核醫科 門朝陽醫師

A 54-year-old male with alcoholic liver cirrhosis, who underwent Ga-67

inflammation scan, was found to have marked two separated hepatic lobes.

Furthermore, HIDA scan and Liver scan with SPECT shows there are small region of adhesion between two hepatic lobes.

Past history& surgery Hx:

liver cirrhosis child A-B ascitis and alcoholism.

UGI bleeding history, hepatic coma Gouty arthritis, right EV, congestive gastropathy.s/p EVL Anxiety disorder Right ureteral stone Right femur intertrochanteric fracture S/P ORIF

and DHS.

Abdominal sono(92/10/27): Liver cirrhosis with splenomegaly Mild ascitis. GB wall thickening Nuclear medicine studies: HIDA scan: r/o cholecystitis Ga-67 inflammation scan: infection? Liver scan with SPECT: study Enterogastric refulx study and GET.

Radiological study:

Abdominal CT

2001-5-22; 2001-10-31;2004-3-1

comparison and shows:

CT report:

We trace his previous CT scans found this case has gradually caudate lobe atrophy. This interesting finding --marked two separated hepatic lobes, may help us to diagnosis unusual type of caudate lobe atrophy with alcoholic liver cirrhosis.

Change in size, shape and radiocolloid uptake of the alcoholic liver during alcohol withdrawal, as demonstrated by single photon emission computed tomography

The volume of the total liver and separate right and left lobes was studied before and after 1 week of alcohol withdrawal in 16 consecutive alcoholics by means of single photon emission computed tomography after intravenous injection of 99Tcm-human albumin colloid; the relative tissue distribution of radioactivity was also followed. The left liver lobe increased in volume more than the right lobe during drinking and decreased more rapidly after alcohol withdrawal. Median volume reductions during 1 week of alcohol withdrawal w ere: total liver 12%, left lobe 26%, and right lobe 8%, indicating that half of the reduction to values of a control group was achieved during this first week. The volume of the right but not of the left lobe was significantly correlated to body size in alcoholics and in controls. The left lobe had a lower capacity to concentrate the radiocolloid than the right lobe in alcoholics and in controls. The liver/spleen, liver/bone marrow and liver/background radioactivity concentration ratios in the alcoholics increased during alcohol withdrawal. We conclude that heavy drinking causes both an increased total liver volume and a change in liver shape, with a relatively more enlarged left than right lobe, as well as a decreased capacity to concentrate radiocolloid. These changes are rapidly reversible during abstinence from alcohol.J Hepatol. 1994 Sep;21(3):417-23. Sweden.

Couinaud Segments

Fig 1-1Anterior and posterior view of liver showing 3-dimensional reconstructions of helical CT scan data in shaded surface projections wh

ich have been segmented according to the Couinaud classification (d

otted line represents the course of the portal vein which is sometimes used to to divide segment IV into segments IVa and IVb). Fig 1-2 Shaded-Surface 3D reconstructions of the liver segments viewed in the transverse plane at the level of the rostral part of the liver and inferiorly from the caudal surface.

Classification and distribution of cirrhosis Commen causes: Alcoholism(western); CAH(HBV)(far east); aut

oimmune(euro caucasians); primary biliary cirrhosis(>90% F) schistosomiasis(equatorial:fibrosis but

cirrhosis found in S. japanicum)

Rare but potential: Wilson; drug induced; biliary atresia hemachr

omastosis; constrictive pericarditis

Rare: cystic fibrosis. Scherosing cholangitis glycogen storage disease. A1 antitrypsin def.

Pathogenesis: The metabolism of ethanol(alcohol) to a

cetaldehyde and acetate dependent to

: alchol dehydrogenase and acetaldehyde dehydrogenase and need

NADH from NAD(NADPH to NADP) In alcoholism the MEOS is induced Unwanted by products: hyperuricemia,

hyperglycemia, ketosis, fatty liver.(redox state of cell in lipid and carbohydrate metabolism, steatosis)

Child’s classification of severity of cirrhosis

Feture points scored for increasing abnormalities 1 2 3 Encephalopathy None 1 and 3 3 and 4 Ascitis None mild mod/sev

Plasma bilirubin <25 25-40 >40

(mol/l)

Plasma albumin >35 28-35 <28

(g/l)

Prothrombin time 1-4 4-6 >6 (secs prolonged)

Total score: 5-6= grade A; 7-9=grade B;10-15=grade C

Alcoholic liver cirrhosis?

Is it typical case?(For gap formation) Or uncommon case of left hepatic lobe

cirrhosis in segment I( Caudate lobe atrophy)?

Or complex to tell due to HBV infection with ascitis and pleural effusion?

Caudate lobe atrophy?by CT

What else could we afford to the clinicians about liver cirrhosis case?

What kind of study or variant do we need to improve in liver cirrhosis case

with EV or case like this?

What do you think?