Pt. preparation
-Oral contrast:
water as a neutral contrast to distend the stomach- to be able to better define the varicies in chirrosis, to eliminate pseudotumours of the stomach.
oral iohexol (Omnipaque) for positive agent
-IV contrast
100-120ml of iohexol 350
100-120ml of iodixanol 320
Phases of acquisition
- non-contrast scanb
- Arterial ph.
-early- 15 sec
-late - 25-30 sec
- Venous ph. - 60 sec
- Late or excretory ph. - 3-4 min
In most of the cases there is no need for non-contrast CT, it might be useful in chirrotic pts to differentiate between regenerating nodules which look denser in native scans than hepatomas.
If you want to diagnose a fatty liver then the most accurate way is do a native scan, with one or two slices and there is no need to scan the whole organ.
Arterial phase imaging is done in cases of hepatomas (liver cc.), of which 30% or more will only be seen in arterial ph. imaging. The late arterial ph (30 sec) is usually applied for the liver.
Early arterial ph. (15 sec) would be good for vessel mapping, but its just too early for tumours to light up.
Routinely the second ph. (60-70 sec) is the venous ph.
Occasionaly like with tumor imaging we make a delayed ph imaging (3-4 min), like when you are looking for delayed ph enhancement of mets like that of cholangiocarcinomas, hemangiomas, but routinely its not done.
Injection rate: 4-5 ml/sec, a total of 100-120ml is used (3ml/sec if IV access is poor)
slice thickness is around 0.6-0.75 mm
FATTY INFILTRATION OF THE LIVER:
Insults to liver (dietary, trauma, ischemia). Diffuse or focal. When focal can simulate tumor or mass like process.
10% undergoing liver biopsy have steatosis. Obesity is the biggest risk factor for steatosis
15-30% of obese pts have steatosis.
Clinical presentation: DM, hyperlipidemia, severe hepatitis, parenteral hyperlimentation, malabsorption, corticosteroids, trauma.
How does it look like on CT?
liver attenuation lower than the spleen or paraspinal muscles, vessels are seen through the zone of fatty liver without distortion or invasion.
LIVER ATTENUATION <40 HU
Others: liver attenuation less than or equal to spleen minus 10HU, liver attenuation equal to or less than the spleen, liver attenuation less than or equal to spleen plus 5 HU, liver splenic attenuation ratio <1.1
The presence of fatty liver is a strong predictor of coronary artery disease.
With fatty infiltartion the vessels become well defined.
LIVER CIRRHOSIS
Fibrosis and necrosis of the liver parenchyma. Alcohol is the most common cause, followed by HCV, HBV, billiary cirrhosis, Primary sclerosing cholangitis, drugs.
Ct findings:
Nodular liver with increase in size of the left lobe with decrease in size of the right lobe.
Increased distance between abdominal wall and liver surface.
Nodularity of the liver will vary with nodules often seen on non contrast CT as high density nodules.
Hypervascular nodules on arterial phase are usually hepatomas, but also can be regenerating nodules.
Commonly occures with varicies, therefore check the venous phase.
High risk of GI bleeding.
Extensive ascites.
Wet bowel due to hypoproteinemia,
-> thickening of bowel wall especially of colon - no need for colonoscopy
Distended vessels of the mesentery
Recanalisation of umbilical veins in abdominal wall.
Regenerating nodules: potentially confusable with hepatomas.
It can be extreemly difficult to differentiate a hepatoma in such livers.
If you don`t do native scan and only do the arterial ph then be careful before calling it a fatty liver as the spleen can enhance very quickly in arterial ph and case a large density difference.
In early phase imaging don`t confuse varicies with lymphnodes.
Regenerating nodule types:
Monoacinar regenerative nodules
- Diffuse noduler hyperplasia
- Nodular regenerative hyperplasia
Multiacinar regenerative nodules
Lobar or segmental hyperplasia
Cirrhotic nodule
FNH
A vascular leasion is a hepatoma until proven otherwise!
If leasion become larger in late phases then its a regenerating nodule, hepatoma don`t get larger in later phases, they stay the same or become smaller or stay isodense.
Small nodules are less likely to be non malignant.
PASSIVE CONGESTION
Facts: due to cardiac disease (RHF, constrictive pericarditis, tricuspid insufficiency).
What do we see?
Retrograde flow in IVC and hepatic veins
Mottled (tarka) enhancement of the liver due to hepatic congestion
Hepatomegaly
Ascites
Periportal edema
BUDD-CHIARI SYNDROME:
Facts: aka hepatic veno-occlusive disease, acute or chronic, regenerating nodules are very common and these can simulate hepatomas.
Acute phase:
- Early enhancement of caudate lobe and central portion of liver around IVC, with decreased enhancement of the rest of the liver.
- Delayed enhancement of peripheral portios of the liver and central portion of low density ( called flip-flop appearance).
- Narrow hypodense hepatic veins and IVC with dense walls.
Chronic phase:
- Non visualization of IVC and hepatic veins.
- Hyperdense nodules or regenerating nodules.
Primary: membranous obstruction of heparic venous outflow
Secondary: thrombosis, tu.
LIVER ABSCESS:
Facts: pyogenic, fungal or amoebic in nature. 90% are pyogenic and E. coli most common in adults as etiology.
Can simulate mets or malignancy therefore history is important!
Right lobe is more commonly involved.
There is a regulra wall with enhancement.
Air fluid level is diagnostic, present in 15%.
Cluster sign is classic on CT.
Can be single or multiple.
Fungal abscess is associated with immunosuppresion.
Amebic and parasitic abscess is frequent amongst travelers.
Pyogenic abscess: Hematogenous spread from GIT, ascending cholangitis or superinfection of necrotic tissue. Clinical presentation: fever, right-sided abdominal pain, weight loss, elevated LFTs. Single or multiple, few mm-s to several cm-s, rim enhancement may occure, may contain gas within the abscess.
Parasitic Abscess-Hydatid: Echinococcus granulosus- hydatid disease or echinococcus cyst - endemic to mediterranean basin and other sheap raising areas.
Humans acquire disease from eating contaminated food.
Many times calcification on the rim of the abscess.
Eosinophilia is common.
Amebic abscess: contaminated water, multiple cluster like cysts, very sick with high fever, travel history is critical.
CT findings: enhancing rim, cystic leasion, zone of edema around border of the leasion, usually solitary but may be multiple.
Candidiasis: immunosuppressed pts, hypodense liver leasions.
HEPATIC INFARCTS
Can simulate an abscess, periphery and wedge shape!
Septic emboli, post biopsy, post transplant,
Infart can turn into abcess.
WHAT CAN SIMULATE A HEPATIC TUMOR?
Abscess, sarcoidosis, angiomyolipoma, hepatic infarct, regenerating nodule, AVM.
SARCOIDOSIS
Up to 94% have liver involvement, most patients areassymptomatic, most common CT finding is hepatomegaly, lesion may be solitary but multiple is more common.
Diff dg: lymphoma, mets.
Mostly accompanied by sarcoid of the spleen.
They are hypovascular lesions, best seen on venous phase.
PORTAL VEIN THROMBOSIS
Partial or occlusive. Acute or chronic. Due to a range of conditions ranging from pancreatitis to hepatoma, abscess, trauma
Arterial phase: perfusion changes in adjacent liver (usually increased).
Portal venous phase imaging: thrombus defined, collateral vessels well seen.
Perfusion changes in liver.
Adjacent zones have hyperemia.
MIP can be tricky and you can easily overlook a thrombus if its no totally occlusive in MIP!
PORTAL VEIN ANEURYSMS:
Rare, assymptomatic, main portal vein mostly, >20mm.
SPLANCHNIC ARTERY ANEURYSMS:
Rare, most common in splenic artery, hepatic artery is second most common.
Rupture is associated with high mortality.
HEREDETARY HEMORRHAGIC TELANGIECTASIA:
RENDU-OSLER-WEBER DISEASE
Telangiectases and AVMs.
Many times assymptomatic.
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