radiologic / pathologic correlation of liver radiologic...

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Radiologic / Pathologic Correlation of Liver

and Gallbladder DiseaseGreg de Prisco, M.D.

Staff RadiologistBaylor University Medical Center

John Woosley, M.D., Ph.D.Professor, Department of Pathology

UNC School of Medicine

Thanks To

• Alvin Silva, M.D.

• Susan Guo, MS II

• Diffuse liver disease– Non-vascular

• Fat deposition• Iron deposition• Hepatitis• Fibrosis/cirrhosis

– Vascular• Passive Congestion• Budd-Chiari syndrome

• Focal Liver Lesions– Benign

• Cysts • Hemangioma• FNH• Adenoma

– Malignant• Metastases • HCC

• Biliary and Gallbladder N.O.S

– PSC– Cholangiocarcinoma– Gallstones– Choledocholithiasis– Porcelain gallbladder

Radiologic Anatomy Review

AOIVC

Spleen

Stomach

Liver

LHVMHV

RHV

Right lobe

Left lobe

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LPV

RPV

HABD

GB

CBDPD

Duo

Panc

FL

Liver Histology Review

Portal areas

Central venules

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Hepatocyte plate

Space of Disse

Sinusoid

Specialized fenestrated endothelium

Kupffer cells

Stellate cell

Diagram of Normal Liver

Sinusoidal endothelium is supported by a thin layer of collagen (blue on trichrome stain)

Sinusoid

Hepatocyte plate

CEA outlines the bile cannalicular system

Diffuse Liver Disease

• Non-vascular– Fat deposition

– Iron deposition

– Hepatitis

– Fibrosis/cirrhosis

Steatosis: Ultrasound

?

L

K

Steatosis: CT

NormalNormal FattyFatty

CT images largely based on density!

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Steatosis: CT


MRI

Steatosis: MR

NormalNormal

In phase = water + fat

Out of phase = water - fat

Steatosis: MR


Geographic Fatty Deposition

Nodular Fatty Deposition

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Macrovesicular steatosis (fat droplets fill and distend hepatocyte cytoplasm) in a centrilobular pattern

Mild Steatohepatitis

Large fat droplets expand hepatocyte cytoplasm and push nucleus to the periphery

Severe steatosis affecting both mid and centrilobular zones, only periportal hepatocytes are spared

Severe Steatohepatitis

Sparing of periportal hepatocytes

Classic example of Mallory’s hyalin – clumps of ropey eosinophilic material within hepatocyte cytoplasm

Fibrosis is perisinusoidal, projecting from central venule

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Broad zones of fibrosis bridge between adjacent central venulesand portal areas.

Advanced Steatohepatitis

Note that steatosisbecomes less prominent as fibrosis advances

Fatty LiverFatty Liver

IronIronFatty LiverFatty Liver

Hemochromatosis vs Hemosiderosis

Hemochromatosis vs Hemosiderosis

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Hemochromatosis

Pancreas

Spleen

Liver

Hemochromatosis

H&E – golden brown pigment within hepatocytes and ductal cells

Iron stain is superimposed on H&E. Dense blue staining of hepatocytes and ductal cells

Iron stained cirrhotic liver from a patient with primary hemochromatosis

A large tumor nodule and smaller satellite nodule contain very little iron

Hemochromatosis with HCC

Hepatitis

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Hepatitis

Chronic Hepatitis

General features

Portal area - normal Portal area – chronic hepatitis

Crisp limiting plate without inflammation or hepatocyteinjury

Interface hepatitis – limiting plate is indistinct with numerous lymphocytes mediating hepatocyte injury

Portal area

Lobular area with lymphocytic infiltrate

Acidophil body – dead hepatocyte with pyknoticnucleus and condensed eosinophilic cytoplasm, surrounded by cytotoxiclymphocytes

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Viral and Autoimmune Hepatitis

Zone of normal hepatocytes

Zone of hepatocyteswith “ground glass”cytoplasm

Normal hepatocyteshave coarsely reticular cytoplasm

Enlarged hepatocytes with finely granular eosinophilic (ground glass) cytoplasm

Immunohistochemical staining for hepatitis B surface antigen show positivity in hepatocytes having ground glass cytoplasm

Hepatocytes may also show incorporation of hepatitis B core antigen within nuclei, detectable by immunohistochemistry

Hepatitis C typically has distinctly nodular lymphocytic aggregates in portal areas

Mild, patchy macrovesicular steatosis is also common

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Portal interface hepatitis with irregular destruction of the limiting plate

Lobular inflammation with acidophil body

Inflammation and hepatocyte necrosis prominent in lobular areas

Interface injury –inflammatory infiltrate damages limiting plate

Inflammatory infiltrate is rich in plasma cells

Cirrhosis

• Imaging: Hepatic– Nodularity

– Morpholigic Changes• Compensated

– Caudate & Lat SegC


– Morpholigic Changes• Decompensated

– periportal space

Cirrhosis




– Posterior notch sign

Cirrhosis

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LM

L




– Posterior notch sign

– Expanded GB sign

Cirrhosis

• Imaging: Extrahepatic– Portal HTN

• Splenomegaly

• Ascites

• Varices

• Gamna-Gandy Bodies

Cirrhosis

MR Elastography

• Mechanical waves are induced in the liver using an external device (“wave machine”)

• Waves are measured with a sensitive phase-contrast MR technique

• Resulting images quantify tissue stiffness

Normal Liver Cirrhotic Liver

Wave images:

Elastographicimages:

cirrhosisnormal

normal cirrhosis

RadioGraphics 2009; 29:1591

Cirrhosis

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This shrunken liver has severe architectural distortion with rounded, variably-sized regenerative nodules encased in dense fibrous connective tissue

Normal liver

Cirrhosis with broad dense blue-staining fibrous septa surrounding round to oval, variably-sized regenerative nodules

Diffuse Liver Disease

• Vascular– Passive congestion

– Budd-Chiari syndrome

RHF: Passive Congestion

Courtesy: Christine Menias, MDWashington University, St. Louis

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X

XX

Budd-Chiari

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Budd-Chiari Syndrome

Centrilobular congestion

Centrilobular congestion

PA

PAPA

Obstruction to hepatic venous outflow leads to centrilobular congestion. Increased venous pressure allows RBCs to enter hepatocyte plates (RBC-trabecular lesion) with hepatocyte atrophy and death

Chronic Budd-Chiari -trichrome stain shows hepatic vein lumen nearly completely occluded by organized thrombus

• Variety of pathology

• Accurate diagnosis

depends on:

- clinical data

- imaging features

- occasionally biopsy

Focal Hepatic Masses

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• Important clinical data

– malignancy?

– chronic liver dz?

– infection?

– lab abnormalities?



• Imaging features

- Ultrasound

- CT

- MR T1 and T2 appearance

- Enhancement pattern

- Hepatobiliary contrast

agent appearance

CT vs MRUnenhanced Enhanced

CTCT

MRMR

T1 weighted

T2 weighted

T1 = water dark

T2 = water bright

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T1 vs. T2

Enhancement

10 minute

3 minutearterial portal venous

Enhancement

10 minute

3 minutearterial portal venous

Timing makes a difference!

Generic Name

Gadodiamide

Gadopentetate dimeglumine

Gadoteridol

Gadoversetamide

Gadobutrol

Gadoterate meglumine

Gadobenate dimeglumine

Gadoxetate disodium

Trade Name

Omniscan

Magnevist

ProHance

Optimark

Gadovist

Dotarem

MultiHance

Eovist

What’s in a name?

Reticuloendothelial cell imaging -SPIO - Ferridex

R.I.P.R.I.P.R.I.P.R.I.P.R.I.P.

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Hepatobiliary Contrast Agents

portal venous 20 minute delayed

Mass lesions

• Benign– Cyst

– Hemangioma

– FNH

– Adenoma

• Malignant– Metastases

– HCC

Cysts

• Common

• Epithelial-lined non vascular spaces

• May be numerous in ADPKD

Cysts• Ultrasound anechoic

• Unenhanced CT hypodense

• T1 low signal

• T2 very high signal

• Nonenhancing

Multiple strips of cyst wall –dense fibrous connective tissue

Cyst wall lining

Cyst wall surface covered by visceral peritoneum

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Cyst lined by biliary type epithelium

Cyst wall surfaced by mesothelium

Hemangioma

• Most common benign solid liver tumor (20%)

• Endothelial-lined vascular spaces

• F > M

Hemangioma

• Ultrasound hyperechoic with or without central hypoechogenicity

• Unenhanced CT hypodense

Hemangioma

• T1 low signal

• T2 very high signal,mimic cysts

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Hemangioma

• 3 enhancement patterns

– Classic - Peripheral, nodular, interrupted, persistent

– Uniform, homogeneous, persistent

– Classic with nonenhancing central scar

Enhancement follows blood pool in all phases!

CTCT

MRMR

Hemangioma

Homogeneous vs. Nodular Enhancement

Hemangiomas mimic cysts on T2

*

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Pitfalls

Metastasis

Hemangioma

Glisson’s capsule becomes convoluted as blood-filled spaces collapse

Normal liver surrounds lesion

Spaces lined by endothelium and focally filed with thrombus

Focal Nodular Hyperplasia

• 2rd most common liver tumor– 3% general population

– 8% all primary hepatic tumors

• Child-bearing females

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• Hyperplastic response to a congenital vascular malformation – Often have a central scar

– Contain bile ducts

• Can occur with hemangiomas


• Stealthy on unenhanced exams

• T1 iso or nearly isointense, central scar hypointense

• T2 majority of lesion isointense, central scar hyperintense


• Enhancement– Uniform homogeneous

arterial enhancement in most of lesion

– Central scar nonenhancing in arterial phase


• Enhancement– Enhances similar to liver in

portal venous phase


• Enhancement– Delayed enhancement of

central scar


• Hepatobiliary contrast– Iso to hyperintense to liver

on delayed hepatobiliary images

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Normal Liver

Irregular pale nodule

Central stellate scar

Central stellate scar

Periphery of lesion has a nodular, cirrhotic-likeappearance without cytologic atypia

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Large, tortuous blood vessels are present within the central scar - atypical vessels have focal fibrointimal hyperplasia

Hepatic Adenoma

• Benign proliferation of hepatocytes

• Young women

• Pathogenesis – Oral Contraceptives (1960)

• Longterm and high dose

– Anabolic steroids

– Glycogen storage disease• Multiple

• Malignant transformation

Hepatic Adenoma

• Unenhanced CT may be iso to hypodense, hyperdense with acute hemorrhage

Hepatic Adenoma

• T1 often have fattydeposition but maybe hyperintense due to hemorrhage

• T2 predominantly hyperintense

Hepatic Adenoma

• Enhancement– Hypervascular

– Heterogeneous • intratumoral hemorrhage,

necrosis

– +/- pseudocapsule

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FNH

Adenoma

Hepatic Adenoma

Hepatic adenoma

Nodular liver lesion

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Nodule has no portal areas

Nodule surrounded by a border of normal liver with portal areas

Bland hepatocytes and large caliber “free-floating” blood vessel that is not supported by connective tissue stroma

Hepatic Metastases

– Most common malignant liver lesion

– After LN, most common site for mets overall

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Hepatic Metastases

– Hypovascular

– Hypervascular

Hypovascular Pattern

– Primaries: colon,

lung, breast,

gastric, prostate,

TCC

Peripheral washout

Hepatic Metastases

Ring-enhancing Metastases

DDx: Abscess, InflammatoryDDx: Abscess, Inflammatory

Hypervascular Pattern

64 M pancreatic tail “mass” resected 1984 Episodic LOC & hypoglycemia

Pancreatic Insulinoma Pancreatic Insulinoma MetastasisMetastasis

• Carcinoid

• Thyroid

• Melanoma

• Renal cell

carcinoma

Diffusion Imaging

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Diffusion Imaging

Liver Metastases

Liver core biopsy consist entirely of tumor with no normal liver parenchyma sampled

Tumor consists of cytologically malignant melanocytes

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Hepatocellular Carcinoma

• Most common primary liver malignancy

• Often arise in cirrhotic liver

• M > F


• Often increased alpha fetoprotein

• Myriad clinical presentations


• T1 appearance can vary– Often isointense

– May be steatotic

– May be hyperintense with hemorrhage, copper, or fat


• T2 often mildly hyperintense – similar to spleen, may be isointense


• Small lesions have arterial uniform enhancement


• Small lesions have arterial uniform enhancement

• Often washout in more delayed phases

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• Large lesions have heterogeneous enhancement

• Uncommonly have pseudocapsule with delayed enhancement


• “Nodule within a nodule” appearance is uncommon,but specific


Infiltrating HCC w PV ThrombusInfiltrating HCC w PV Thrombus

• Vascular invasion commonly seen


• Vascular invasion commonly seen

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Hepatocellular carcinoma

Cirrhotic background

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Nodular liver with fibrous septae containing prominent lymphoid follicles – typical of hepatitis C cirrhosis

Cirrhotic liver with regenerative nodules surrounded by dense fibrous bands

Partially-encapsulated tumor nodule

Cirrhotic liver

Tumor

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Thick hepatocyte plates composed of cytologically atypical hepatocytes, prominent Mallory bodies

Hypervascular Lesion KeysLESION

– Small Hemangioma

– Large Hemangioma

– FNH

– Adenoma

– HCC

– MetastasesCarcinoid, Thyroid, Melanoma,

Renal, Islet cell

HINTS– Early and persistent enhancement

– Nodular enhancement +/- scar

– Early homogenous enhancement,

delayed enhancing scar, HBA

– Heterogenous, pseudocapsule

– Enhancing lesion in cirrhotic,

washout, mild T2 hyperintensity,

pseudocapsule

– Early, heterogeneous, ring, washout, HBA

Biliary Tract and Gallbladder

• Biliary– PSC

– Cholangiocarcinoma

• Gall Bladder– Gallstones and Choledocholithiasis

– Porcelain gallbladder

GB

RHDLHD

CHDCD

Normal MRCP

CBD

PD

Primary Sclerosing Cholangitis

Courtesy: Christine Menias, MDWashington University, St. Louis

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PSC with CBD fibrosis

PSC with intrahepatic periductal fibrosis

Early damage -concentric periductal fibrosis

Trichrome stain highlights concentric “onion skin” fibrosis

Late damage – duct is obliterated leaving behind a fibrous nodule of scar tissue

“Widowed artery” – ducts are paired with an artery of similar caliber; when this duct has become obliterated, the artery is said to be widowed

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Trichrome stain highlights nodular scar of obliterated duct

Gross appearance of late PSC with biliary cirrhosis

Residual liver parenchyma in puzzle-piece like pattern, often with striking bile-staining

Small intrahepatic bile stones can sometimes be seen

Usual cirrhotic liver pattern with broad fibrous septa surrounding round to oval, variably-sized regenerative nodules

Biliary cirrhotic liver pattern with broad fibrous septa surrounding “puzzle-piece” areas of liver parenchyma – the larger ones often retain normal liver architecture (portal areas and central veins)

Cholangiocarcinoma

• Cholangiocarcinoma– 2nd most common primary

hepatic malignancy– Etiologies

• PSC• Caroli’s• Choledochal cyst• Thoratrast

– 3 locations• Hepatic bifurcation• Distal CBD• Intrahepatic (5-15%)

Cholangiocarcinoma

• Imaging appearance variable due to location and growth pattern

– Mass forming

– Periductal infiltrating

– Intraductal

Cholangiocarcinoma

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Cholangiocarcinoma

• Intrahepatic, peripheral– Varies due to amount of

fibrosis and necrosis

– Atrophy

– Capsular retraction

– Hypovascular• Progressive, delayed

hyperenhancement due to

fibosis

Cholangiocarcinoma

• Intrahepatic– Biliary Duct Dilataton

Cholangiocarcinoma – Intrahepatic

46 YO man with longstanding PSC, multiple bouts of ascendingcholangitis, and chronic liver failure undergoes transplantation

Septum with paired artery and bile duct. Bile duct is lined by dysplastic epithelium.

Dysplastic epithelium transitions into frankly invasive cholangiocarcinoma.

Low power view emphasizes the intense desmoplastic stroma that often accompanies cholangiocarcinoma.

Gallstones

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Gallstones

Gallstones

WES Triad

Choledocholithiasis

Choledocholithiasis

Normal Acute large duct obstruction

Normal portal area

Expanded portal area

Interlobular bile duct Proliferating

ducts

Centrilobular cholestasis with bile-stained hepatocyte cytoplasm and canalicular bile plugs

Bile-stained macrophages

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Interlobular bile duct infiltrated by PMNs

Extensive biliary fibrosis

Sheets of PMNs with residual fragment of ductal epithelium

Ruptured duct with bile leakage

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Giant cell and macrophages engulfing inspissated bile

Leakage of bile with detergent-like bile salts results in hepatocellular necrosis (bile infarct)

Porcelain Gallbladder

Porcelain Gallbladder

Porcelain gallbladder with calcification of the gallbladder wall

Summary

• Diffuse Liver Disease

• Focal Liver Lesions

• Common biliary and gallbladder disease

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Ode to the Liver

“…While the heart plucks mandolin strings,you suck and score, you distinguish and divide,

you increase and lubricate,you give home to life’s enzymes

and grams of experience collecting liquors at this song’s party

and after cleaning up,you are warmly last to say

goodbye.”

-Pablo Neruda

radiologic / pathologic correlation of liver radiologic...

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