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Liver Diseases: Diagnosis & Imaging Techniques

The document discusses various conditions of the liver, biliary system, and pancreas. It provides details on imaging methods used to examine each organ and describes the pathophysiology, causes, and radiographic features of various diseases including cirrhosis, fatty liver, pyogenic abscess, hydatid disease, hemangioma, hepatocellular carcinoma, metastases, portal hypertension, cholecystitis, cholelithiasis, cholangiocarcinoma, pancreatitis, chronic pancreatitis, and pancreatic neoplasms.

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0% found this document useful (0 votes)
19 views49 pages

Liver Diseases: Diagnosis & Imaging Techniques

The document discusses various conditions of the liver, biliary system, and pancreas. It provides details on imaging methods used to examine each organ and describes the pathophysiology, causes, and radiographic features of various diseases including cirrhosis, fatty liver, pyogenic abscess, hydatid disease, hemangioma, hepatocellular carcinoma, metastases, portal hypertension, cholecystitis, cholelithiasis, cholangiocarcinoma, pancreatitis, chronic pancreatitis, and pancreatic neoplasms.

Uploaded by

j.doe.hex_87
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© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PPT, PDF, TXT or read online on Scribd

THE LIVER

Methods of examination

1. US
2. CT
3. MRI
4. Nuclear medicine
CIRRHOSIS

Pathologically cirrhosis consists of varying amounts of hepatic


necrosis, fibrosis, fatty infiltration and nodular regeneration
Types:
[Link] sclerosing cirrhosis – minimal regenerative activity
of hepatocytes, little nodule formation, liver is hard and small.

2. Nodular cirrhosis – regenerative activity with presence of


many small nodules; initially the liver may be enlarged.

Causes – alcohol, hepatitis B, hemochromatosis


Radiographic features
Liver
- Small liver, increased echogenicity, heterogeneous
- Nodular surface
- Regenerating nodules – hypoechoic
- Unequal distribution of cirrhosis in different segments – left
lobe appears larger than right lobe; lateral segment of left lobe
enlarges, medial segment shrinks; ratio of the width of the
caudate lobe to the right hepatic lobe is 0,6
Portal hypertension
- Collaterals – left gastric, paraesophageal, mesenteric,
splenorenal
- Splenomegaly
- Ascites
Complications – hepatocellular carcinoma, esophageal
varices with bleeding
FATTY LIVER
Causes – obesity, alcohol, hyperalimentation, debilitation,
chemotherapy, steroids
Radiographic findings
US – fat increases liver echogenicity, renal cortex appears
more hypointense relative to liver than normal, intrahepatic
vessel borders become indistinct or cannot be visualized,
nonvisualization of diaphragm
CT – fatty areas are hypodense, hepatic and portal veins
appear dense because of decreased parenchymal density
PYOGENIC ABSCESS
Pathogens – Escherichia Coli, aerobic streptococci, anaerobes
Causes – ascending cholangitis, trauma, surgery, portal
phlebitis.
Radiographic features
- CT – hypodense with peripheral enhancement, no fill-in.
- Double target sign – wall enhancement with surrounding
hypodense zone.
- 30% contain gas.
- any abscess can be drained percutaneously, particularly: deep
abscesses, no response to treatment, nonsurgical
candidates.
HYDATID DISEASE
Humans are intermediate hosts of the dog tapeworm (taenia
echinococcus). Two forms:
[Link] – more common, few large cysts
[Link] – less common, more invasive
Radiographic features
[Link]
- well-delineated cysts
- size of cysts usually very large
- daughter cysts within larger cysts ( multiseptated cysts) are
pathognomonic
- rimlike cyst calcification
- double rim sign: pericyst, endocyst
- waterlily sign
- enhancement of cyst wall
[Link]

- poorly marginated, multiple, hypodense liver lesions.


- lesions are infiltrative (chronic granulomatous reaction with
necrosis, cavitation).
-calcifications are punctate and dystrophic, not rimlike.

Complications
- rupture into peritoneal, pleural, pericardial cavity
- obstructive jaundice due to external compression or intrinsic
obstruction of biliary tree
HEMANGIOMA
- Frequency – 4-7% of population, 80% in [Link]
may enlarge particularly during pregnancy or estrogen
administration.
US
- hyperechoic lesions 80%.
- hypoechoic lesions especially in fatty liver.
- giant hemangiomas are heterogeneous.
- anechoic peripheral vessels may be demonstrated by color
Doppler .
CT
- hypodense, well-circumscribed lesion on precontrast scan
globular or nodular intense enhancement.
MRI
- hyperintense on heavily T2W sequences.
- imaging modality of choice.
Nuclear imaging (SPECT)
- decreased activity on early dynamic images.
HEPATOCELLULAR CARCINOMA (HCC)
Risk factors – cirrhosis, chronic hepatitis B, hepatotoxins,
metabolic disease in paediatric patients
 
Radiographic features
General
- three forms – solitary, multiple, diffuse
- portal and hepatic vein invasion is common
- metastases – lung, adrenal, lymph nodes, bone
CT
- hypodense mass lesion
- early arterial enhancement
-Pseudocapsule

US
- most small HCC are hypoechoic
- larger HCC are heterogeneous
-high-velocity Doppler pattern

Angiography
- hypervascular
- AV shunting is typical
- Dilated arterial supply
METASTASES
30% of patients who die of malignancy have liver metastases.
Colorectal carcinoma, stomach, pancreas, breast, lung
Sensitivity for lesion detection: CTAP – high-dose delayed
CT – CECT,MRI – US
- Echogenic MTS – GI malignancy, HCC, vascular
- Hypoechoic MTS – lymphoma, bull’s eye pattern
(hypoechoic halo around lesion)
- Calcified metastases – all mucinous metastases – colon,
thyroid, ovary, kidney, stomach
- Cystic metastases – necrotic leyomiosarcoma
PORTAL HYPERTENSION
Criteria – hepatic wedge pressure  10 mm Hg. Causes:
Presinusoidal
Extrahepatic (obstruction of portal vein) – thrombosis, compression
Intrahepatic (obstruction of portal venules) – hepatic fibrosis, infection
 Sinusoidal
Cirrhosis ,sclerosing cholangitis
Postsinusoidal
Budd-Chiari syndrome, congestive heart failure
 
Radiographic features
- Portal vein diameter  13 mm
- Collateral vessels – gastroesophageal varices via coronary vein,
azygos; SMV collateral – mesenteric varices; splenorenal varices;
IMV collateral – hemorrhoids
- Splenomegaly
- Ascites
THE BILIARY SYSTEM
Methods of examination

1. Abdominal plain film – gas or calcium in the biliary tract


2. US
3. CT
4. MRI + MRCP
5. ERCP
6. PTC
7. Scintigraphy
ACUTE CHOLECYSTITIS
Causes - gallstone 95%
US
- Luminal distension  4cm
- Wall thickening  5 mm (edema, congestion)
- Gallstones
- Pericholecystic fluid
Complications
- Gangrenous cholecystitis: rupture of GB
- Emphysematous cholecystitis
- Empyema
CHRONIC CHOLECYSTITIS

- GB wall thickening (fibrosis, chronic inflammation)


- Gallstones
- Failure of GB to contract
CHOLELITIASIS
Types:
Cholesterol stones are caused by precipitation of
supersaturated bile
- Pigment stones – precipitate of calcium bilirubinate
- Mixed stones
Predisposing factors:
- Obesity
- Hemolytic anemia
- Abnormal enterohepatic circulation of bile salts
- Diabetes
- Cirrhosis
- Hyperparathyroidism
US – method of choice – hyperreflective image with
prominent posterior shadow; mobility of stones (exception –
stones impacted in neck or stones adherent to wall)
CHOLANGIOCARCINOMA
Adenocarcinoma of the biliary tree.
Clinical – jaundice, pruritus, weight loss.
Treatment – pancreaticoduodenectomy or palliative procedures (
stent placement, biliary bypass)
Location – hilar (originates from epithelium of main hepatic ducts or
junction –Klatskin tumor) + peripheral – originates from
epithelium of intralobular ducts
Radiographic features
- Dilated intrahepatic ducts
- Hilar lesions – central obstruction + lesions are usually infiltrative
so that a mass is not usually apparent + encasement of portal veins
causes irregular enhancement by CT
- Peripheral lesions – may present as a focal mass or be diffusely
infiltrative + retain contrast materials on delayed scans + occasionally
invade veins
- ERCP very useful
THE PANCREAS
Methods of examination

1. CT
2. US
3. MRI + MRCP
4. Arteriography
PANCREATITIS
Classification
- Mild acute pancreatitis (interstitial edema)
- Severe acute pancreatitis (necrosis, fluid collections)
- Chronic pancreatitis

Causes
- Alcohol
- Cholelitiasis
- Abdominal trauma
- Hyperlipidemia, hypercalcemia
- Drugs – azathioprine, sulfonamides
- Peptic ulcer
- Pregnancy
Imaging – CT staging
Grade A – normal pancreatic appearance
Grade B – focal or diffuse enlargement of pancreas
Grade C – pancreatic abnormalities and peripancreatic
inflammation
Grade D – 1 peripancreatic fluid collection
Grade E – 2 peripancreatic fluid collections and/or gas
Complications
- Necrosis
- Acute fluid collections – enzyme-rich pancreatic fluid, no
fibrous capsule
- Pseudocyst – encapsulated collection of pancreatic fluid
- Abscess
- Hemorrhage
CHRONIC PANCREATITIS
Progressive, irreversible destruction of pancreatic parenchyma
by repeated episodes of mild or subclinical pancreatitis.

Radiographic features
Commonly small, atrophic pancreas
Fatty replacement, fibrosis, calcifications
Irregular dilatation of pancreatic duct

Complications
Pseudocysts
Obstructed CBD
Venous thrombosis – splenic, portal, mesenteric
Carcinoma
Malabsorbtion
NEOPLASM
Types
Exocrine pancreatic tumor – adenocarcinoma, cystic
neoplasm
Endocrine pancreatic tumor – insulinoma, gastrinoma
Other tumors – lymphoma, metastases
ADENOCARCINOMA
Clinical – jaundice, weight loss, Courvoisier sign
(enlarged, nontender gallblader)

Radiographic features
Mass effect
Alterations of density
Extrapancreatic extension
Vascular involvement
Metastases

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