Hepatobilary Flashcards

Question

Does this Lesion meet Threshold growth criteria for HCC?

Answer 1

* No. * there is an increase in diameter of just over 50% but in an 8 month period. so doesn't reach threshold growth criteria.

Answer 2

* Early * progressed * nodule in a nodule * infiltrating * angioinvasice

Answer 3

* First Stage of HCC * the precursor to Progressed HCC * \<2cm diameter * usually 10-15mm * Vaguely nodular * no capsule * vascular invasion and intrahepatic mets are very rare * blood supply changes not mature * so unlikely to demonstrate typical HCC imaging features.

Answer 4

* Overtly malignant and distinctly nodular * usually, over 2cm diameter but may be \< 2 cm * vascular invasion * intrahepatic mets * established blood supply changes with angiogenesis and change to portal venous drainage (from HV) * Typical imaging findings of HCC. * Tumour capsule characteristic, with internal fibrous septa. Image shows: 1. NR APHE 2. Wash out 3. Capsule

Answer 5

* more than 30% of patients present with Multifocal disease

Answer 6

* Small progressed HCC within a dysplastic Nodule * Infrequent * Important to look for a recognise * In this picture we see: * a T1 bright dysplastic nodule on the pre contrast * then art phase can be

Answer 7

* Difficult. * non-mass forming malignancy * Ill-defined margins * typical arterial hyperenhancement and washout often not both present * poor prognosis * venous invasion common. In the HBP image, the bright areas are normal hepatocytes which have taken up contrast. The rest (dark) is infiltrating HCC.

Answer 8

* Invades PV, HV and IVC * Often extensive at dix * V. Poor Prognosis * usually seen as a contraindication to liver transplant * LI-RADS 'tumour in vein" TIV

Answer 9

* HCC tumour thrombus is usually grossly expansile * where as bland clot is usually not expansile.

Answer 10

* Mosaic Architecture + Sepat * Corona enhancement * Fat

Answer 11

* Progressed hypervascular HCC * Enhancement of peritumoural venous drainage area * early drainage of contrast from HCC into surrounding sinusoids * late arterial phase to early PV phase * fades out subsequently. * There's a higher risk of satellite nodules/mets within the area of the corona. * include the corona in the treatment/resection volume.

Answer 12

* Fat is quite common in HCC. * Good indicator of hepatocellular origin of a nodule in a cirrhotic patient. * seen in dysplastic nodules as well. Other liver lesions containing fat: * HCC * Dysplastic Nodules * HNF 1-alaph inactivated hepatocellular adenoma (HNF 1a HCA) * Hepatic angiomyolipoma in the non-cirrhotic liver. * VERY RARE in FNH. Picture shows: * HCC with macroscopic fat within it on CT. * This becomes more obvious on IP and OP imaging on MRI * Markedly steatotoic HCC usually slightly better prognosis

Answer 13

* Large HCC with inhomogenous T1 IP imaging. * large amounts of fat on OP * Quite a lot of art phase enhancement with wash out on the PVP (portal venous phase) * doesn't look like FNH. and the presence of fat would certainly go against that as well. * Fat containing HCC is best seen in OP MRI *

Answer 14

* Fat containing HCC is best seen in OP MRI * high-grade dysplastic nodules and HCC may contain fat The presence of fat tends not to be critical in HCC, as other typical features are usually present. Fat-containing HCCs usually have a better prognosis.

Answer 15

* HCC are usually T2 bring (mild to moderate) * but small lesions may not be t2 bright. * around 80% of progressed HCC are T2 bright. This may be homogenous or heterogenous * LEARNING POINT * a t2 bright nodule in a cirrhotic liver is highly suspicious for malignancy.

Answer 16

* HCCs have densely packed cells * 80% poorly differentiated HCCs show true restriction. ie on ADC * only 50% of well-differentiated HCCs demonstrate restricted diffusion. * Things to note * background liver is cirrhotic and fibrous and therefore diffusion restricted. * therefore DWI is insensitive * DWI restricting nodules are non-specific as diffusion restriction is seen in HCC and cholangiocarcinoma. * LEARNING POINTS * a diffusion restricted nodule in cirrhosis is highly sus for malignancy (not specific for HCC) * The absence of diffusion restriction in a lesion fulfilling criteria for HCC or a lesion suspicious for HCC means nothing.

Answer 17

* Primovist/gadoxetic acid/EOB = liver specific MRI contrast agents * EOB/primovist-MRI doesn't really help you with typical Progressed HCC. * The hepatocyte uptake of EOB relies mainly on the expression of OATP transporters on the surface membrane.

Answer 18

* Hepative veins * triphasic flow pattern * artial contraction (right atrium) Normal hepatic vein Doppler Dr Bahman Rasuli◉ and Dr Matt A. Morgan◉ et al. The hepatic veins have a characteristic spectral Doppler waveform. Alterations in the normal hepatic vein waveform may reveal or confirm abnormalities in the heart or liver. Terminology The shape of the hepatic vein spectral Doppler waveform is primarily determined by pressure changes in the right atrium, or more exactly the blood flow resulting from the resultant pressure gradients. Multiple terms have been used to describe the hepatic vein waveform, including "phasic", "triphasic", "tetrainflectional", and "periodic". Some prefer the term "periodic" since the term "triphasic" already has a specific application in arterial spectral Doppler waveforms and since "periodic" suggests that the waveform is transmitted by cardiac motion rather than systolic flow. Radiographic features The normal periodic hepatic vein waveform is typically described in four parts: a wave: atrial contraction coinciding with the "p wave" on the electrocardiogram, contraction elevates pressure within the right atrium creating a gradient for late diastolic filling of the right ventricle this also creates a pressure gradient favouring a lesser degree of retrograde flow into the IVC and hepatic veins the small reversal of flow typically results in a small wave above the baseline, reversed from the overall net flow back to the heart s wave: ventricular systole as systole commences, right ventricle contraction results in longitudinal, apically orientated traction on the tricuspid annulus the resultant "stretching" of the right atrium results in a drop in pressure, creating a gradient for anterograde flow from the inferior vena cava and hepatic veins, most pronounced at mid-systole this typically forms the highest velocity deflection seen in the waveform v wave: atrial overfilling a transitional inflection point as blood fills the right atrium, the flow from the hepatic veins and IVC slows, resulting in the s wave returning back to baseline if the atrium fills to capacity then there may be a small amount of flow "recoil" backward, resulting in a v wave that rises above the baseline d wave: tricuspid valve opening as the tricuspid valve opens, blood flows from the right atrium into the right ventricle, resulting in a net flow of blood away from the liver and the waveform again dives back down below the baseline this wave is almost always lower in magnitude than the s wave Sometimes a c wave occurs as a second small inflection above the baseline, right after the a wave, reflecting the effect of the tricuspid valve bulging into the right atrium. Differential diagnosis Alterations in the normal hepatic venous Doppler waveform often indicate cardiac dysfunction, although it may also reflect disease of the hepatic parenchyma and/or vasculature. The consequent haemodynamic perturbations may manifest as: * increased pulsatility (exaggeration of anterograde/retrograde velocities)tricuspid regurgitation * abnormally high amplitude of the a and v waves * diminished or reversed s wave * congestive heart failure * abnormally high amplitude of the a and v waves * maintenance of a dominant anterograde S wave \> D wave * this presumes tricuspid valvular competence * decrease in phasicity (diminution of anterograde/retrograde velocities)cirrhosis * often associated with spectral broadening of the Doppler envelope and truncation of the a wave * hepatic veno-occlusive disease (e.g. Budd-Chiari)

Answer 19

* Low-velocity 10-20cm/s flow pattern * respiratory vaiation present * pulsation in PV flow is seen in tricuspid regurg and low BMI * Portal Veins In terms of complexity, the portal venous waveform is somewhere between those of the hepatic artery and hepatic veins. A model for understanding portal venous flow requires accepting two pieces of information. First, physiologic flow should always be antegrade, which is toward the transducer and therefore creates a waveform that is above the baseline. Second, hepatic venous pulsatility is partially transmitted to the portal veins through the hepatic sinusoids, which accounts for the cardiac variability seen in this waveform. It should also be kept in mind that the flow velocity in this vessel is relatively low (16–40 cm/sec) compared with that in the vessel coursing next to it, namely, the hepatic artery. The normal portal venous waveform (Fig 23) should gently undulate and always remain above the baseline. The peak portal velocity (V1) corresponds to systole, and the trough velocity (V2) corresponds to end diastole. At first, one may incorrectly reason that systole should cause back pressure and create the trough; however, such is not the case. The primary influence on variation in portal venous pressure is atrial contraction, which occurs at end diastole. Atrial contraction, toward end diastole, transmits back pressure, first through the hepatic veins, then to the hepatic sinusoids, and ultimately to the portal circulation, where forward portal venous flow (velocity) is consequently decreased (the trough). In fact, prior studies of patients with increased portal venous pulsatility secondary to tricuspid regurgitation have noted that the portal venous waveform resembles an inverted hepatic venous waveform (1). Therefore, at end diastole, the atrium contracts and the portal venous waveform reaches a low point (trough). The degree of undulation is highly variable but may be quantified with a PI (Fig 24). It is important to note that the PI calculation for the portal vein is different from that for the hepatic arteries (arterial PI = (V1–V2)/Vmean). In the portal veins, the PI is calculated as V2/V1, with V1 normally being greater than 0.5.

Answer 20

* low impedance/resistance wave form * artery flow pattern * same flow direction as the portal vein * https://pubs.rsna.org/doi/10.1148/rg.311105093 Radiographics article

Answer 21

* The liver is 8-10HU higher than the spleen on non-contrast CT * The HA contributes 25% of blood flow to the liver * the PV contributes 75% of blood flow to the liver * Most tumours have only arterial blood supply.

Answer 22

* extends from the umbilicus to the diaphragm * divides the medial and lateral segments of the left lobe of the liver * The falciform ligament is a broad and thin peritoneal ligament. It is sickle-shaped and a remnant of the ventral mesentery of the fetus. It is situated in an anteroposterior plane but lies obliquely so that one surface faces forward and is in contact with the peritoneum behind the right rectus abdominis and the diaphragm, while the other is directed backward and is in contact with the left lobe of the liver. It contains between its layers a small but variable amount of fat and its free edge contains the obliterated umbilical vein (ligamentum teres) and if present, the falciform artery, and paraumbilical veins. The falciform ligament divides the left and right subphrenic compartments but may still allow passage of fluid from one to the other.

Answer 23

* Round ligament/obliterated umbilical vein * lies in the free edge of the falciform liagement * hyperechoic structure in the left lobe of the liver * LAND MARK * gastroesophageal junction

Answer 24

* extends from the GB to the porta hepatis * divides the (American left and right lobes) * ie divides segs 2/3 from the rest.

Answer 25

* Between the caudate lobe and the lateral segment of the left lobe * contains the hepatogastric ligament.

Answer 26

* SSFSE or fast gradient echo scout images * Axial T1W gradient echo in and out phase * axial FS T2 dual TE * Axial DWI * Axial 3D gradient echo T1 pre and post con (art, PV and equilibrium phases)

Answer 27

* MR technique to noninvasively quantify the stiffness of the liver * a mechanical driver is placed adjacent to the liver to generate shear waves within the abdomen at a predetermined frequency (40-120Hz) * MR images are then aqcuried with a gradient echo sequence as the waves propagate thru theliver * the velocity and wavelength of theawves propagating depend on the stiffness of the tissue. * velocity and wavelength increase with greater tissue stiffness. * used to assess liver fibrosis

Answer 28

* viral * hep A, B, NonA Non B, delta * CMV * EBV * HSV * Rubella * Yellow fever * Chemical Hepatitis * Etoh * Drucgs * isoniazine * halothane * chlorpromazine * phenytoin * methyldopa * panadol * Toxins CCl4

Answer 29

* GB wall thickening may occur * increased echogenicity of portal triads in acute hepatitis * ddx cholangitis * decreased echogencity in chronic hepatits * echogenicity * patterns are difficult to evaluate and there is interobserver variability * only fatty liver substantially increases echogenicity of the eliver * Acute hepatitis is a clinical and laboratory diagnosis. Starry sky appearance appears as bright echogenic dots throughout a background of decreased liver parenchymal echogenicity. It has poor sensitivity and specificity.

Answer 30

* Increased T1 and T2 relaxation times in the liver * high signal bands paralleling portal vessels on T2 (periportal oedema) * There is severe gallbladder wall T2 hyperintensity in keeping with oedema, which compresses the mucosa of the gallbladder. Cystic duct, CBD pancreatic duct are within normal limits with no obstructing lesions seen. Marked high T2 signal is also demonstrated within the periportal spaces consistent with oedema. Liver also appears slightly enlarged with recanalisation of the umbilical vein noted. Overall findings suggestive of acute hepatitis and could account for the markedly deranged LFTs. * Case Discussion This case demonstrates markedly abnormal gallbladder wall and periportal oedema with a normal CBD. Appearances suggest an acute hepatitis. Full viral hepatitis screen was carried out and found to be negative. The patient then absconded from the ward.

Answer 31

* Small liver * increased echogenicity * coarse * heterogenous * nodular surface * Hypoechoic regenerating nodules (image) * Simple cysts and haemangiomas are rare in cirrhotic livers * Unequal distribution of cirrhosis in different segments (ie sparring) * left lobe appears larger than right * lateral seg of left lob (II and III) enlarges * IVa and IVb shrink * the caudate lobe enlarges * Portal hypertension * hepatic wedge pressure \>10mmhg * collaterals * left gastric * paraoesophageal * mesenteric * retroperitoneal veins * spleonreal * Splenomegally ascites

Answer 32

* hepatic fibrosis with the formation of **nodules that lack a central vein** * Two types * **Chronic sclerosing cirrhosis** * minimal regnerative activity of hepatocytes * little nodule formation * liver is hard and small * **Nodular cirrhosis:** * regenerative activity with presence of many small nodules * initially the liver may be enlarged.

Answer 33

* Etoh * Hepatitis B * Biliary cirrhosis * Hemochromatosis * Heart failture * Wilson disease * A-Antitrypsin * Drugs

Answer 34

* 10% of patients develop cirrhosis * haemangiomas are much less common 2%

Answer 35

1. Obesity 2. etoh 3. hyperalimentation (IV nutrition) 4. debilitation 5. Chemo 6. hepatitis 7. steroids 8. cushing syndrome

Answer 36

* renal cortex appears more hypointense relative to liver than normal * intrahepatic vessel borders become indistinct or cannot be visualised * nonvisualisation of diaphragm bc of increased beam attunuation

Answer 37

* usually geographic (ie straight borders) * may occasionally have all features of a tumous * ie areas of fatty liver are interspersed with normal liver * adjacent to falciform ligament, usually anterolateral edge of medial segment * lack of mass effect * vessel distribution and architecture are preserved in areas of fat * rapid change with time * fat appearance or resultoion bay be as fast as 6 days

Answer 38

* Focal fatty sparing typically has a geographic appearance and occurs in characteristic locations 1,3: * adjacent to the porta hepatis (segment 4) * gallbladder fossa (picture) * adjacent to the falciform ligament * subcapsular parenchyma * MRI Requires both in- and out-of-phase imaging and contrast to adequately assess 1. Pseudolesions (focal sparing) are better seen on out-of-phase imaging, but otherwise, appear normal and similar to the rest of the liver on T2 and contrast-enhanced sequences 1. Hepatobiliary contrast agents such as gadoxetate disodium can show greater delayed uptake and biliary excretion when compared to the fatty liver due to a greater concentration of functioning hepatocytes 4. The rest of the liver demonstrates: T1: hyperintense T2: mildly hyperintense IP/OP: signal drop out on the out-of-phase sequence

Answer 39

* NCCT: 55-65HU * Normal liver is 10 HU denser than Spleen * each mg of triglyceride per gram of liver decreases liver density by 1.6 HU *

Answer 40

* Fatty areas are hypodense, while normal liver appears relatively hyperdense * herpative veins and poeral veins appear dense relative to decreased parenchymal density * common focal fatty deposit segment 4 near fissure for falciform lig. * Most radiologists use a HU cut off of \< 40. * MRI in and out of phase imaging to verify the presence of fat

Answer 41

* **Focal confluent fibrosis** * wedge shaped area of low attenuation on NCCT * T1 hypo and T2 hyper on MRI * Retraction of overlying liver capsule. 90% * Total lobar or segmental involvement can be seen * Located in medial segment of the left lobe +/- anterior segment of the right lobe * may show delayed persistent enhancement * https://radiopaedia.org/articles/confluent-hepatic-fibrosis * Confluent hepatic fibrosis Dr Mostafa El-Feky◉ and Dr Matt A. Morgan◉ et al. Confluent hepatic fibrosis is a possible result of chronic injury to the liver, most commonly from cirrhosis or hepatic vascular injury. Radiographic features Confluent hepatic fibrosis is a cause of wedge-shaped or concave-marginated abnormalities in the cirrhotic liver: it occurs more frequently in the medial and anterior segments of the liver and tends to extend from the hilum to the periphery. CT wedge-shaped regions of hypoattenuation on non-contrast CT hypoattenuating on the arterial and portal venous phases the fibrosis may gradually enhance MRI wedge-shaped regions of moderate T2 hyperintensity T1 hypointensity (possible increased T1 signal from cholestasis) progressive postcontrast enhancement on the dynamic sequence but does not show enhancement on the delayed phase with hepatospecific contrast agents lack fat signal intensity Confluent hepatic fibrosis is categorised as LR1 or LR2 in the LI-RADS classification system. If findings are indeterminate between fibrosis and hepatocellular carcinoma, it should be graded LR3 or LR4. Differential diagnosis The main differential diagnoses are: hepatocellular carcinoma enhancement pattern allows differentiation not associated with volume loss or capsular retraction cholangiocarcinoma peripheral cholangiocarcinoma may also show capsular retraction but generally is more masslike dilated intrahepatic bile ducts are also more common in cholangiocarcinoma than with confluent hepatic fibrosis hepatic epithelioid haemangioendothelioma may show capsular retraction but otherwise has a different appearance and enhancement pattern Practical points For unknown reasons, confluent fibrosis is more common in primary sclerosing cholangitis and alcohol-related cirrhosis than with viral cirrhosis. References

Answer 42

* "Very Poor French & MATH" so no Sugar (glycogen) for you * Von Gierke * Pompe * Forbes * McArdle * Anderson * Tarui * Hers

Answer 43

* Primary liver findings * hepatomegally * US: increased echogenicity * looks like fatty liver * CT * increased Density * 55-90 HU * Opposite to fatty liver * nephromegally * Hepatic complications * HCC * Hepatic adenoma

Answer 44

* Gaucher disease is a rare genetic disorder passed down from parents to children (inherited). When you have Gaucher disease, you are missing an enzyme that breaks down certain types of fatty substances (lipids). These lipids can build up in organs such as your spleen and liver. * Gaucher disease (GD) is the most common lysosomal storage disorder in humans. It is an autosomal recessive, multisystem disease arising from a deficiency of glucocerebrosidase or beta-glucosidase activity, resulting in the accumulation of a glycolipid (glucocerebroside) within the lysosomes of macrophages, particularity in the bone marrow, spleen and liver. * Radiographic features * Plain radiograph * Skeletal involvement is seen in 70-100% of patients and primarily involves long bones (tibia, humerus, femur) as well as vertebrae. Ribs, hands and wrists, ankles and feet, and mandible may also be involved 6. * Features of skeletal involvement include: * osteopenia * osteonecrosis * pathological/crush fractures * endosteal scalloping * Erlenmeyer flask deformities * H-shaped vertebrae * paranasal sinus obliteration due to medullary expansion 9 * MRI * spleen * massive splenomegaly * splenic nodules (30%) 1 * splenic infarcts (33%) * liver * hepatomegaly: less marked than the degree of splenomegaly * T2: hyperintense stellate areas representing inflammation and fibrosis 3 * areas of hepatic ischaemia * skeletal system * long bones are most severely affected * reduced T1 and T2 signal from involved bone marrow (due to infiltration of Gaucher cells) * bone marrow burden (BMB) score may be obtained from MRI images 4 * may give a "salt and pepper pattern" due to scattered involvement * features of superimposed osteonecrosis * metaphyseal notching of humeri * pathological fractures * Erlenmeyer flask deformity

Answer 45

* Hemochromatosis * iron overload * The clinical finding is **Bronze diabetes** * cirrhosis * DM * hyperpigmentation * Types * Primary * AR * defect in intestinal mucosa causing increased iron absorption * iron excess in parenchymal cells, ie liver, pancreas, myocardium, pituitary, thyroid synovium * leads to cellular damage, organ dysfunction and malignancy * secondary * non-genetic cause of iron accumulation * Multiple transfusions * iron is deposited in phagocytic cells in the spleen and liver (KUPFFER CELLS) * less toxic * Radiographic features General visceral features of haemochromatosis are increased organ density (CT) and reduced organ signal intensity (MRI). Secondary imaging features include hepatomegaly, cirrhosis and signs of heart failure. The pattern of iron deposition is important. Predominant involvement of the liver, without deposition in spleen or bone marrow, is consistent with non-RES iron deposition and is characteristic of primary haemochromatosis. Iron deposition in the spleen and bone marrow, but to a lesser degree in the liver is consistent with RES deposition and is most likely due to haemosiderosis, which may or may not be associated with secondary haemochromatosis. * Diagnosis Visceral iron results in susceptibility artefact which leads to T2\* signal loss. The result is a low signal that is seen on all sequences, but particularly gradient echo and T2. It is useful to compare organ signal to that of skeletal muscle, with lower organ signal than muscle indicating the presence of iron. Gradient in-phase and out-of-phase sequences are particularly useful, demonstrating changes that are the opposite of those seen in hepatic steatosis. In haemochromatosis, the liver on in-phase sequence (which is usually obtained second, and thus more susceptible to T2\* effects) demonstrates low signal, whereas the out-of-phase sequence demonstrates higher signal 6. In primary haemochromatosis, spleen and bone marrow signal is typically normal and low pancreatic signal is usually only seen if there is cirrhosis.

Answer 46

* Hyperechoic liver

Answer 47

* Dense liver \>75 HU * much denser than spleen * Intrahepatic vessels stand out as low density structures

Answer 48

* Primary hemochromatosis * The Liver pancreas and myocardium hypointense on T2W and T2\* gradient echo sequence in **primary hemochromatosis** with sparing of the spleen and the bone marrow. * In secondary hemochromatosis * there is decreased signal intensity of the liver, spleen and bone marrow with sparing of the pancreas * the amount of iron can be quantified using Gradient echo sequences with T2\* weighting and progressively longer TEs. Free websites allow calc of estimated hepatic iron concentration * iron deposition and decreased in signal intensity in the kidneys are only seen in intravascular hemolysis cause by mechanic stress in pts with heart valves, paroxysmal noctural hemoglobuinuria and in hemolytic crisis of sickle cell disease * Signal changes in the liver are in keeping with iron deposition in haemochromatosis. A second cavernous haemangioma is shown in segment IV. T2 BLADE fat-suppressed with an echo train of 116ms. The segment VIII mass is hyperintense, "lightbulb bright"'. There is a diffuse signal drop throughout the liver (susceptibility). Low signal liver parenchyma on T1 in-phase. The mass is hyperintense relative to the liver. Paradoxical increase in signal of the liver parenchyma on T1 out-of-phase, yet the mass is hyperintense relative to liver parenchyma. 40-minute post IV gadoxetate sodium (hepatocyte-specific contrast agent). Case Discussion There are several causes for increased hepatic attenuation on CT. In this case, the differentiating feature of primary haemochromatosis is the increased density of the liver only. In secondary haemochromatosis (e.g. frequent transfusions), the spleen would be expected to be hyperdense as well. CT is not suitable for quantifying iron load in the liver, although this was practised in some institutions until the 1990s 1. However, MR quantification of iron content in the liver, using several gradient recalled echo sequences, is a non-invasive alternative to biopsy. Cavernous haemangiomas of the liver are classically hypointense relative to liver parenchyma on T1-weighted imaging. In this case, the haemangiomas appear relatively hyperintense because of the diffuse signal drop in the liver parenchyma secondary to iron deposition; there is little, if any iron deposition in the haemangioma. A hyperdense liver on non-contrast CT is an 'old chestnut' radiology exam case. Watch out for ancillary features that may point to the diagnosis such as pulmonary fibrosis and pacemaker (amiodarone), or increased density in the spleen and pancreas (secondary haemochromatosis).

Answer 49

HCC in primary hemochromatosis

Answer 50

* Pathogens * e coli * areobic strep * anerobes * Causes * ascendig cholangits * trauma * pylephlebitis * Pylephlebitis, or infective suppurative thrombosis of the portal vein, is a serious condition with significant morbidity and mortality, which can complicate intraabdominal sepsis of any etiology.

Answer 51

* CT * hypodense mass or masses with peripheral enhancement, no fill-in * Double target sign * wall enhancement with surrounding hypodense zone (edema) * 30% contain gas

Answer 52

* amebic abscess * entamoeba histolytica * imaging features * abscesses do not contain gas unless secondarily superinfected * irregular shaggy borders * internal sepations 30% * multiple abscesses 25% * Treatment * conservative - metronidazole * abscess drainage indicated if no response to rx or non-surgical candidate.

Answer 53

* dog tapeworm Taenia echinococcus. * THe embroys penetrate the human intestinal mucosa and disseminate to theliver and lungs \> spleen, kidneys, bone, CNS. * Two species * dogs * echinococcus granulosus more common, few large custs * echinococcus multilocularis host is rodents. less common, more invasic * Most pts get the disease in child hood. initiallly the cutsts are 5mm and then enlarge 1cm/year until symptomatic.

Answer 54

* well-delineated cysts (multilocular \> unilocular) * size of cyts usually very large * daughter cysts within larger cysts is pathognomonic * rim like cyst calcification in 30% * double rim sign (pericyts endocyst) * **Water lily sign** * The water-lily sign, also known as the camalote sign, is seen in hydatid infections when there is detachment of the endocyst membrane which results in floating membranes within the pericyst that mimic the appearance of a water lily. It is classically described on plain radiographs (mainly chest X-ray) when the collapsed membranes are calcified but may be seen on ultrasound, CT, and MRI. * enhancement of cyst wall.

Answer 55

* poorly marginated multiple hypodense liver lesions * lesions infiltrative * chronic granulomatous reaction with necrosis, cavitation * calcification punctate and dystrophic, not rim like * https://www.hindawi.com/journals/crira/2014/638375/

Answer 56

* Type 1: * pure fluid collection * unilocular * well defined cyst * ameniable to Percut drainage * Type II * partial/complete detachment of membrane floating in cyst * amenable to percut drainage * Type III * multisepatated or multilocular * ameniable to percut drainage * Type IV * heterogeneous cystic mass * NOT ameniable * Type V: * calcifed wall * NOT ameniable.

Answer 57

* Rupture into peritonela, pleura, pericardial cavity * obstructive jaundice and a result of compression/obstruction of biliary tree, filary fistual * Super infection (bacterial) requiring prolonged drainage * anaphylaxis, shock, DIC (\<1%)

Answer 58

Fig. 3—34-year-old man with AIDS and bacillary peliosis. A, Transverse contrast-enhanced CT image shows large ill-defined, hypoattenuating lesion (white arrow) with heterogeneous peripheral enhancement within left liver lobe. Smaller subcapsular hypoattenuating lesion (black arrow) with ring enhancement can also be seen in right liver lobe. B, Transverse contrast-enhanced CT image (different scan level) shows multiple enlarged lymph nodes, feature typically seen in bacillary peliosis. C, Transverse contrast-enhanced CT image obtained after 9 months shows progression of disease with multiple hypoattenuating lesions disseminated within liver parenchyma with multiple small accumulations of contrast material in center of lesions (so-called target sign). D, After treatment with antibiotics, transverse contrast-enhanced CT image shows resolution of liver lesions and lymphadenopathy https://www.ajronline.org/doi/pdf/10.2214/AJR.05.0167 * PEliosis Hepatitis * rare benign disorder a/w steroid medication, sprue, diabetes, vasculitis, hematologic disorders * bacillary peliosis hepatitis is caused by Bartonella species in HIV positive patients * Multiple spherical lesions with centrifugal or centripetal enhancement. * On angio lesions seen as multiple nodular vascular lesions on late arterial phase *

Answer 59

1. Hepatocellular 2. cholangiocellular 3. mesenchymal 4. Heterotopic tissue

Answer 60

* Benign Hepatocellular tumours * adenoma * Focal nodular hyperplasia * Regenerating nodule * Malignant Hepatocellular tumours * HCC * Fibrolamellar HCC

Answer 61

* benign Cholangiocellular tumours * bilary cystadenoma * bileduct adenoma * Malignant cholangiocellular tunours * cholangioca * cystadenoca

Answer 62

* Beign mesenchymal * hemangioma * fibroma * lipoma * Malignant * angiosarcoma * thorotrast * Primary lymphoma * AIDS

Answer 63

* Benign * Adrenal * pancreatic * Malignant * mets

Answer 64

* benign * adrenal * pancreatic * malignant * mets

Answer 65

differentiation of solid vs cystic masses. For further differentiation of solid tumours \> 1cm MRI or CECT is needed (MRI preferred)

Answer 66

A homogeneous hyperechoic lesion is seen with well-defined borders and normal surrounding hepatic parenchyma, typical of hepatic haemangioma. Case Discussion A hepatic haemangioma is a relatively benign hypervascular liver lesion. It is the most common benign tumour of the liver. It is frequently diagnosed as an incidental finding on imaging and most patients are asymptomatic. A peripheral location within the liver is most common. * Frequency: * 4% of pop * 80% in females * may enlarge in preg or with Estrogen administration * Two types: * Typical Hemangioma (common) * small * asymptomatic * discovered incidently * Giant hemangioma * \>5cm * uncommon * may be symptomatic * Hemorrhage * thrombosisis * Kasaback-Merritt syndrome: * sequestration of thrombocytes in hemagnioma causing thrombocytopenia

Answer 67

Kasabach-Merritt Syndrome Kasabach-Merritt phenomenon (KMP), first described in 1940, is a rare but life-threatening coagulopathy of infancy which presents with thrombocytopenia, microangiopathic hemolytic anemia, and consumptive coagulopathy in the setting of a rapidly enlarging vascular tumor.

Answer 68

* 80% Hyperechoic * 10% hypoechoic which may have a hyperechoic rim * espec in fatty liver (picture) * Markedly echogenic liver due to hepatic steatosis makes the haemangioma appear hypoechoic. Note the absence of echogenic walls to vessels. * https://radiopaedia.org/cases/hepatic-steatosis-and-haemangioma * Giant hemangiomas are heterogenous * Anechoic peripheral vessels may be demonstrated on USS DOppler * Posterior acoustic enhancement is common (even in hypoechoic lesions)

Answer 69

* Hypodense, well circumscirbed lesion on precontrast scan * Globular or nodule intense peripaherl enhancement during artphase * Fill in occurs within minutes (longer for giant hemangiomas) (but also occurs for mets) * Multiple giant liver haemangiomata demonstrating characteristic peripheral puddling enhancement with gradual central filling. The enhancing components follow aortic density. Central cleft due to cystic degeneration/liquefaction. Incidental atrial septal defect noted on the delayed phase scans.

Answer 70

* Liver hemangioma * Hyperintense (similar to CSF) on heavily T2W seqeucne**s (LIGHT BULB SIGN)** * Post gad peripheral nodular enhancement with pentripetal fill in * imaging modality of choice

Answer 71

* decreased activity on early dynamic images * increased activity on delayed 1-2 hour blood pool imagines * only useful if lesion is \> 3cm due to limited spatial resolution.

Answer 72

* hepatocytes * kupffer cells * bile ducts

Answer 73

* 75% in young women * a/w OCP is quesitonable * Hepatic neoplasm with no malignant transformation. conservative mx * 20% are multiple.

Answer 74

* Can be difficult to detect as composed of normal cells (Kuppfer, hepatocytes bile ducts) * central fibrous scar is common * Exogenous oestrogens do not cause FNH, nor do they cause an increase in size of these masses. * USS * isoechoic * may have central vascularity with spokewheel pattern on colour doppler * MRI * lesion isointense to liver * central scar hyper intense on T2W * art enhancement * delayed enhancement of the central scarone hour delayed enhancement after Gd BOPTA * Hypervascular on Angiography

Answer 75

* Pathology The origin of focal nodular hyperplasia is thought to be due to a hyperplastic growth of normal hepatocytes with a malformed biliary drainage system, possibly in response to a pre-existent arteriovenous malformation 1,4. The arterial supply is derived from the hepatic artery whereas the venous drainage is into the hepatic veins. Focal nodular hyperplasia does not have a portal venous supply 9. Focal nodular hyperplasia is divided into two types 4: typical: 80% atypical: 20% * Macroscopically, typical lesions demonstrate a mass which is often quite large with well-circumscribed margins but poorly encapsulated. A characteristic feature is a prominent central scar with radiating fibrous septa, but this is present in less than 50% of cases 7. A large central artery is usually present with spoke wheel like centrifugal flow 3,4 (no portal veins). Histologically the lesion is composed of abnormal nodular architecture, malformed vessels, and cholangiolar proliferation. Nearly normal hepatocytes are arranged in one to two cell-thick plates. Bile ductules are usually found at the interface between hepatocytes and fibrous regions 1,2. Kupffer cells are present 4,7. There is no malignant potential 1.

Answer 76

Associations Association with other benign lesions is commonly seen (~25%) 8: * hepatic haemangiomas (most common) 6 * hereditary haemorrhagic telangiectasia * arteriovenous malformations (AVM) * anomalous venous drainage * hepatic adenoma (possible but not proven) 16 * congenital absence of portal vein/portal vein atresia * Budd-Chiari syndrome * portal shunts * idiopathic portal hypertension * portal or pulmonary hypertension 7

Answer 77

* composed of hepatocytes * no bile ducts or Kypffer cells * they are cold on Tcm99 sulfur colloid scnas).

Answer 78

OCP and glycogen storage disease Esp von Gierke disease they may resolve completely after discontinuation of hormone tx.

Answer 79

1. hemorrhage 2. infarction 3. malignant degeneration Liver adenomatoisis is a distinct entity. although the adeomas in liver adenomatosis are histologically similar to other adenomas, they are not steroid dependant, b ut are multiple, progressive, symptomatic and more likely to lead to impaired liver function, hemorrhage and malignant degeneration.

Answer 80

* usually solitary * encapsulated * may have dozens if have a glycogen storage disease or adenomatosis * CT * peripherally hypodense (lipid accumulation in hepatocytes) * Normal liver * adenomas are isodense (as they are made up of hepatocytes) * Fatty liver * adenomas are hyperdense on all phases and non con. * USS * nonspec. * may be hyper, hypo or iso * MRI * capsule on delayed phase * arterial enhancement * drop out on OP imaging

Answer 81

The incidence of hepatic adenomas is unknown, with studies showing migration from the classically described female predominance related to the use of oral contraceptives to an increased prevalence in men, particularly recognising that obesity and metabolic syndrome are emerging risk factors for adenomas 18. Hepatic adenoma is traditionally considered the most frequent hepatic tumour in young women on the oral contraceptive pill. They are found in certain situations, including 3: * oral contraceptive use (especially the first generation pills which have a high concentration of oestrogens) * anabolic steroids: typically young men * glycogen storage diseases: * type I (von Gierke disease) * type III (Cori or Forbes disease) * obesity * metabolic syndrome 18 * diabetes mellitus 19

Answer 82

Pathology Hepatic adenomas are usually solitary (70-80% of cases 10) and large at the time of diagnosis (5-15 cm) 3,13. They are most frequently seen at a subcapsular location in the right lobe of the liver and are often round, well-defined pseudo-encapsulated masses. Occasional dystrophic calcification may be present. When multiple, usually \>10 adenomas 9, the term hepatic adenomatosis is used. Multiple lesions are frequently observed in patients with type I glycogen storage disease. Von Gieke Macroscopic appearance The lesion is well-circumscribed, often subcapsular with yellow colouration on account of frequently abundant fat and lack of bile. Haemorrhagic change is frequent. The tumour may be surrounded by a fibrous pseudocapsule 15. Histology Histologically, hepatic adenomas are characterised by proliferation of pleomorphic hepatocytes without normal lobular architecture. These cells frequently have abundant glycogen (thus the link with von Gierke disease) 5. They are traditionally described as being devoid of bile ducts and Kupffer cells, although this has been shown not to be the case, with a diminished number of Kupffer cells found in many cases 1,3-4. This has an important implication for Tc-99m sulfur colloid scans (see below).

Answer 83

Molecular classifications According to the original 2006 Bordeaux classification, there are four subtypes of hepatic adenomas 17: 1. inflammatory hepatic adenoma * most common subtype * highest bleed rate 2. HNF-1 alpha mutated hepatic adenoma * second most common subtype * often multiple 3. beta catenin-mutated hepatic adenoma * least common subtype * higher risk in men on anabolic steroids and patients with glycogen storage disease, familial adenomatous polyposis 4. unclassified hepatic adenoma

Answer 84

At least five masses are seen at liver parenchyma with maximum diameters of 60×40mm. The masses show early homogenous enhancement and become isodense with surrounding parenchyma on delayed images. Case Discussion Path proven hepatic adenomas which are benign, generally hormone-induced, liver tumors. Hepatic adenoma is traditionally considered the most frequent hepatic tumor in young women on the oral contraceptive pill. https://radiopaedia.org/cases/hepatic-adenoma-multiple

Answer 85

* Asia, Japan, Africa: 5-20% * Western hemisphere 0.2-0.8%

Answer 86

* Cirrhosis: 5% develop HCC * Chronic hep B: 10% develop HCC * Hepatoxins: aflatoxin, OCPs, Thorotrast * Metabolic disease in paediatric Patients * galatosemia * glycogen stroage disease

Answer 87

* Solitary 25% * Multiple 25% * Diffuse 50%

Answer 88

* PV 35% * Hepatic Veins 15% * rare in other malignancies * HCC typically occurs in abnormal livers (cirrhosis, hemochromatosis)

Answer 89

* Lung \> Adrenal * LNs \> Bone * 10-20% at autopsy, bone mets may be painful

Answer 90

* hypodense mass lesion * may appear hyperdense in fatty liver * enhancement * early arterial enhancement * prominent AV shunting causes early enhancement * remains enhanced on PV phase * Venous invasion 40% * Calcs * more commonly seen in fibrolamellar HCC * 40% * better prognosis * younger pts * normal afp * central scar calcification

Answer 91

* Most small HCCs are hypoechoic * larger HCCs are heterogenous * Fibrolamellar HCCs are Hyperechoic * feeding tumour vessels may be seen on colour doppler

Answer 92

* T1: * hyperintense 50% (bc of fat in lesions) * iso/Hypo 50% * Hypointense capsule in 25-40% * T1 hyper and T2 hypo lesion may represent a dysplastic nodule * Short term f/u MRI may be useful as there may be interval development of enhancement, capsule and T2 hyperintensity suggesting progression to HCC.

Answer 93

* Hypervascular * AV shinting is typical * Dilated arterial supply * DSA: angiography hypervascular tumour **threads and streaks pattern:** sign of tumour thrombus in the portal vein * https://pubs.rsna.org/doi/10.1148/radiol.2361030114

Answer 94

* malignant hepatocellular tumour with distinct clinical and pathological differences to HCC * Lobulated heterogenous mass with a central scar in an otherwise normal liver * It is uncommon to find evidence of cirrhosis, vascular invasion or multifocal disease in F-HCC. * Hypointense (on all MR sequences) fibrous scar. * this widely described imaging features has been used to discriminate btwn Firbolemella ca and FNH * however in rare cases, Fibrolamella ca may demonstrate a hyperintense scar on T2, which simulates the hyperintense scar of FNH. * Dense heterogenous enhancement in the artery and portal phases. * the scar usually does not enhance and is best visulaied on delayed images

Answer 95

* GIT malignancy * HCC * Vascular mets

Answer 96

* Most mets are hypovascular * lymphoma * bull's eye pattern * hypoechoic halo around lesion * nonspecific sign but frentltly seen in bronchogenic Ca * Hypoechoic rim represents compressive liver tissue, tumour fibrosis * Calcified mets * hyperechoic with distal shadowing * All mucinous mets * colon \> Thyroid * ovary kidney * stomach * Cystic mets * necrotic leiomyosarcoma * mucinous mets

Answer 97

A hyperechoic liver lesion on ultrasound can arise from a number of entities, both benign and malignant. A benign hepatic haemangioma is the most common entity encountered, but in patients with atypical findings or risk for malignancy, other entities must be considered. Benign * hepatic haemangioma: commonest hyperechoic liver lesion by far (present in 4% of the population) 1,4 * focal nodular hyperplasia * hepatic adenoma with high fat content * focal fatty change: focal hepatic steatosis * hepatic angiomyolipoma * inflammatory pseudotumour of the liver * lipoma * Malignant hepatic metastases * colorectal carcinoma (up to 50% of hyperechoic liver metastases) * treated breast cancer * endocrine tumours of the pancreas * renal cell carcinoma * thyroid carcinoma * melanoma * some sarcomas * choriocarcinoma * hepatocellular carcinoma: particularly in a cirrhotic liver 3 * cholangiocarcinoma The presence of hyperechogenicity can be a result of fat within a liver lesion 2, although some non-fat-containing lesions may also be echogenic (e.g. hepatic haemangioma).

Answer 98

Peripheral wash out sign is characteristic of mets https://link.springer.com/article/10.1007/s00261-019-02034-y

Answer 99

AngioSarcoma * Rare malignancy * Tumour arises from endothelial cells * Risk factors * thorotrast 10% * vinyl chloride * arsenic * hemochromatosis * neurofibromatosis * Multilocular mass with disseminated appearance and cystic areas * Can mimic Haemangiomas on CT * * Primary hepatic angiosarcoma (PHA) is a rare hepatic tumor, originating from endothelial and fibroblastic tissue, primarily made up of vessels and composed of abundant vasculature. It represents only 0.1–2% of all primary liver malignancies [1]. PHA commonly occurs in ages from 60 to 70 years. * Hepatic angiosarcoma is a rare malignancy but is still the third most common primary liver tumour. They have a variable appearance on both CT and MRI, reflecting the pleomorphic histological nature. Prognosis is very poor, with survival uncommon beyond one year from diagnosis.

Answer 100

* **Epitheliod hemangioendothelioma** * female predominance * middle age * associated with OCP and vinyl chloride * Predominant periphery of the liver, * intratumorsal calcification, * changes of the liver contour with * capsular retraction and * compensatory hypertrophy of the normal liver * Invasion of the PVs and Hepatic veins

Answer 101

* HCC * Ho extrahepatic spread * \<5cm single or multiple * Child A or B Cirrhosis * Mets * \<5cm, single lesion * Vascular lesion * carcinoid * islet cell tumour

Answer 102

* localise lesion uss or ct * advance 20g needle * instill 15-30ml/lesion * withdraw needle * lesions. typically rxd 3 times or until no tumour is apparent * efficacy is comparable to surgery * larger lesions more difficult to treat * mets are more difficult to treat * alcohol doesn't diffuse as well and there is no capsule

Answer 103

* Alternating current at frequencies above 250khx is used to generate heat and destroy tumour tissue. * Indications * Single tumour \<5cm * ideally \<3cm * completely surrounded by hepatic tissue * 1cm or deeper to hepatic capsule * and 2cm or more away from large hepatic or portal veins * Palliation in pts with large liver tuours who have severe pain caused by capsular distension.

Answer 104

* conscious sedaition * localise lesion on CT or US * single or multiple electrodes used * the size of the coagulated area can be increased by use of multiple electrodes or by using a cluster probe (up to 9 separate electrode tips). * can be done percut/laparoscopy or laparotmy * Complicaitons * more likely when tumour is superficial or close to hilar structures. * prolonged ablation time * several lesions treated simultaneously * intraperitoneal hx * liver abscess * intestinal perf * pain fever

Answer 105

* the liver is the most common intraabdominal site of injury * sybcapsular hematoma * hypodense or hyperdense lenticular fluid collection contained by the liver capsule caused by blunt trauma * Laceration * single or multiple stellate configurations usually of low density relative to enhanced parenchyma * Clots may appear high density caused by penetrating or blut trauma * Complications * perihepatic hx * intraperitoneal or extraperionteal hx

Answer 106

* hepatic wedge pressure \> 10mmHg * Portal hypertension is a clinical syndrome defined by a pathological increase in portal pressure. The development of cirrhosis of the liver is characterized by clinical manifestations related to portal hypertension like esophageal varices, ascites, bleeding, and encephalopathy. Direct measurement of portal pressure is invasive, inconvenient, and clinically impractical. Currently, the most commonly used parameter is the Hepatic Venous Pressure Gradient (HVPG), i.e., the difference between the wedged (WHVP) and the free hepatic venous pressures. HVPG represents the gradient between pressures in the portal vein and the intra-abdominal portion of inferior vena cava. When blood flow in a hepatic vein is stopped by a wedged catheter, the proximal static column of blood transmits the pressure from the preceding communicated vascular territory (hepatic sinusoids) to the catheter. Thus, WHVP reflects hepatic sinusoidal pressure and not the portal pressure itself. In the normal liver, due to pressure equilibration through interconnected sinusoids, wedged pressure is slightly lower than portal pressure, though this difference is clinically insignificant. In liver cirrhosis, the static column created by balloon inflation cannot be decompressed at the sinusoidal level due to disruption of the normal intersinusoidal communications; therefore, WHVP gives an accurate estimation of portal pressure in cirrhosis. The normal HVPG value is between 1 to 5 mmHg. Pressure higher than this defines the presence of portal hypertension, regardless of clinical evidence. HVPG \>or= 10 mmHg (termed clinically significant portal hypertension) is predictive of the development of complications of cirrhosis, including death. HVPG above 12 mmHg is the threshold pressure for variceal rupture. The main advantages of HVPG are its simplicity, reproducibility, and safety. This review summarizes the technique of the HVPG measurement. * https://pubmed.ncbi.nlm.nih.gov/18695309/

Answer 107

* Presinusoidal * extrahepatic obstruction of the PV * thrombosis * tumor * compression * inhepatic obstruction of Portal venules * hepatic fibrosis * congenital toxic * copper * PVC * myelofibrosis wilson disease sarcoid * infection * malaria * schistosomiasis * sinusoidal * cirrhosis (most common cause) * sclerosisng cholangitis * post sinusoidal * Budd chiari syndrome * CHF

Answer 108

* Portal vein \>13mm * US: * reversal of flow in right portal flow with normal directional flow in the left PV feeding a recanalised umbilical vein * Collaterals * Gastro-oesophageal varices via coronary vein, azygous * Superior mesenteric vein collateral: mesenteri varices * splenorenal varices * IMV collateral -\> hemorrhoids * Recalization of umbilical vein -\> caput medusa * retroperitoneal colalterals that communicate with phrenci, adrenal and renal veins * Splenomegaly * ascites * mural thickening of stomach, proximal colon, portal gastrophaty/colopathy * Portal biliopathy * venous drainage of the CBD is handled by epicholedochal (saint) and para choledochal (petren) venous Plexi * dilatation of these veins bc of extrahepatic portal venous obstruction can cause mural irregularities and compression of the biliary tree, Appears as irregular strictures of the extrahepatic and intrahepatic bile ducts, segmental dilated segments with beaded appearance, ectasia and pruning of the intrahepatic bile ducts.

Answer 109

* Direct commnication between branches of HA and PV. * Appears as wedge shaped areas of hyperattenuation on late arterial phase CT * Types * Contribute arterial blood to the Portal venous blood supply of venous sinusoids * Transsinusoidsal * most commonly seen in hepatic cirrhosis but may also occur bc of focal infection or nodules of disease compromising portal circulation * when they are seen in cancer pts, attention should be paid to the apex of the lesion where small mets may be evolving. * Transtumoural: * most common in the setting of HCC where a perinodular arteriolar plexus appears to cause a wedge of aterialised parenchyma * both transsinusoidal and transtumor mechanisms contribute to this effect * this pattern is also seen after RF Albation * Transplexal * the wall of the large bile ducts carry a vascular plexus that communicates with HA and drains to both hepatic sinusoids and the portal vein * this type of shunting manifests from the perihilar level. * they are encountered in cirrhosis PV thormosis or occlusion and in the setting of lobar infection * Aerterioportal communication via vasa vasorum of PV * trans vasal * occurs commonly in conjunction with transplexal shunting and is commonly seen in PV occlusion or HCC.

Answer 110

* Thombosis of the main hepatic veins branches of hepatic veins or IVC with possible extension into the PV. * Clinical * ascites * pain * hepatosplenomegaly * Causes * idiopathic 50-75% * Secondary * coag anomalities * clotting disorders * polycythemia * Tumours * HCC, RCC * Trauma * OCP * Chemo * Mottled peripheral hypodensity to the right liver, mainly in the periphery of segments V, VI, VII and VIII. The right and middle hepatic veins do not opacify. The left and caudate lobes of the liver have a normal appearance with normal opacification of enlarged left hepatic veins. The portal veins opacify normally. As best as can be determined the peripheral right portal vein branches opacify normally. The hepatic artery is not well seen secondary to timing of the CT. Splenomegaly. Cholecystectomy. Adrenal glands, kidney and pancreas have a normal appearance. No free fluid or free gas. Bilateral pleural effusions, larger on the left. Minor bibasal atelectasis. Conclusion: Appearances are of right liver hypoperfusion, probably from venous congestion from complete right and middle hepatic vein thrombosis. This represents Budd-Chiari syndrome.

Answer 111

* Veins * absent hepatic veins * Flow in IVC rersed, turbulent diminished or absent * Flow in PV may be reversed or diminished * intrahepatic collateral vessels * Narrowing of the intrahepatic IVC * Liver * hemorragic infarction appears hypoechoic by IS * Caudate lobe is often spared (emisary veins drain directly into the IVC) and appears enlarged, small right lobe * CT * increased central (periportal) parenchymal enhancement * Patchy peripheral enhancement: geographic szones of poorly opacified parenchyma interspersed with well opaciifed zones * Hepatic Venoocclusive disease, which causes progressive occlusion of small vessels, is clinically indistinguishable from BCS * Causes * Toxins from bish tea (jamaica) * Chemotherapy * Bone marrow transplant (GVH)

Answer 112

* Malignancy * chronic pancreatitis * hepatitis * Trauma * Shunts * Hypercoagualble states (pregnancy)

Answer 113

* US * echogenic clot in vein * PV enlargement * Hepatofugal flow * flow in the HA and PV should always be in the same direction: hepatopetal flow (ie towards the liver peripheray) * Opposite flow directs (ie toward the hepatic hilum) in the PV and HA indicate hepatofugal flow. * CT * Clot in PV with collaterals * GO, umbilical collateral vessels * Cavernous transformation * numerous worm-like vessels at the porta hepatis reconstituting intrahepatic portal venous system * Splenomegaly ascities.

Answer 114

pancreatitis

Answer 115

* Aorta * iliac artery * splenic artery * hepatic artery

Answer 116

* Transplant criteria commonly used by the united network of organ sharing. * max diameter of tumour is 5cm if single * no more than 3 liver tumours with max diameter of 3cm * Min of 2cm.

Answer 117

* an expanded set of criteria proposed by the University of California San Francisco (UCSF), * newer and more liberal criteria * solitary tumor smaller than 6.5 cm, * or patients having 3 of fewer nodules, * with the largest lesion being smaller than 4.5 cm * or having a total tumor diameter less than 8.5 cm without vascular invasion, to undergo OLT.

Answer 118

* UGI bleeding secondry to ulcers * biliary : * obstruction * leak fistula * biloma * sludge * Vascular complications * HA thrombosis * most common serious vasuclar complication * more common in kids * usually need another transplant * US shows no arterial flow in liver * Extensive collaterals to the liver * the waveforms of these collateral vessels are abnormal, showing parvus tardus waveform, RIs of Less than 0.5 and systolic acceleration time of greater than 0.1s. * usually occurs at the anastomotic site within 3 moths of transplant * nonanastomic stensois may indicate rejection or hepatic necrosis. * PV thormobisi * less frequent than HA thrombosis US echogenic thrombus can be seen within the lumen of the vessle * HV thormbsis * quite rare because no surgical anastomosis is involved * Rejection * 40%

Answer 119

* Atelectasis and Pleural effusions common * increased periportal attenuation (periportal Collar 70%) (periportal oedema) * ascites * splenomegaly * noninfected loculated intraperitoneal fluid collections * abscesses * hepatic, splenic * perihepatic * pancreatic * Hepatic infarction 10% * Hepatic hematoma * Sludge * inspissated thick bile 15% * maybe extensive and cause biliary casts * Splenic infarction * hepatic calcification * IVC thomrbosis * Pseudoaneusym of HA * Recurrent Hepatic Tumour. Bile cast syndrome (BCS) is a complication of orthotopic liver transplantation (OLT). It is characterized by the presence of biliary casts and debris causing biliary obstruction. It occurs in 4 %-18 % of OLT recipients 1. It can present as cholangitis and graft damage or loss.

Answer 120

* abnormal cholangiograms are seen in 80% of patients with HA stenosis -\> bile duct ischemia * but on in 30% of patients with patent HA * complications include * non-anastomotic strictures 25% * anastomotic strictures 5% * intraluminal filling defects 5% * sludge * casts * Bile leak 5%

Answer 121

* **passive hepatic congestion** * COngested liver in cardiac disease * stasis of blood in liver bc of impaired hepatic venous drainage * Early enhancement of dilated IVC and hepatic veins on CT bc of contrast reflux from RA into IVC * Heterogenous rerticulated mosaic parenchymal patten of liver * Periportal edema * enlarged liver and ascites * cardiomegaly.

Answer 122

* hepatic sarcoidosis * non-caseating granulomas are evident in multiple organs. * most common finding is non-specific hepatosplenomegaly * diffuse parenchymal heterogeneity or multinodular pattern with low attenuating nodules in liver and spleen that gradually become isodense after contrast * Advanced disease may simulate cirrhosis * nodules hypointense on T1 and T2 * periportal adenopathy. https://www.eurorad.org/case/15636 Non-enhanced abdominal CT (Fig. 1) showed cirrhotic changes of the liver, with increased size of the left and caudate lobe, contour irregularity, and parenchymal heterogeneity. Contrast-enhanced abdominal CT (Fig. 1) revealed a pattern of multiple hypodense macro-nodules. Signs of portal hypertension or involvement of the spleen were absent. Abdominal MRI (Fig. 2) was scheduled. T1-weighted MR-images showed large confluent hypointense nodules. Nodules appeared slightly hyperintense in T2-weighted MR-images, hypointense on T2-weighted fat-saturated MR-images, and demonstrated signal dropout on opposed-phase images. Abdominal lymph nodes were not enlarged. No foci of abnormal enhancement or restricted diffusion were detected. Vascular architecture and bile duct morphology were intact. A liver biopsy was performed, revealing non-caseating epithelioid granulomas, large regenerative nodules with fat deposition and fibrotic changes (Fig. 3). A subsequent chest CT (Fig. 4) revealed mild hilar and mediastinal lymphadenopathy. Intrapulmonary nodules were also seen. Resolution of chest imaging findings was noted after 6 months of treatment with corticosteroids and azatheioprine.

Answer 123

* HELLP * Haemolysis * elevated liver enzymes * Low platelets * Variant of preeclampsia in primigravidas. rarely seen in multis * intrahepatic or subcapsular fluid collection (hematoma) on US or CT * Liver infarction with small or large peripheral wedge shaped hypoattenuating lesions

Hepatobilary Flashcards

(155 cards)