3_primer_mankad_hoey_20150316195806 Flashcards
Hepatic Artery Variants
50-60% from CHA via Coeliac axis, then CHA divides to proper HA and GDA10% CHA divides into RHA and GDA10% CHA divides into LHA and GDANormal HA velocity 30-60 cm/s; RI 0.6±0.06; continuous diastolic flow
Portal Vein
Hepatopetal, non-pulsatile, mild respiratory variationFlow velocity 20-30 cm/sDiameter 12-14 mm
Hepatic Vein
Triphasic with respiratory and cardiac variationHV sampling occurs at its confluence
Cirrhotic nodules
Regenerative (hepatocytes and stroma; not seen on US unless large; on CT are high attenuation if siderotic)Cirrhotic (regenerative nodules with surrounding fibrosis)Dysplastic (hepatic adenomas with areas of dysplasia; due to HBV and HCV)
Imaging features of Cirrhosis
Decrease size of right lobe and medial left lobe, with caudate lobe hypertrophyMRI:Regenerative nodules: high T1W, low T2W;Dysplastic: high T1W, very low T2W, with post Gd enhancement;Neoplastic: arterial enhancement with PV washout; nodule-in-nodule on T2W (high T2W neoplastic within low T2W dysplastic nodule)
Haemochromatosis
Primary (AR) due to increased uptake of transferrinSecondary - erythrogenic, Bantu siderosis or transfusional (>30 units blood)CT - high attenuation liver with low attenuation PV branchesMR - Liver low T1W and T2W relative to muscle, with susceptibility on GRE; pancreas low late in disease, spleen normal in primary but low in secondary disease
Liver Abscess
Cause: 80-90% bacterial, 5% amoebic, 50%), ofetn contain gas and 60-70 y/o peakAmoebic: due to entamoeba histolytica, usually 30-50 y/o, usually single, in peripheral right lobe and often >5 cmImaging: raised right hemidiaphragm, hypoechoic initally, then developing thick reflective wallCT signs specific to pyogenic abscess: Double target sign (enhancing wall with surrounding oedema), cluster sign (clustered abcesses)MR: Low T2W, high T2W, enhancing wall, low signal wall on T2W with surrounding perilesional oedemaNM: Uptake of sulphur colloid; Gallium taken up by pyogenic but not amoebic
Hepatic Haemangioma
Commonest benign liver lesion (70 to 80%), usually 4 cm = giant cavernous haemangioma.Associations: FNH, HHT, Kasabach-Merritt Syndrome (Haemangioma and thrombocytopaenia).Supplied from hepatic artery, may rupture spontaneously.Usually hyperechoic on US, ± posterior acoustic enhancement, no flow on DopplerCT: low attenuation with early peripheral nodular enhancement, delayed centripetal fill in to maximal at 15 minutes.MR: Sharply defined, low T1W, very high T2W, central fibrous scar, similar enhancement to CT.
FNH
Second commonest benign liver lesion, usually right lobe, FCentral scar (containing AVM), usually on liver surface, non-encapsulated ± pedunculated,, very vascular, contains Kupffer cells, non-calcifiedUS: Homogeneously hyperechoic with hypoechoic central scar in 15-20%, displaces vessels around it, enlarged central artery and peripheral draining veins visible on DopplerCT: Ill-defined, transiently high attenuation in PV phase with gradual equilibration, central scar on delayed, ‘spoke-wheel’ pattern in 20-30%MR: Isointense on T1W and T2W, central scar hypointense on T1W and hyperintense (in 75%) on T2W; initial Gd avid enhancement with gradual equilibration (early enhancement of central scar); SPIOd (Kupffer specific) cause lesion enhancement
Hepatocellular adenoma
Women on COCP and men on anabolic steroids, 20-40 y/o, usually 5-10 cm, subcapsular in right lobeContain mixture of hepatocytes, Kupffer cells and fat, but no portal tracts; usually contains haemorrhage and necrosisUS: Heterogeneous, solid, with hypoechoic rimCT: well defined, ±hyperdense if areas of haemorrhageMR: can’t be distinguished from HCC, predominantly hyperintense T1W and isointense T2WNM: Photopaenic on sulphur colloid, no uptake on Gallium
HCC
Commonest visceral malignancy, peak 60-70 y/o;Solitary (30%), Multifocal (60-70%) and diffuse (5%) forms; invades PV in 50-60% and IVC in in siderotic noduleLarge HCC: Mosiac pattern (confluent nodules, small septae, best seen on T2W), tumour capsule (hypointense) in 60-80%, extracapsular extension with satellite nodules in 50-70%, tumour thrombus as high T1W and T1 GRE in PV, with arterial enhancementNM: photopaenic on sulphur colloid, avid uptake on Gallium
Fibrolamellar HCC
No RFs for HCC, 30-40 y/oSolitary lobulated lesion, central scar, pseudocapsule of hepatic tissue, central amorphous calcification in 30-40%Regional LNs 50-60%, rarely metastasises, no vascular invasionUS: Heterogeneous with hyperechoic central scarCT: Lobulated enhancing mass with non-enhancing central scarMR: Hypointense T1W, hyperintense T2W with heterogenous enhancement; scar hypointense on T1W and T2W and non-enhancing
Liver metastases
Usually colon, breast, lung or pancreas; solitary in 10%, both lobes in 75%US: variable, echogenic usually GIT or GU; no Doppler flow except with carcinoidExclusion criteria for metastatectomy - advanced primary, >4 metastases, extrahepatic metastases, <30% liver remaining post surgeryCalcified liver metastases: gastric, melanoma, RCC, colon, ovarianHypervascular metastases: thyroid, renal, carcinoid, melanoma, pancreatic islet cellHaemorrhagic metastases: Colon, thyroid, breast, choriocarcinoma, melanoma
Budd Chiari Syndrome
Hepatic vein of IVC obstruction, 60-70% idiopathicCauses of thrombotic obstruction (5 P’s): Pregnancy, Pill, Polycythaemia Rubra Vera, abnormal Platelets, PNHNon-thrombotic obstruction: Right heart failure, constrictive pericarditis, right atrial tumour, IVC membraneUS: Hepatosplenomegaly, ascites, caudate lobe hypertrophy, ascites, prominent portosystemic anastomoses and azygos/hemiazygos systems, absent / reversed flow in hepatic veins, hepatic arterial resistance index >0.7CT: Heterogenous liver enhancement, caudate large and normally enhancing, poor opacification of hepatic veins
Hepatic veno-occlusive disease
Post radiation / chemotherapyMR: occlusion of centrilobular venules without major hepatic vein thrombosisUS: Bidirectional flow in portal veins without hepatic vein / IVC obstruction, GB wall thickening
Portal vein thrombosis
Causes: idiopathic (neonates), malignancy (in 30% of HCC, also cholangioCa, pancreatic Ca, liver metastases), hypercoaguable, trauma (iatrogenic - umbilical vein catheter), peritonitis, pancreatitis, ascending cholangitisUS: Echogenic material on PV, increased PV diameter, thickened lesser omentum
Peliosis hepatis
Rare benign dilatation of sinusoidal blood filled spaces in reticuloendothelial system (liver, spleen, marrow, lymph nodes, lungs)Causes: AIDS, TB, Anabolic steroids, CRF, tamoxifenUS: Multiple hyper-/hypoechoic areasCT: Enhancing, round lesions in organs; initially low attenuation then isoattenuating with time
Biliary anatomy
RPHD into LHD 20%RPHD, RAHD, LHD trifluence 10%75% cystic duct inserts into middle third of extrahepatic CHD, 10% distal CHDCBD / PD / Ampulla - 75% Y, 25% V, 5% UCHD measured at level of HA, normal <7 mmSecretin transiently distends pancreatic duct (maximal at 2 minutes post injection) prior to MRCP
Choledochal cysts
Cystic dilatations of CBD; 30-40% present at <1 y/o.Clinical features: Intermittent obstructive jaundice, RUQ pain and RUQ mass (25% triad)Associations: Biliary, pancreatic anomalies and liver cysts
Caroli’s disease
Segmental dilatation of intrahepatic bile ducts, autosomal recessive, causes biliary stasis with intrahepatic calculi then secondary pyogenic cholangitis, intrahepatic abscesses, increased risk cholangiocarcinomaAssociations: Medullary sponge kidney (80%), Infantile polycystic kidney disease’Central dot sign’ - specific, portal radicals surrounded by abnormally dilated / ectatic bile ducts
Chemotherapy cholangitis
Most commonly associated with floxuridine; strictures of CHD and bifurcation, sparing of distal CBD
Cholelithiasis
Cholesterol (70-80%) but 70% mixed, 20% radiopaque, associated with cirrhosisPigment (30%) 2-5 mm, faceted, calcium bilirubinate, 50% radiopaqueWall-echo-shadow complex (double arc sign) when GB contracted over GS (but also seen with porcelain GB and emphysematous cholecystitis)Sludge (echogenic bile) - 100% fasting patients at 6 weeks (decreased CCK)
Biliary Enteric fistulae
Most commonly biliary-duodenal (70%; can cause GS ileus)Causes: Chronic cholecystitis with GS erosion into GIT (90%), Penetration of posterior DU into CHD (5%)
Bouveret syndrome
Obstruction of stomach or duodenum by GS