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 :
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Methods of examination
4. Nuclear medicine
Pathologically cirrhosis consists of varying amounts of hepatic necrosis, fibrosis, fatty infiltration and nodular regeneration
1.Chronic 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
- 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
- Collaterals – left gastric, paraesophageal, mesenteric, splenorenal
Complications – hepatocellular carcinoma, esophageal varices with bleeding
Causes – obesity, alcohol, hyperalimentation, debilitation, chemotherapy, steroids
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
Pathogens – Escherichia Coli,aerobic streptococci, anaerobes
Causes – ascending cholangitis, trauma, surgery, portal phlebitis.
- 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.
Humans are intermediate hosts of the dog tapeworm (taenia echinococcus). Two forms:
E.granulosus – more common, few large cysts
E.multilocularis – less common, more invasive
- 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
- enhancement of cyst wall
- Frequency – 4-7% of population, 80% in females.Hemangiomas may enlarge particularly during pregnancy or estrogen administration.
- hyperechoic lesions 80%.
- hypoechoic lesions especially in fatty liver.
- giant hemangiomas are heterogeneous.
- anechoic peripheral vessels may be demonstrated by color Doppler .
- hypodense, well-circumscribed lesion on precontrast scan
globular or nodular intense enhancement.
- hyperintense on heavily T2W sequences.
- imaging modality of choice.
Nuclear imaging (SPECT)
- decreased activity on early dynamic images.
- increased activity on delayed blood pool images.
Risk factors – cirrhosis, chronic hepatitis B, hepatotoxins, metabolic disease in paediatric patients
- three forms – solitary, multiple, diffuse
- portal and hepatic vein invasion is common
- metastases – lung, adrenal, lymph nodes, bone
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
Criteria – hepatic wedge pressure 10 mm Hg. Causes:
Extrahepatic (obstruction of portal vein) – thrombosis, compression
Intrahepatic (obstruction of portal venules) – hepatic fibrosis, infection
Cirrhosis ,sclerosing cholangitis
Budd-Chiari syndrome, congestive heart failure
- Portal vein diameter 13 mm
- Collateral vessels – gastroesophageal varices via coronary vein, azygos; SMV collateral – mesenteric varices; splenorenal varices; IMV collateral – hemorrhoids
Causes - gallstone 95%
- Luminal distension 4cm
- Wall thickening 5 mm (edema, congestion)
- Pericholecystic fluid
- Gangrenous cholecystitis: rupture of GB
- Emphysematous cholecystitis
- GB wall thickening (fibrosis, chronic inflammation)
- Failure of GB to contract
Cholesterol stones are caused by precipitation of supersaturated bile
- Pigment stones – precipitate of calcium bilirubinate
- Mixed stones
- Hemolytic anemia
- Abnormal enterohepatic circulation of bile salts
US – method of choice – hyperreflective image with prominent posterior shadow; mobility of stones (exception – stones impacted in neck or stones adherent to wall)
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
- 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
- Mild acute pancreatitis (interstitial edema)
- Severe acute pancreatitis (necrosis, fluid collections)
- Chronic pancreatitis
- Abdominal trauma
- Hyperlipidemia, hypercalcemia
- Drugs – azathioprine, sulfonamides
- Peptic ulcer
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
- Acute fluid collections – enzyme-rich pancreatic fluid, no fibrous capsule
- Pseudocyst – encapsulated collection of pancreatic fluid
Progressive, irreversible destruction of pancreatic parenchyma by repeated episodes of mild or subclinical pancreatitis.
Commonly small, atrophic pancreas
Fatty replacement, fibrosis, calcifications
Irregular dilatation of pancreatic duct
Venous thrombosis – splenic, portal, mesenteric
Exocrine pancreatic tumor – adenocarcinoma, cystic neoplasm
Endocrine pancreatic tumor – insulinoma, gastrinoma
Other tumors – lymphoma, metastases
Clinical – jaundice, weight loss, Courvoisier sign (enlarged, nontender gallblader)
Alterations of density