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FUNDAMENTALS OF BODY CT > Liver > Flashcards

Liver Flashcards

1
Q

Anatomic segments of the Liver

A

Couinaud classification: I-VIII segments. Each segment is self contained: Hepatic artery, portal vein, biliary tract and hepatic vein. Divides liver in three vertical planes (right HV, left HV and middle HV) and one transverse plane (left and right HP)

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2
Q

Drainage of the Caudate lobe

A

Directly to IVC

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3
Q

Anatomic variants of Liver irrigation

A

Classic hepatic artery (55%)

  1. Accesory Hepatic Vein: Drains segment 5-6 to IVC
  2. Common trunk of MHV and LHV before joining IVC (65-86%)
  3. Left hepatic artery <– Left gastric artery
  4. Right hepatic artery <– SMA
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4
Q

Proceso Papilar

A

Normal caudate lobe variant, it extends towards the lesser sac, may simulate a mass or enlarged lymphnode

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5
Q

Clasificación anatómica clásica de hígado

A

Lóbulo caudado, Lóbulo izquierdo lateral (superior, inferior), medial (superior inferior), Lóbulo derecho anterior (superior, inferior) y posterior (superior, inferior)

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6
Q

Normal Liver Hounsfield Units

A

40-60 HU. <40 is hypodense (or >10 HU difference between spleen and liver) . >75 is hyperdense

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7
Q

Riedel Lobe

A

Right lobe of the liver that extends far caudal (normal anatomic variant)

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8
Q

Diaphragmatic Slips

A

Infolding os the diaphragm that ident the normal smooth contour of the liver (normal)

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9
Q

Liver CT protocol

A

Phases: non-contrast, arterial (25 secs), porto-venous (65 secs), equilibrium (2-3 mins), late (10-20 mins)

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10
Q

Third Inflow (Concept)

A

Systemic veins causes perfusion abnormalities in predictable areas of the liver, they communicate with portal venous branches, focally decreasing portal venous flow and resulting in an increase in hepatic arterial flow in the same area

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11
Q

Third Inflow (Common Areas)

A

A) Segments 4-5: Cholecystic vein (may allow direct spread of CA from gallblader)
B) Segment 4 (posterior): Aberrant right gastric vein (Gastric CA spread)
C) Segment 2-3: Aberrant left gastric vein (Gastric CA spread)
D) Segment 4 (dorsal): Parabiliary veins
E) Segment 3-4 (anterior): Epigastric-paraumbilical veins (Collaterals in portal hypertension)

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12
Q

Third Inflow (Tumours)

A

A) Hipervascular tumours may have intratumoral arterioportal shunts. They produce transient, peripheral wedge-shaped enhancement zones during arterial phase (Pitfall: don’t mistake them with a tumour)
B) Tumor invasion/thrombosis/compression may obstruct portal veins, generating decreased attenuation of parenchyma.

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13
Q

Confident diagnosis of fatty infiltration

A
  1. Angulated geometric margins
  2. Interdigitating margins
  3. Abscence of mass effect, vessel displacement or narrowing by encasement
  4. Rapid change over time
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14
Q

Causes of increased liver attenuation

A

1) Iodine: Amiodarone
2) Gold: Gold Salts
3) Iron: Hemochromatosis 1°, 2° (Hemosiderosis)
4) Copper: Wilson disease
5) Glycogen: Glycogen storage diseases

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15
Q

Cirrhosis CT findings

A
  • Fatty infiltration with hepatomegaly
  • Hereogeneous parenchymal attenuation/enhancement
  • Nodular or irregular lobulated surface
  • Atrophy of right lobe with hypertrophy of the left and caudate lobes
  • Total liver volume loss (shrunken and deformed)
  • Prominece of porta hepatis and intrahepatic fissures
  • Signs of portal hipertension (Ascites, splenomegaly, etc.)
  • Serous cysts adjacent to intrahepatic and extrahepatic bile ducts
  • Enlarged lymph nodes (>1 cm) at porta hepatis and portocaval spaces
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16
Q

Diferential diagnosis of Cirrhosis

A

Treated breast cancer metastases, miliary metastases, Budd-Chiari syndrome and fulminant hepatic failure

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17
Q

Laënnec cirrhosis

A

Alcoholic micronodular cirrhosis, related to absortion of alcohol directly from the stomach to the right hepatic lobe in the portal venous system (atrophy right lobe and hypertrophy of left/caudate lobes)

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18
Q

Cirrhosis causes

A

Chronic alcoholism, chronic viral hepatitis, NASH, primary schlerosing cholangitis, primary biliary cirrhosis and genetic diseases (Autoimmune hepatitis, wilson disease, hemochromatosis, etc.)

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19
Q

Nodules in cirrhosis

A

1) Regenerative nodules
2) Dysplasic nodules
3) Small HCC nodules

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20
Q

Small HCC Nodule characteristics

A

1) Isointense on non-contrast CT
2) Hypervascular on arterial phase
3) Rapid wash-out on venous phase

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21
Q

Most frequent hepatic metastatic diseases

A

Breast cancer, small cell lung carcinoma, melanoma, carcinoid, pancreatic carcinoma

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22
Q

Hepatic simple cysts characteristics

A

1) Uniform low attenuation.
2) Sharp margination.
3) Imperceptible wall.
4) No contrast enhancement.

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23
Q

Focal Confluent Fibrosis

A

Focal, wedge-shaped, fibrotic mass, extending from the porta hepatis to the liver periphery, with capsular retraction.

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24
Q

Portal Hypertension Findings

A

1) Portosystemic collateral vessels (Esophageal, para esophageal, gastric varices, paraumbilical veins, caput medusae, splenorenal shunts and perisplenic collaterals)
2) Portal vein and branches enlarged >13 mm
3) Splenic and SMA enlarged >10 mm
4) Splenomegaly
5) Ascites

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25
Q

Types of Portal Vein Thrombosis

A

Classified as bland (low attenuation, non enhancing filling or partially filling the lumen) or neoplasic (low attenuation, arterial enhancement)

26
Q

Causes of Portal Vein Thrombosis

A

1) HCC
2) Cirrhosis
3) Hepatoma
4) Hypercoagulability
5) Pancreatitis
6) Pancreatic CA
7) Trauma
8) Mesenteric inflammation

27
Q

“Cavernous Transformation”

A

Development of numerous periportal collateral veins in response to chronic portal vein thrombosis

28
Q

Passive Hepatic Congestion

A

Causes: Right heart failure, constrictive pericarditis, pericardial effusion. Generates: Rise in Venous pressure, IVC, hepatic veins, chronic congestion and statis in the hepatic sinusoids, inchemic injury, fatty infiltration and cirrhosis
Nutmeg liver (mottled mosaic pattern)

29
Q

Budd-Chiari Syndrome generalities

A

Generates increase of portal vein pressure due to hepatic venous outflow obstruction
FR: Pregnancy, ACO, QT, RT, policytemia vera.
Causes: Neoplasic obstruction of HV or HVI (HCC, RCC, adrenal carcinoma), chronic idiopathic fibrosis and congenital

30
Q

Acute Budd-Chiari Syndrome CT findings

A

Acute (1-3 months): Liver is enlarged and hypoattenuating, but with normal morphology on noncontrast CT, hepatic veins and IVC are narrowed, after contrast the caudate lobe and liver surrounding the IVC show early enhancement, and in portal phase liver periphery is enhanced while the contrast medium is being washed out (Flip-flop appereance).

31
Q

Chronic Budd-Chiari Syndrome CT findings

A

Enlarged caudate lobe, dysmorphic liver, atrophy and multiple regenerative nodules (1-4 cm), portal hypertension, azygos vein is enlarged

DD: HCC nodules: Key: BCS nodules remain relatively hyperdense in the portal venous phase

32
Q

Hereditary Hemorragic Talangiectasia

A

Osler-weber-rendu syndrome, autosomal dominant disorder with variable penetrance characterized by multiorgan talangiectasias and AV malformations

33
Q

Hereditary Hemorragic Talangiectasia CT findings

A

1) Talangiectasias: Hypervascular masses 1-10 mm, high density at no contrast.
2) Confluent vascular channels: >1 cm, coalescense of talangiectasias.
3) Vascular malformations: Arterial phase filling of portal vein (Hepatic artery to portal vein shunt) and hepatic vein (Hepatic artery to hepatic vein shunt).
4) Dilation of Hepatic common artery >10 mm.
5) Biliary alterations (Cysts, strictures, dilatation).
6) Other organs: Pancreas, heart, lungs, GI, etc.

34
Q

Hepatic Sarcoidosis

A

Non caseating granulomas in various organs. 94% have liver involvement and 70% spleen. CT findings:
1) Hepatomegaly.
2) Innumerable hypoattenuating lesions (<2 cm).
3) Hypovascular.
4) Diffuse lymphadenophaty (30%), sometimes massive >2 cm (10%).
5) Usually Asymptomatic.

35
Q

Viral Hepatitis findings in CT

A

Heterogeneous enhancement, periportal edema, focal low attenuation areas and gallbladder wall thickening.

36
Q

Metastases generalities and types

A

Most common malignant tumor in liver (18:1), wide spectrum of appereances:
1) Low attenuation, well defined, solid mass, vague peripheral enhacement, target sign.
2) Hypervascular metastases: washout during delayed phase
3) Cystic necrotic Tumors: Low attenuation centrally, non-enhancing.
4) Calcified.

37
Q

Hypervascular metastases examples (7)

A

1) Carcinoid
2) Choriocarcinoma
3) Melanoma
4) Pancreatic neuroendocrine tumour
5) Pheochromocytoma
6) Renal Cell Carcinoma
7) Thyroid carcinoma

38
Q

Cystic/necrotic metastases examples (4)

A

1) Mucinous colon carcinoma
2) Lung carcinoma
3) Melanoma
4) Carcinoid

39
Q

Calcified metastases examples (3)

A

1) Mucinous adenocarcinoma
2) Osteosarcoma
3) Chondrosarcoma

40
Q

Hepatocellular Carcinoma

A
  • Most common primary hepatic malignancy
  • RF: Cirrhotic liver, males, >50 y/o
  • Elevated Alpha-fetoprotein
  • 40% of HCC in cirrhotic livers are missed
  • Use LI-RADS for standarized evaluation (specially <2 cm)
41
Q

LI-RADS (Who?)

A

Yes: Patients with cirrhosis, chronic hepatitis B or current/prior HCC
No: <18 years old, cirrhosis secondary to vascular cirrhosis or congenital hepatic fibrosis

42
Q

LI-RADS major criteria (4)

A

1) Hyperenhacement of the lesion in arterial phase
2) Lesion “washout” in portal venous and delayed phases
3) Peripheral rim of hyperenhacement of the capsule or pseudocapsule
4) Increase in diameter of the mass (>50% in 6 months)

43
Q

LI-RADS tumor in vein criteria (4)

A

1) Unequivocal soft tissue in hepatic or portal veins (definite)
2) Ocluded vein with ill-defined walls (not definite)
3) Occluded or obscured vein in contiguity with malignant mass (not definite)
4) Heterogeneous vein enhancement not attributable to artifact (not definite)

44
Q

LI-RADS ancillary signs for HCC (5)

A

1) nonenhancing capsule
2) Nodule-in-nodule appereance
3) Mosaic architecture
4) Fat in mass
5) Hemorrage within or adjacent to the lesion

45
Q

LI-RADS ancillary signs favoring benignity (5)

A

1) Stable size >2 years
2) Unequivocal reduction in size
3) Enhancement pattern that parallels blood pool enhacement
4) Vessels transverse mass without displacement or distortion
5) presence of iron in mass

46
Q

Imaging features of HCC >2 cm (6)

A

1) Pattern of growth: 50% Solitary tumor, 30% diffuse infiltrative tumor, 20% multinodular tumor
2) Dominant mass with nearby satellite lesions
3) Avid contrast enhancement in arterial phase with washout in portal-delayed phase
4) Calcifications 25%, tumor invasion of hepatic 12-54% and portal veins 29-65%, may extend to IVC and right atrium.
5) Fat deposition
6) Extrahepatic spread to: lungs, pleura, lymphnodes in abdomen, bones and adrenal glands

47
Q

Peripheral mass-forming intrahepatic Cholangiocarcinoma

A
  • Second most common primary malignant liver tumor (10-20%)
  • Adenocarcinoma of bile ducts
  • Solid mass with sharp rounded, lobulated, ill-defined margins
  • Large at diagnosis >15 cm
  • Low attenuation, bile duct dilation peripheral to the tumor
  • Peripheral enhancement in arterial phase (peripheral to central cells), portal venous washes out (isodense to hypodense, delayed gradual central enhancement
  • <3 cm may be hypervascular
  • It can invide the portal vein
48
Q

Fibrolamellar Carcinoma

A
  • Rare (<1% of HCC), slow growing tumour, arrises from normal liver, young (<40 years old), no elevated AFP.
  • Large mass (often >12 cm).
  • Enhancement mainly during arterial and portal venous phase
  • Fibrous tissue extends in the mass and separates it on “islands”, coalescenses into a central scar (observable during elimination phase).
  • Cirrhoses, vascular invasion and multifocal carcinoma are rare with FMC
  • 50% have enlarged porta hepatis, lymphnodes.
49
Q

Hepatic Lymphoma

A

Secondary lymphoma:
- Diffuse or multiple.
- Diffuse infiltration with only hepatomegaly.
- Multiple well defined, large.
homogeneous low attenation nodules.
May show target sign.

50
Q

Hepatic Adenoma

A

Rare, women 90% who use ACO or men with anabolic steroids
- Surgical required because: risk of rupture or malignancy.
- AFP normal
- Contrast washout rapidly, no enhance at portal-venous and elimination phases.
- Intratumoral hemorrage is common 25-40%
- Calcifications 10%

51
Q

Hepatic Adenomatosis

A

> 10 Hepatic adenoma in the liver

52
Q

Focal Nodular Hyperplasia

A
  • Second most common benign hepatic tumor.
    Homogeneous enhancement in arterial phase.
  • Washout in portal venous phase.
  • Incidentally, asymphtomatic, 95% < 5 cm
  • Fibrous bands and central stellate fibrous scars are characteristic.
  • No treatment needed
53
Q

Cavernous Hemangioma

A
  • Second most common focal mass of the liver (7% of people).
  • Large thin-walled, blood-filled vascular spaces lined by epithelium and separated by fibrous septa.
  • Hypodense, isoatenuation with arterial blood, arterial phase: early, peripheral, discontinous, nodules.
  • Porto-venous phase: Progressive fill in-enhancement from the periphery
  • Delayed phases: Idem
  • Rarely seen in cirrhosis
54
Q

Hepatic Cysts

A
  • 20% of population
  • Low density with internal attenuation of water (<20 HU), Solitary or multiple, non enhancement
55
Q

Biliary Cystoadenomas

A

Uncommon cystic neoplasm that arises from mucin-secreting columnal epithelum, risk of malignan transformation 20%, complex cystic mass 3-40 cm, well defined thick fibrous capsule, internal septation

56
Q

Von Meyenburg complexes

A

Biliary hematomas, small <15 mm, benign, asymptomatic, appear as simple cysts with predilection for the subcapsular region, absence of communication with the biliary tree (different than Carioli Disease),

57
Q

Polcycystic Liver Disease

A
  • Autosomal dominant polycystic kidney disease (70%)
  • Autosomal dominant polycystic liver disease (30%)
  • Asymptomatic, generally normal hepatic function.
  • Complications are uncommon: Massive hepatomegaly, abdominal pain, intracystic hemorrage, infection, portal hypertension
  • Cysts: Peripheral simple cysts (>8 cm), peribiliary cysts (<1 cm)
58
Q

Pyogenic Abcess

A
  • Pus and debris in area of destroyed liver
  • Direct extension from bowel infection
  • Causes: Appendicitis, diverticulitis, trauma
  • 85% pyogenic, E.Coli is the most frequent
  • Characteristics: Usually solitary, multiloculated, thickened enhancing walls
  • Density: 0-45 UH
  • Gas bubbles within the lesion in 20% of cases
  • Biliary obstruction and thrombophlebitis are most common associated findings
59
Q

Amebic abcess

A
  • Caused by Entamoeba histolytica
  • 3-7% of amebiasis
  • 6% of liver abcess
  • Similar image than pyogenic abcess
60
Q

Hydatid Cyst

A
  • Echinococcus granulosus
  • Adquired by contaminated food
  • Eosinophilia is common
  • Hydatid sand and daughter cysts
61
Q

Fungal Abcess

A
  • Immunecompromised patients
  • Diseminated microabcesses
  • Candida albicans is the most common pathogen
  • CT: Innumerable hypoattenuating hypovascular lesions (2-20 mm in size)
  • May have peripheral ring enhancement
  • Complications: Cholangitis, rupture of microabcesses
  • Healing might calcify the lessions

FUNDAMENTALS OF BODY CT (8 decks)

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