hyperdense NECT and high-T1.
  • Other features include restricted diffusion, mild-moderate T2 (rather than very high), hyperintensity (but not marked), lesional fat/iron sparing, blood products, increase in size.

Fibrolamellar carcinoma – Variant of HCC in 5%, in young adults with no risk factors for HCC, no elevation of AFP. Unknown aetiology. Cords of tumour with surrounding fibrous bands emanating from central scar. Large, lobulated, echogenic central scar with calcification. Heterogeneous arterial and PV enhancement with delayed in scar. Hypo/iso-T1, hyper-T2. Satellite nodules in 10-15%, haemorrhage/necrosis in 10% (may be massive -> multicystic). Tends to be advanced at presentation, but better prognosis than HCC due to no underlying chronic disease.

Cholangiocarcinoma (CCA)

Second most common primary hepatic tumour, from epithelium of ducts. 90% adenocarcinomas. Patterns include mass forming, periductal infiltrating or intraductal polypoid. Increased risk with choledochal cyst, UC, PSC, Caroli disease, oriental cholangitis, cirrhosis, HCV infection, Hispanics, exposure to Thorotrast; but most have none of these. Might only see abrupt stricture and thickening of duct. Presents late, poor prognosis with only ~20% resectable. Mixed variants have elements of HCC and CCA. Metastases to LN, lungs, bones (esp vertebrae), adrenals, brain.

  • Intrahepatic/peripheral CCA (10%) – Intrahepatic hypodense mass, adjacent biliary dilatation in 25%, capsular retraction. Central fibrosis with central T2 hyperintensity and outer T2 hypointensity. Irregular/lobulated border due to early adjacent metastases that coalesce with the tumour. Target appearance with peripheral low hepatobiliary uptake and DWI. Early thin rim enhancement with delayed and gradual central enhancement from fibrosis. May have central hepatobiliary phase hyperintensity due to very slow transit and pooling of contrast in the extracellular space (rather than intracellular uptake).
  • Hilar CCA (Klatskin tumour, 80%) – Near junction of RHD and LHD. Usually poorly differentiated, aggressive. Usually small, obstructing both RHD and LHD. May obstruct PV causing liver atrophy on one side. Delayed enhancement, diffusion restriction. Bismuth-Corlette classification of CCA and biliary strictures:
    • Type I – CHD/CBD >20mm from RHD/LHD confluence.
    • Type II – CHD involving the confluence.
    • Type IIIa – II and RHD (right secondary intrahepatic duct).
    • Type IIIb – II and LHD.
    • Type IV – RHD and LHD (ie both secondary intrahepatic ducts) or multifocal. Unresectable.
  • Extrahepatic CCA (5%) – Distal bile duct between upper border pancreas and ampulla, may be periampullary. Tend to be small <30mm at presentation causing obstruction. Stenosis/obstruction of CBD in 95%, intraductal polyp in 5%.

Epithelioid Haemangioendothelioma

Rare, low grade malignancy intermediate between an angiosarcoma and haemangioma. Geographic, multiple, capsular retraction.


Usually diffusely infiltrative and undetectable, multiple-nodular in 10%, occasionally large poorly defined masses. Low T1, high T2.


20x more common than primary tumours, most commonly GIT, breast, lung, pancreas. Widely variable appearances. Most have band of peripheral enhancement on arterial phase with rapid washout. Degree of vascular staining is unrelated to tumour blood flow. Displaced/compressed/occluded adjacent vessels. Arterial encasement or shunting is rare. Tendency to outgrow blood supply with central necrosis. Hypervascular metastases include neuroendocrine tumours, carcinoid, RCC, melanoma, thyroid, choriocarcinoma. Hypovascular metastases include lung, oesophagus, pancreas. Mixed vascularity in breast, eye, cholangiocarcinoma, sarcoma. Variable hypo/hyper-echoic, homo/heter-geneous. 90% multiple.

Hepatic Cystsic Lesions

  • Benign cysts – 5% of population. Most solitary, occasionally multiple (esp ADPKD even in absence of renal cysts, other polycystic disease, tuberous sclerosis) where tend to cluster (bunch of grapes) with varing size. Most septated with lobular rather than spherical contour. Anechoic with thin walls/septa, acoustic enhancement, occasionally internal debris (esp current/previous infection), near water HU, nonenhancing. DDx hydatid, abscess, biliary cystadenoma.
  • Echinococcal/hydatid cyst – From E.granulosus or E.multilocularis tapeworm (endemic to central/northen Europe, Mediterranean, north Asia, China, Japan, Turkey, parts of North America). Affects liver in 95% with single/multiple cysts with well-defined walls that usually enhance, 50% calcify, 75% have daughter cysts. Water-lily sign – rupture of daughter cysts, with collapsed cysts floating within the larger cyst. Aspiration -> risk of anaphylactic reaction. Tx mebadazole or excision.
  • Biliary cystadenoma – Benign cystic tumour lined by cuboidal/columnar epithelium resembling normal biliary epithelium. F>M middle aged. Cystic, unilocular or multilocular. Almost always intrahepatic (rarely extrahepatic biliary tree). May have mural nodules, septal/wall calcification. May recur after excision, potential to transform into biliary cystadenocarcinoma.

Multiple Biliary Hamartomas

(Von Meyenburg complexes). Rare bile duct hamartomas, clusters of disorganised dilated ducts, asymptomatic, usually incidental. Prevalence 3% at autopsy, <1% on imaging (too small to see). May be associated with ADPKD, polycystic liver disease. Usually small small echogenic, occasionally larger hypoechoic, hypodense, high T1 and T2, usually nonenhancing.

Gallbladder Lesions


(Hyperplastic cholecystosis). Benign hyperplasia of gallbladder mucosa and smooth muscle causing focal (most), segmental (may cause hourglass GB with focal thickening midportion) or diffuse mural thickening. Fundus almost always involved. Rokitansky-Aschoff sinuses – intramural diverticula within hypertrophied small muscle wall, commonly containing cholesterol crystals (causing comet tail reverberation artefact). Multiple cystic bubbly lesions. Gallstones common. No malignant potential. DDx cholesterolosis – gross triglyceride/cholesterol deposits in lamina propria causing “strawberry GB”.

Gallbladder Polyps

Common. Echogenic nonshadowing non-mobile nodules.

  • Cholesterol polyps (most) – <10mm, commonly multiple.
  • Adenomatous polyps (rare) – Indistinguishable from cholesterol polyps. If >10mm or definite growth then may be malignant and should be resected.

Gallbladder Carcinoma

F:M 4:1, >60yo. Pain, anorexia, weight loss, jaundice. Increased risk with porcelain GB, cholelithiasis. Gallstones in 95%, may mask the carcinoma. 95% are adenocarcinomas, 5% squamous cell carcinomas, rarely carcinoid or carcinosarcoma. Patterns include infiltrating (most, poorly defined thickening that may involve the entire GB) or exophytic (irregular cauliflower mass >10mm, may be heterogeneous due to enveloped stones, necrotic debris). Most common fundus or neck. Dilated ducts. Only 20% are diagnosed preoperatively. May locally extend into liver (most), bile ducts or bowel. Metastases to periportal, peripancreatic nodes and liver. Most unresectable at diagnosis with poor prognosis.


Traumatic injury includes:

  • Haemoperitoneum – HU 30-45.
  • Sentinel clot – Focal clotted blood (>60HU) adjacent to organ.
  • Active bleeding – Hyperdense 85-350HU fluid in arterial phase.
  • Free gas – Insensitive sign of bowel injury.
  • Free contrast in peritoneum – From oral contrast or ruptured bladder.
  • Subcapsular haematomas – Crescent-shaped.
  • Intraparenchymal haematomas – Irregular-shaped low density in enhanced organ.
  • Laceration – Jagged linear low density blood within enhanced organ.
  • Infarction/ischaemia – Reduced contrast enhancement extending to capsule.


Portal vein provides 2/3 of blood flow, hepatic artery 1/3. Be cautious with calling heterogeneity due to perfusion effects in the presence of capsular retraction.

Transient hepatic attenuation/intensity differences (THAD/THID) – Phenomenon on enhanced CT (THAD) or MRI (THID). Lesion or area of parenchyma visible on arterial phase, from localised mismatch in arterial vs portal venous blood supply. From siphoning effect, relative portal hypoperfusion/thrombosis or arterioportal shunt. May be associated with hepatic tumours.

Portal Hypertension

Increased resistence to portal blood flow with raised portal venous pressure leading to portosystemic collaterals. Prehepatic causes include portal vein thrombosis or extrinsic compression, massive splenomegaly increasing splenic ven blood flow. Post-hepatic causes include severe RH failure, constrictive pericarditis, hepatic vein obstruciton. Intrahepatic causes incude cirrhosis (most), schistosomiasis, massive fatty change, sarcoidosis, nodular regenerative hyperplasia. Increased resistance of flow through sinusoids (contraction of myofibroblasts, scarring, vasoconstriction), hyperdynamic circulation increasing portal venous blood flow (splanchnic arterial vasodilation). Risk of variceal bleeding and hepatic encephalopathy. Hepatic a may be enlarged and tortuous. Portal vein >13mm, SMV/splenic vein >10mm, portal vein thrombosis, portal/mesenteric vein calcifications. Consequences include:

  • Ascites – Generally serous; from sinusoidal hypertension (leaking fluid into the space of Disse), hypoalbuniaemia, percolation of hepatic lymph into the peritoneal cavity (when exceeds thoracic duct capacity), splanchnic vasodilatation. Mesenteric/omental/retroperitoneal oedema.
  • Portosystemic venous shunts – Portal hepatofugal flow or flow in dilated paraumbilical vv is highly specific. Collaterals include coronary, gastro-oesophageal (40%, risk of massive haematemesis), splenorenal, paraumbilical, haemorrhoidal and retroperitoneal veins.
  • Congestive splenomegaly – Gamna-Gandy bodies (siderotic nodules) are organised foci of haemorrhage with haemosiderin/iron, fibrosis and calcium in spleen. May cause thrombocytopenia or pancytopenia.
  • Hepatic encephalopathy.

Noncirrhotic portal fibrosis and idiopathic portal hypertension is common in India, Japan. ?From gut bacterial infection with septic embolisation of portal vein.

Portal Vein Thrombosis

From cirrhosis (25%), tumour invasion/compression (HCC, pancreatic cancer), hypercoagulable states, abdominal sepsis with pyelophlebitis (eg pancreatitis, diverticulitis, appendicitis), pancreatitis, trauma, neonatal umbilical sepsis or umbilical vein catehterisation (subclinical presenting years later), unknown in 10%. May cause or exacerbate portal hypertension. Hypodense, echogenic plug (may be anechocoic/hyperechoic depending on age), high-T1 acute, iso-T1 chronic in portal vein. Internal arterial Doppler confirms tumour thrombus. Cavernous transformation of the portal vein – small adjacent collaterals expand creating tangled vessels. Usually no ascites (occlusion is presinusoidal). Acute occlusion may cause bowel congestion and infarction. Intrahepatic branches, if occluded cause sharply demarcated red-blue infarct of Zahn with severe hepatocellular atrophy and haemostasis in sinusoids, but no actual infarct/necrosis.

Budd-Chiari Syndrome

From obstructed >/=2 hepatic veins (obstructed single main hepatic vein is clinically silent). Thrombosed hepatic vv from tumour, hypercoagulable states, trauma. 10% idiopathic ?unrecognised thrombogenic disorder. Impaired flow to R and L lobes causing ‘flip-flop’ early central enhancement (peripheral weak) then delayed peripheral enhancement (central washed out). Caudate lobe spared and enlarged, drains directly into IVC, may obstruct/compress the IVC. ‘Comma sign’ – intrahepatic collaterals on CT/MR. Multiple hepatic regenerative nodules up to 30mm with hypervascular enhancement persisting on PV phase (cf HCC). Liver becomes swollen and red-purple, severe centrilobular congestion and necrosis, centrilobular fibrosis if chronic. Ascities.

Obliterative hepatocavopathy – obstruction of the hepatic portion of IVC, from thrombosis or membrane.

Vascular Malformations

May be associated with HHT. Types include hepatic artery -> vein (aorto-venous, may cause high output CHF); artery -> portal vein (aortoportal, portal HTN); portal vein -> hepatic vein (porto-venous, clinically silent). Strange diffuse hyperenhancement, early HV/PV enhancement, enlarged hepatic artery.

Hepatic Congestion

Impaired venous drainage from CHF or constrictive pericarditis causes passive congestion of the liver. Distended IVC and hepatic veins with reflux of contrast, incresaed pulsatility of the portal vein, heterogeneous liver enhancement, hepatosplenomegaly, cardiomegaly, pleural effusion, ascites. Congested centrilobular sinusoids with corresponding hepatocytes becoming atrophic, if chronic leads to cardiac sclerosis (rarely cirrhosis). Additional left heart failure or shock with hepatic hypoperfusion causes centrilobular haemorrhagic necrosis with variegated mottled appearance (nutmeg liver’), sharply demarkated with viable periportal hepatocytes on microscopy.

Liver Infarct

Rare due to double blood supply. Hepatic artery occlusion (embolism, neoplasia, polyarteritis nodosa, sepsis) may compress adjacent portal vein and cause a localised infarct, occasionally haemorrhagic.

Peliosis Hepatis

Rare dilation of the sinusoids of unkown aetiology. ?Focal apoptosis of hepatocytes or sinusoidal endothelial cells, Bartonella. Associated with chronic illness (cancer, TB), AIDS, post-transplant immunodeficiency, drugs; 20-50% idiopathic. Usually asymptomatic, may cause intra-abdominal haemorrhage, hepatomegaly or liver failure. Multiple hypodense blood-filled cyst like lesions of high T2, low T1, centrifugal enhancement without washout, no mass effect. May have haemorhage and dystrophic calcification.

Sinusoidal Obstruction Syndrome

(Previously veno-occlusive disease). In 25% of allogenic bone marrow transplants, usually within 3/52; also seen in chemotherapy. Mortality up to 30%. Toxic injury to the sinusoidal endothelium with sloughing causing obstruction to the hepatic venules with centrilobular congestion and necrosis, later fibrosis.

Gallbladder Torsion

Rare, elderly women. Floating GB from long, loose or absent mesentery. Tapered cystic duct, high T1 in wall, coagulation necrosis with intramural haemorrhage. Complete torsion -> ischaemia, gangrene.