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PRESENTER : DR. ANNU SHRI
HEPATIC INFLAMMATORY
AND
INFECTIOUS DISEASES
ANATOMY
IMAGING TECHNIQUE OF LIVER
οƒ˜ ULTRASONOGRAPHY
οƒ˜ COMPUTED TOMOGRAPHY
οƒ˜ MAGNETIC RESONANCE IMAGING
οƒ˜ RADIONUCLIDE SCANNING
οƒ˜ IDEAL ORGAN.
οƒ˜ EASY TO APPROACH.
οƒ˜ STANDARD ULTRASOUND – GREY SCALE.
οƒ˜ DOPPLER EVALUATION.
οƒ˜ CONTRAST ENHANCED ULTRASOUND.
οƒ˜ ELASTOGRAPHY.
ULTRASOUND
VARIOUS HEPATIC PROTOCOLS :
οƒ˜ NON-CONTRAST MDCT
οƒ˜ MONOPHASE MDCT : Portal venous phase ( 30 sec delay).
οƒ˜ DUAL PHASE MDCT : Arterial (Arterial bolus tracking) & Portal venous.
οƒ˜ TRIPLE PHASE MDCT: NCCT , Arterial and Portal venous phase.
COMPUTED TOMOGRAPHY
VARIOUS SEQUENCES USED:
οƒ˜ T2 WEIGHTED
οƒ˜ T1 WEIGHTED IP, OP, WATER ONLY, FAT ONLY.
οƒ˜ T2 WEIGHTED FAT- SAT
οƒ˜ T1 WEIGHTED FAT- SAT : - TRIPLE ARTERIAL PHASE
- PORTAL VENOUS PHASE
- MRCP
- EQUILIBRIUM PHASE
MRI
οƒ˜ VIRAL HEPATITIS
οƒ˜ ALCOHOLIC HEPATITIS
οƒ˜ RADIATION INDUCED HEPATITIS
οƒ˜ PELIOSIS HEPATIS
INFLAMMATORY DISEASES
INFECTIOUS DISEASES
οƒ˜ PYOGENIC LIVER ABSCESS
οƒ˜ AMEBIC LIVER ABSCESS
οƒ˜ FUNGAL ABSCESS
οƒ˜ INFLAMMATORY PSEUDOTUMOUR
οƒ˜ GRANULOMA ( TB , SARCOIDOSIS)
οƒ˜ EOSINOPHILIC ABSCESS
οƒ˜ PARASITIC DISEASE
οƒ˜ HEPATIC SARCOIDOSIS
οƒ˜ HEPATIC CANDIDIASIS
οƒ˜ HEPATIC SCHISTOSOMIASIS
οƒ˜ CAUSE – hepatitis A(picorna virus), B (hepadna), C(flavivirus), E, F(togavirus)
& G (GBV-C).
οƒ˜ Uncomplicated acute hepatitis clinical recovery within 4 months.
οƒ˜ > 6 month – Chronic hepatitis
οƒ˜ USG- periportal cuffing. Chronic - coarsening of echotexture.
-GB wall thickening / contraction. -periportal lyphadenopathy
- hepatosplenomegaly.
VIRAL HEPATITIS
Acute hepatitis.
A, Sagittal, and B, transverse,
images of the left lobe of the
liver show marked increased
thickness and echogenicity of
the soft tissue surrounding the
portal vein branch, called
periportal cuffing.
C, Sagittal, and D, transverse,
views of the gallbladder with
marked mural thickening, such
that the lumen is virtually
obliterated. The gallbladder wall
shows a multilayered appearance
with extensive hypoechoic
pockets of edema fluid.
A B
C D
Acute hepatitis. Acute hepatitis in
patient with fever, abnormal liver
function tests, and incidental
gallstones.
A, Transverse view of porta
hepatis, and B, transverse view of
left lobe of liver, show thick,
prominent echogenic bands
surrounding the portal veins in the
portal triads, called periportal
cuffing.
C, Sagittal, and D, transverse,
views of the gallbladder show
moderate edema and thickening of
the gallbladder wall. The
allbladder is not large or tense, and
the patient does not have acute
cholecystitis. As this case
illustrates, incidental cholelithiasis
may be confusing
A B
C D
Acute viral hepatitis in a 39-year-old man as seen on contrast-enhanced MDCT
acquired during the arterial phase (A) and the portal venous phase (B). Note the
heterogeneous contrast enhancement in the edematous enlarged liver.
A B
Precontrast OP (A) and contrast-enhanced fat-saturated (B) T1-weighted hepatic MRI in a
54-year-old man with chronic viral hepatitis.
A B
MRI :- generalised hepatomegaly with edematous liver (hyper intense on T2WI and early post contr.)
- periportal T2 hyperintense signal
Chronic hepatitis :- absence of patchy enhancement suggest low inflammatory rx.
- progressive enhancement in delayed phase suggest presence of liver fibrosis.
οƒ˜ 3 Distinct overlapping entities:
οƒ˜ Fatty liver. Alcoholic hepatitis. Cirrhosis
ALCOHOLIC HEPATITS
On CT :-
οƒ˜ Sharply defined hypodense area in liver corresponding to radiation ports.
οƒ˜ Represents edema or fatty infiltration of involved area.
οƒ˜ Onset : 2-6 wks after therapy
οƒ˜ Dose > 35 Gy to liver.
οƒ˜ Resolve in 3-5 months.
On MRI:-
οƒ˜ Geographic areas of oedema on T1 & T2WI.
RADIATION HEPATITIS
οƒ˜ Pathogenesis:- unknown / general outflow obstruction of the sinusoids with
breakdown of the sinusoidal barriers .
οƒ˜ Agents associated :- anabolic steroids, corticosteroids, tamoxifen,
diethylstilbestrol, azathioprine, and oral contraceptives.
οƒ˜ Microscopically :- dilatated sinusoids with multiple blood-filled lacunar spaces.
οƒ˜ Macroscopically:- hepatomegaly.
οƒ˜ MDCT :- multiple small hypodense lesions <1 cm in diameter on noncontrast
images; centrifugal contrast uptake during portal venous phase. --Thrombosed
venous branches remain hypodense during parenchymal phase imaging.
PELIOSIS HEPATIS
Contrast-enhanced fat-saturated T1-weighted hepatic
MRI shows peliosis hepatis (arrows) that developed in
this 59-year-old woman while she was being treated
with tamoxifen.
οƒ˜ MRI :- small hypointense lesions on T1WI /
hyperintense on T2WI.
οƒ˜ Larger lesions imaging characteristics of
blood at different phases of organization.
Contrast-enhanced fat-saturated T1-weighted hepatic MRI
shows peliosis hepatis (arrows) that developed in this 51-year-
old woman while she was being treated with steroids.
οƒ˜ Miliary TB (MC Form)
οƒ˜ Radiological abnormalities absent because of its diffuse micronodular
nature.
οƒ˜ Macronodular tuberculomas :- solitary / multiple.
οƒ˜ On USG :- Hypoechoic.
οƒ˜ On CT:- hypodense lesions with/ without rim enhancement.
οƒ˜ Tubercular abscess rupture – cholangitis (bile ducts)/ pylephlebitis (PV)
οƒ˜ Old healed granuloma – multiple small intrahepatic calcifications.
TUBERCULOSIS
οƒ˜ Most common hepatic presentation of multisystem sarcoidosis - Boeck’s
sarcoid - Noncaseating epithelioid granulomas (submillimeter to 1 to 2 cm)
scattered throughout the liver.
οƒ˜ Unknown pathophysiology.
οƒ˜ Bihilar lymphadenopathy.
οƒ˜ Coexisatance with primary sclerosing cholangitis /other autoimmune
diseases.
οƒ˜ Larger granulomas contain greater amounts of reticulin and are
surrounded by fibrotic hepatic parenchyma, reflecting a more vigorous
immunologic response.
SARCOIDOSIS
οƒ˜ Acute complications:- Hepatic failure due to
intrahepatic cholestasis -Portal hypertension.
οƒ˜ Multisystem sarcoidosis mortality (10%) - due to
cor pulmonale, lung fibrosis, and liver cirrhosis.
οƒ˜ NCE MDCT :- Multiple intrahepatic and
intrasplenic hypodense lesions accompanied by
nonspecific hepatosplenomegaly.
- On post-contrast : Isodense.
οƒ˜ MRI demonstrates :- Noncaseating epithelioid
granulomas as hypointense intrahepatic and
intrasplenic nodules on T1 and T2WI.
οƒ˜ Advanced-stage hepatic sarcoidosis may present
as liver cirrhosis.
Contrast-enhanced MDCT shows multisystemic
sarcoidosis of the liver and spleen. With disseminated
distribution of innumerable hepatic lesions.
Contrast-enhanced MRI with multisystemic sarcoidosis
of the liver and spleen.
οƒ˜ Routes :- biliary tree routes, following suppurative cholangitis and
cholecystitis.
οƒ˜ Other routes are through the portal venous system in diverticulitis or
appendicitis and hepatic artery.
οƒ˜ Presenting features:- fever, malaise, anorexia and right upper quadrant pain.
Jaundice (25%)
οƒ˜ D/D’S :- Amebic or echinococcal infection, simple cyst with hemorrhage,
hematoma, and necrotic or cystic neoplasm.
οƒ˜ Ultrasound-guided liver aspiration
PYOGENIC (BACTERIAL) LIVER
ABSCESS
οƒ˜ On USG:- Frankly purulent abscesses appear
cystic, with the fluid ranging from echo free to
highly echogenic.
οƒ˜ Solid with altered echogenicity -early
suppuration.
οƒ˜ Hypoechoic- Necrotic hepatocytes.
οƒ˜ Gas-producing organisms can give rise to
echogenic foci with a posterior reverberation
artifact.
οƒ˜ Fluid-fluid interfaces, internal septations and
debris.
οƒ˜ Wall can vary from well defined to irregular and
thick.
A
B
C
Early lesions. A and B, Rapid evolution from
phlegmon to liquefaction. A, Poorly defined mass effect or phlegmon
in segment 7 of the liver. B, At 24 hours later, there is a central
area of liquefaction. C, Early abscess is poorly marginated and bulges
the liver capsule. It is difficult to characterize this mass as solid or
cystic. There was no vascularity within this or other masses.
Mature abscess cavities in three patients. D to F, Classic mature
abscess as a well-defined mass with liquefaction and internal debris.
D E F
G H I
Abscesses related to gas-forming organisms. G, Multiple gas bubbles seen as innumerable bright echogenic foci within a poorly defined
hypoechoic liver mass. H, Sagittal image of the left lobe of the liver, and I, confirmatory CT scan, show a liver mass with extensive gas content.
οƒ˜ On NECT – marked
hypodensity , due to presence
of pus in centre.
οƒ˜ On CECT- Enhancing
peripheral rim.
οƒ˜ Lobulated contour or
circumferential transitional
zones of intermittent
attenuation.
οƒ˜ Cluster sign :- smaller lesion
<2 cm clustering together or
into large abscess.
οƒ˜ Double target sign : due to
perilesional edema.
οƒ˜ Gas bubbles / air fluid level.
A, On precontrast CT scan there is a hypodense mass (arrow). B, On arterial-
phase CT the mass has a target-like appearance (arrow)β€”a hypodense center
surrounded by an enhanced hyperdense middle and a hypodense periphery.
Transient wedge-shaped segmental enhancement is also observed surrounding
the mass (arrowhead).
A
B
οƒ˜ On MRI :- Hypointense on T1WI.
οƒ˜ Hyperintense on T2WI.
οƒ˜ Signal void due to presence of gas.
οƒ˜ On post contrast – early intensely enhancing abscess wall
- prominent perilesional enhancement.
A, On fat-suppressed T2-weighted MRI there is an inhomogeneous hyperintense mass (arrow) with a very hyperintense area, suggesting a collection of
pus. B, On arterial-phase Gd-enhanced T1-weighted MRI the peripheral part of the mass shows wedge-shaped segmental enhancement (arrowhead).
Septum-like enhancement in the mass is also observed (arrow). C, On the equilibrium-phase image a nonenhanced cystic mass with an enhanced
irregular thick wall is visualized (arrow).
οƒ˜ Entameba histolytica.
οƒ˜ Amoebic liver abscess (mc extraintestinal manifestation)
οƒ˜ Protozoan reaches the liver by penetrating through the colon, invading the
mesenteric venules and entering the portalvein. Or via lymphatics or
directly extends into the liver from the hepatic flexure.
Pathology
Destructionof liver necrotic tissue including the viable organism lesion
increases in size + central cavitation+ active organism.
Solitary lesion - right lobe. (venous drainage from infected right colon, via
the superior mesenteric vein to the portal vein)
AMEBIC ABSCESS
οƒ˜ On USG :- round or oval lesion, absence of
a prominent abscess wall, hypoechogenicity
compared to normal liver.
οƒ˜ Fine low level internal echoes, distal
enhancement and continuity with the
diaphragm.
οƒ˜ Two patterns 1. Round or oval shapes.
2.Hypoechoic appearance
with fine internal echoes
οƒ˜ On CT:- lowattenuation lesions, (density
dependenton stage of development and
internal contents).
οƒ˜ Early stages-similar to solid tumors.
οƒ˜ Older abscesses - cystic in appearance.
οƒ˜ The zone of inflammation - isodense to
hypodense on unenhanced CT scans
οƒ˜ Enhances after contrast administration.
οƒ˜ Thin outer rim of lower attenuation.
οƒ˜ Uncommon
οƒ˜ Opportunistic infection seen in Immunocompromised hosts- On intensive
chemotherapy, AIDS, lymphoma, acute leukemia.
οƒ˜ Liver involved secondary to hematogenous spread of mycotic infections in
other organs, mc primary site- lungs.
οƒ˜ candida is the most common
FUNGAL INFECTION
οƒ˜ On CT - most common pattern is multiple small, rounded areas of
decreased attenuation. Areas of scattered increased attenuation
representing calcification.
οƒ˜ Liver lesions characteristically form a honeycomb abscess that contains 1-
to 2-mm fungus balls.
οƒ˜ Periportal areas of increased attenuation, correlating with fibrosis.
οƒ˜ Candida microabscesses have been reported as cold lesions on both
sulphur colloid and gallium scans.
οƒ˜ On MR - increased signal intensity on T1WI & STIR sequences.
Hepatic and splenic microabscesses (Candida) in a patient with acute myelogenous leukemia. A, In the arterial phase of dynamic CT there are
multiple small nodules with faint peripheral ringlike enhancement in the liver and spleen (arrows). B, On equilibrium-phase CT they appear hypodense
compared with the background liver (arrows).
οƒ˜ Echinococcus granulosus and Echinococcus multilocularis.
οƒ˜ Echinococcus alveolaris - rare , most aggressive.
οƒ˜ Humans – intermidiate hosts.
οƒ˜ In human liver, cysts grow to 1 cm during the first 6 months and 2-3 cm
annually, depending on host tissue resistance. (right lobe)
οƒ˜ Hydatid Cyst Structure:- 3layers
a. Outer - pericyst, modified host cells, form a dense and fibrous protective
zone.
b. Middle laminated - ectocyst allows passage of nutrients.
c. Inner - germinal layer, scolices (the larval
stage of the parasite) and the laminated membrane are
produced. (true wall).
HYDATID DISEASE
οƒ˜ On USG:- well-defined anechoic cyst.
οƒ˜ Snowstorm sign.
οƒ˜ US water lily sign.(floating memberanes)
οƒ˜ Wheel spoke sign (internal septae)
A, Baseline sonogram shows a fairly simple cyst
in the right lobe with a small mural nodule and a
fleck of peripheral calcium anteriorly. B, Three
weeks later the patient presented with right
upper quadrant pain and eosinophilia. The
detached endocyst is floating within the lesion.
Hydatid liver disease:
spectrum of
appearances. A, Classic
appearance showing a cyst
containing multiple
daughter cysts. B,
Sonogram, and C,
confirmatory CT scan,
show a unilocular and
simple cyst, a fairly
uncommon morphology
for hydatid
disease. D, Sonogram
shows a complex mass.
Anteriorly, multiple ringlike
structures suggest hydatid
disease. At surgery, cystic
mass showed
thick debris and
innumerable scolices. E,
Sonogram, and F,
confirmatory CT scan,
show an indeterminate
mass with a thin rim of
calcification. G, Complex
mass similar to that seen in
D. There are fingerlike
projections within, again
suggestive of hydatid
disease.
H, Sonogram, and I,
confirmatory CT scan,
show a central liver mass
with rim and internal
punctate calcification.
οƒ˜ Hepatic schistosomiasis is caused by Schistosoma mansoni(most severe), S.
japonicum, S. mekongi, and S. intercalatum.
οƒ˜ Most common parasitic infections in humans, affect 200 million people
worldwide.
οƒ˜ Ova reach the liver through the portal vein and incite a chronic
granulomatous reaction, terminal portal vein branches become occluded.
οƒ˜ Presinusoidal portal hypertension, splenomegaly, varices, and ascites.
οƒ˜ On USG:- Widened echogenic portal tracts, meas. upto 2 cm.
οƒ˜ Most affected region - porta hepatis.
οƒ˜ Liver size is enlarged. As the periportal fibrosis progresses, liver
becomes contracted, and the features of portal hypertention appears.
SCHISTOSOMIASIS
οƒ˜ MC opportunistic infection in
immucompatients(AIDS).
οƒ˜ MC cause of life-threatening infection in
patients with HIV.
οƒ˜ Similar sonological pattern is seen in:-
Mycobacterium avium-intracellulare and
cytomegalovirus.
PNEUMOCYSTIS CARINII
Disseminated P.
carinii infection in AIDS patient who previously
used pentamidine
inhaler. Sonogram shows innumerable tiny,
bright echogenic
foci without shadowing throughout the liver
parenchyma.
Hepatic inflammatory and infectious dis.
Hepatic inflammatory and infectious dis.

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Hepatic inflammatory and infectious dis.

  • 1. PRESENTER : DR. ANNU SHRI HEPATIC INFLAMMATORY AND INFECTIOUS DISEASES
  • 3. IMAGING TECHNIQUE OF LIVER οƒ˜ ULTRASONOGRAPHY οƒ˜ COMPUTED TOMOGRAPHY οƒ˜ MAGNETIC RESONANCE IMAGING οƒ˜ RADIONUCLIDE SCANNING
  • 4. οƒ˜ IDEAL ORGAN. οƒ˜ EASY TO APPROACH. οƒ˜ STANDARD ULTRASOUND – GREY SCALE. οƒ˜ DOPPLER EVALUATION. οƒ˜ CONTRAST ENHANCED ULTRASOUND. οƒ˜ ELASTOGRAPHY. ULTRASOUND
  • 5. VARIOUS HEPATIC PROTOCOLS : οƒ˜ NON-CONTRAST MDCT οƒ˜ MONOPHASE MDCT : Portal venous phase ( 30 sec delay). οƒ˜ DUAL PHASE MDCT : Arterial (Arterial bolus tracking) & Portal venous. οƒ˜ TRIPLE PHASE MDCT: NCCT , Arterial and Portal venous phase. COMPUTED TOMOGRAPHY
  • 6.
  • 7. VARIOUS SEQUENCES USED: οƒ˜ T2 WEIGHTED οƒ˜ T1 WEIGHTED IP, OP, WATER ONLY, FAT ONLY. οƒ˜ T2 WEIGHTED FAT- SAT οƒ˜ T1 WEIGHTED FAT- SAT : - TRIPLE ARTERIAL PHASE - PORTAL VENOUS PHASE - MRCP - EQUILIBRIUM PHASE MRI
  • 8. οƒ˜ VIRAL HEPATITIS οƒ˜ ALCOHOLIC HEPATITIS οƒ˜ RADIATION INDUCED HEPATITIS οƒ˜ PELIOSIS HEPATIS INFLAMMATORY DISEASES INFECTIOUS DISEASES οƒ˜ PYOGENIC LIVER ABSCESS οƒ˜ AMEBIC LIVER ABSCESS οƒ˜ FUNGAL ABSCESS οƒ˜ INFLAMMATORY PSEUDOTUMOUR οƒ˜ GRANULOMA ( TB , SARCOIDOSIS) οƒ˜ EOSINOPHILIC ABSCESS οƒ˜ PARASITIC DISEASE οƒ˜ HEPATIC SARCOIDOSIS οƒ˜ HEPATIC CANDIDIASIS οƒ˜ HEPATIC SCHISTOSOMIASIS
  • 9. οƒ˜ CAUSE – hepatitis A(picorna virus), B (hepadna), C(flavivirus), E, F(togavirus) & G (GBV-C). οƒ˜ Uncomplicated acute hepatitis clinical recovery within 4 months. οƒ˜ > 6 month – Chronic hepatitis οƒ˜ USG- periportal cuffing. Chronic - coarsening of echotexture. -GB wall thickening / contraction. -periportal lyphadenopathy - hepatosplenomegaly. VIRAL HEPATITIS
  • 10. Acute hepatitis. A, Sagittal, and B, transverse, images of the left lobe of the liver show marked increased thickness and echogenicity of the soft tissue surrounding the portal vein branch, called periportal cuffing. C, Sagittal, and D, transverse, views of the gallbladder with marked mural thickening, such that the lumen is virtually obliterated. The gallbladder wall shows a multilayered appearance with extensive hypoechoic pockets of edema fluid. A B C D
  • 11. Acute hepatitis. Acute hepatitis in patient with fever, abnormal liver function tests, and incidental gallstones. A, Transverse view of porta hepatis, and B, transverse view of left lobe of liver, show thick, prominent echogenic bands surrounding the portal veins in the portal triads, called periportal cuffing. C, Sagittal, and D, transverse, views of the gallbladder show moderate edema and thickening of the gallbladder wall. The allbladder is not large or tense, and the patient does not have acute cholecystitis. As this case illustrates, incidental cholelithiasis may be confusing A B C D
  • 12. Acute viral hepatitis in a 39-year-old man as seen on contrast-enhanced MDCT acquired during the arterial phase (A) and the portal venous phase (B). Note the heterogeneous contrast enhancement in the edematous enlarged liver. A B
  • 13. Precontrast OP (A) and contrast-enhanced fat-saturated (B) T1-weighted hepatic MRI in a 54-year-old man with chronic viral hepatitis. A B MRI :- generalised hepatomegaly with edematous liver (hyper intense on T2WI and early post contr.) - periportal T2 hyperintense signal Chronic hepatitis :- absence of patchy enhancement suggest low inflammatory rx. - progressive enhancement in delayed phase suggest presence of liver fibrosis.
  • 14. οƒ˜ 3 Distinct overlapping entities: οƒ˜ Fatty liver. Alcoholic hepatitis. Cirrhosis ALCOHOLIC HEPATITS
  • 15. On CT :- οƒ˜ Sharply defined hypodense area in liver corresponding to radiation ports. οƒ˜ Represents edema or fatty infiltration of involved area. οƒ˜ Onset : 2-6 wks after therapy οƒ˜ Dose > 35 Gy to liver. οƒ˜ Resolve in 3-5 months. On MRI:- οƒ˜ Geographic areas of oedema on T1 & T2WI. RADIATION HEPATITIS
  • 16. οƒ˜ Pathogenesis:- unknown / general outflow obstruction of the sinusoids with breakdown of the sinusoidal barriers . οƒ˜ Agents associated :- anabolic steroids, corticosteroids, tamoxifen, diethylstilbestrol, azathioprine, and oral contraceptives. οƒ˜ Microscopically :- dilatated sinusoids with multiple blood-filled lacunar spaces. οƒ˜ Macroscopically:- hepatomegaly. οƒ˜ MDCT :- multiple small hypodense lesions <1 cm in diameter on noncontrast images; centrifugal contrast uptake during portal venous phase. --Thrombosed venous branches remain hypodense during parenchymal phase imaging. PELIOSIS HEPATIS
  • 17. Contrast-enhanced fat-saturated T1-weighted hepatic MRI shows peliosis hepatis (arrows) that developed in this 59-year-old woman while she was being treated with tamoxifen. οƒ˜ MRI :- small hypointense lesions on T1WI / hyperintense on T2WI. οƒ˜ Larger lesions imaging characteristics of blood at different phases of organization. Contrast-enhanced fat-saturated T1-weighted hepatic MRI shows peliosis hepatis (arrows) that developed in this 51-year- old woman while she was being treated with steroids.
  • 18. οƒ˜ Miliary TB (MC Form) οƒ˜ Radiological abnormalities absent because of its diffuse micronodular nature. οƒ˜ Macronodular tuberculomas :- solitary / multiple. οƒ˜ On USG :- Hypoechoic. οƒ˜ On CT:- hypodense lesions with/ without rim enhancement. οƒ˜ Tubercular abscess rupture – cholangitis (bile ducts)/ pylephlebitis (PV) οƒ˜ Old healed granuloma – multiple small intrahepatic calcifications. TUBERCULOSIS
  • 19. οƒ˜ Most common hepatic presentation of multisystem sarcoidosis - Boeck’s sarcoid - Noncaseating epithelioid granulomas (submillimeter to 1 to 2 cm) scattered throughout the liver. οƒ˜ Unknown pathophysiology. οƒ˜ Bihilar lymphadenopathy. οƒ˜ Coexisatance with primary sclerosing cholangitis /other autoimmune diseases. οƒ˜ Larger granulomas contain greater amounts of reticulin and are surrounded by fibrotic hepatic parenchyma, reflecting a more vigorous immunologic response. SARCOIDOSIS
  • 20. οƒ˜ Acute complications:- Hepatic failure due to intrahepatic cholestasis -Portal hypertension. οƒ˜ Multisystem sarcoidosis mortality (10%) - due to cor pulmonale, lung fibrosis, and liver cirrhosis. οƒ˜ NCE MDCT :- Multiple intrahepatic and intrasplenic hypodense lesions accompanied by nonspecific hepatosplenomegaly. - On post-contrast : Isodense. οƒ˜ MRI demonstrates :- Noncaseating epithelioid granulomas as hypointense intrahepatic and intrasplenic nodules on T1 and T2WI. οƒ˜ Advanced-stage hepatic sarcoidosis may present as liver cirrhosis. Contrast-enhanced MDCT shows multisystemic sarcoidosis of the liver and spleen. With disseminated distribution of innumerable hepatic lesions. Contrast-enhanced MRI with multisystemic sarcoidosis of the liver and spleen.
  • 21. οƒ˜ Routes :- biliary tree routes, following suppurative cholangitis and cholecystitis. οƒ˜ Other routes are through the portal venous system in diverticulitis or appendicitis and hepatic artery. οƒ˜ Presenting features:- fever, malaise, anorexia and right upper quadrant pain. Jaundice (25%) οƒ˜ D/D’S :- Amebic or echinococcal infection, simple cyst with hemorrhage, hematoma, and necrotic or cystic neoplasm. οƒ˜ Ultrasound-guided liver aspiration PYOGENIC (BACTERIAL) LIVER ABSCESS
  • 22. οƒ˜ On USG:- Frankly purulent abscesses appear cystic, with the fluid ranging from echo free to highly echogenic. οƒ˜ Solid with altered echogenicity -early suppuration. οƒ˜ Hypoechoic- Necrotic hepatocytes. οƒ˜ Gas-producing organisms can give rise to echogenic foci with a posterior reverberation artifact. οƒ˜ Fluid-fluid interfaces, internal septations and debris. οƒ˜ Wall can vary from well defined to irregular and thick. A B C Early lesions. A and B, Rapid evolution from phlegmon to liquefaction. A, Poorly defined mass effect or phlegmon in segment 7 of the liver. B, At 24 hours later, there is a central area of liquefaction. C, Early abscess is poorly marginated and bulges the liver capsule. It is difficult to characterize this mass as solid or cystic. There was no vascularity within this or other masses.
  • 23. Mature abscess cavities in three patients. D to F, Classic mature abscess as a well-defined mass with liquefaction and internal debris. D E F G H I Abscesses related to gas-forming organisms. G, Multiple gas bubbles seen as innumerable bright echogenic foci within a poorly defined hypoechoic liver mass. H, Sagittal image of the left lobe of the liver, and I, confirmatory CT scan, show a liver mass with extensive gas content.
  • 24. οƒ˜ On NECT – marked hypodensity , due to presence of pus in centre. οƒ˜ On CECT- Enhancing peripheral rim. οƒ˜ Lobulated contour or circumferential transitional zones of intermittent attenuation. οƒ˜ Cluster sign :- smaller lesion <2 cm clustering together or into large abscess. οƒ˜ Double target sign : due to perilesional edema. οƒ˜ Gas bubbles / air fluid level. A, On precontrast CT scan there is a hypodense mass (arrow). B, On arterial- phase CT the mass has a target-like appearance (arrow)β€”a hypodense center surrounded by an enhanced hyperdense middle and a hypodense periphery. Transient wedge-shaped segmental enhancement is also observed surrounding the mass (arrowhead). A B
  • 25. οƒ˜ On MRI :- Hypointense on T1WI. οƒ˜ Hyperintense on T2WI. οƒ˜ Signal void due to presence of gas. οƒ˜ On post contrast – early intensely enhancing abscess wall - prominent perilesional enhancement. A, On fat-suppressed T2-weighted MRI there is an inhomogeneous hyperintense mass (arrow) with a very hyperintense area, suggesting a collection of pus. B, On arterial-phase Gd-enhanced T1-weighted MRI the peripheral part of the mass shows wedge-shaped segmental enhancement (arrowhead). Septum-like enhancement in the mass is also observed (arrow). C, On the equilibrium-phase image a nonenhanced cystic mass with an enhanced irregular thick wall is visualized (arrow).
  • 26. οƒ˜ Entameba histolytica. οƒ˜ Amoebic liver abscess (mc extraintestinal manifestation) οƒ˜ Protozoan reaches the liver by penetrating through the colon, invading the mesenteric venules and entering the portalvein. Or via lymphatics or directly extends into the liver from the hepatic flexure. Pathology Destructionof liver necrotic tissue including the viable organism lesion increases in size + central cavitation+ active organism. Solitary lesion - right lobe. (venous drainage from infected right colon, via the superior mesenteric vein to the portal vein) AMEBIC ABSCESS
  • 27. οƒ˜ On USG :- round or oval lesion, absence of a prominent abscess wall, hypoechogenicity compared to normal liver. οƒ˜ Fine low level internal echoes, distal enhancement and continuity with the diaphragm. οƒ˜ Two patterns 1. Round or oval shapes. 2.Hypoechoic appearance with fine internal echoes
  • 28. οƒ˜ On CT:- lowattenuation lesions, (density dependenton stage of development and internal contents). οƒ˜ Early stages-similar to solid tumors. οƒ˜ Older abscesses - cystic in appearance. οƒ˜ The zone of inflammation - isodense to hypodense on unenhanced CT scans οƒ˜ Enhances after contrast administration. οƒ˜ Thin outer rim of lower attenuation.
  • 29. οƒ˜ Uncommon οƒ˜ Opportunistic infection seen in Immunocompromised hosts- On intensive chemotherapy, AIDS, lymphoma, acute leukemia. οƒ˜ Liver involved secondary to hematogenous spread of mycotic infections in other organs, mc primary site- lungs. οƒ˜ candida is the most common FUNGAL INFECTION
  • 30.
  • 31. οƒ˜ On CT - most common pattern is multiple small, rounded areas of decreased attenuation. Areas of scattered increased attenuation representing calcification. οƒ˜ Liver lesions characteristically form a honeycomb abscess that contains 1- to 2-mm fungus balls. οƒ˜ Periportal areas of increased attenuation, correlating with fibrosis. οƒ˜ Candida microabscesses have been reported as cold lesions on both sulphur colloid and gallium scans. οƒ˜ On MR - increased signal intensity on T1WI & STIR sequences. Hepatic and splenic microabscesses (Candida) in a patient with acute myelogenous leukemia. A, In the arterial phase of dynamic CT there are multiple small nodules with faint peripheral ringlike enhancement in the liver and spleen (arrows). B, On equilibrium-phase CT they appear hypodense compared with the background liver (arrows).
  • 32. οƒ˜ Echinococcus granulosus and Echinococcus multilocularis. οƒ˜ Echinococcus alveolaris - rare , most aggressive. οƒ˜ Humans – intermidiate hosts. οƒ˜ In human liver, cysts grow to 1 cm during the first 6 months and 2-3 cm annually, depending on host tissue resistance. (right lobe) οƒ˜ Hydatid Cyst Structure:- 3layers a. Outer - pericyst, modified host cells, form a dense and fibrous protective zone. b. Middle laminated - ectocyst allows passage of nutrients. c. Inner - germinal layer, scolices (the larval stage of the parasite) and the laminated membrane are produced. (true wall). HYDATID DISEASE
  • 33. οƒ˜ On USG:- well-defined anechoic cyst. οƒ˜ Snowstorm sign. οƒ˜ US water lily sign.(floating memberanes) οƒ˜ Wheel spoke sign (internal septae) A, Baseline sonogram shows a fairly simple cyst in the right lobe with a small mural nodule and a fleck of peripheral calcium anteriorly. B, Three weeks later the patient presented with right upper quadrant pain and eosinophilia. The detached endocyst is floating within the lesion.
  • 34. Hydatid liver disease: spectrum of appearances. A, Classic appearance showing a cyst containing multiple daughter cysts. B, Sonogram, and C, confirmatory CT scan, show a unilocular and simple cyst, a fairly uncommon morphology for hydatid disease. D, Sonogram shows a complex mass. Anteriorly, multiple ringlike structures suggest hydatid disease. At surgery, cystic mass showed thick debris and innumerable scolices. E, Sonogram, and F, confirmatory CT scan, show an indeterminate mass with a thin rim of calcification. G, Complex mass similar to that seen in D. There are fingerlike projections within, again suggestive of hydatid disease. H, Sonogram, and I, confirmatory CT scan, show a central liver mass with rim and internal punctate calcification.
  • 35. οƒ˜ Hepatic schistosomiasis is caused by Schistosoma mansoni(most severe), S. japonicum, S. mekongi, and S. intercalatum. οƒ˜ Most common parasitic infections in humans, affect 200 million people worldwide. οƒ˜ Ova reach the liver through the portal vein and incite a chronic granulomatous reaction, terminal portal vein branches become occluded. οƒ˜ Presinusoidal portal hypertension, splenomegaly, varices, and ascites. οƒ˜ On USG:- Widened echogenic portal tracts, meas. upto 2 cm. οƒ˜ Most affected region - porta hepatis. οƒ˜ Liver size is enlarged. As the periportal fibrosis progresses, liver becomes contracted, and the features of portal hypertention appears. SCHISTOSOMIASIS
  • 36. οƒ˜ MC opportunistic infection in immucompatients(AIDS). οƒ˜ MC cause of life-threatening infection in patients with HIV. οƒ˜ Similar sonological pattern is seen in:- Mycobacterium avium-intracellulare and cytomegalovirus. PNEUMOCYSTIS CARINII Disseminated P. carinii infection in AIDS patient who previously used pentamidine inhaler. Sonogram shows innumerable tiny, bright echogenic foci without shadowing throughout the liver parenchyma.

Editor's Notes

  1. Indications for MRI of the liver include: β€’ Characterization of diffuse or focal hepatic lesions of uncertain etiology β€’ Determination of the extent and segment localization of hepatic malignancies prior to planned partial liver resection β€’ Follow-up in cases of known primary or secondary hepatic malignancies
  2. Decreased parenchmal echogenicity against which portal v eins appear brighter than normal.
  3. Attenuation is not altered as seen in fatty liver Hepatomegaly , gb wall thickening , periportal hypodensity.
  4. heterogenous contrast enhancement & T2 hyperintense signals signify ongoing severe inflammation) Chr – periportal lymph nodal enlargement. PV remains patent nd maintain shape.
  5. Bull’s-eye: 1 to 4 cm lesion with hyperechoic center and hypoechoic rim. It is present when neutrophil counts return to normal. The echogenic center contains inflammatory cells (Fig. 4-20). β€’ Uniformly hypoechoic: most common, corresponding to progressive fibrosis (Fig. 4-21, A). β€’ Echogenic: variable calcification, representing scar formation