Gallbladder, Liver, Pancreas and Spleen

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GALLBLADDER functions as a reservoir for bile produced by the liver. It is 7-10 cm long, 3 cm wide at its broadest measure, and has a capacity of 30-50 mL

portions of the duodenum are labeled in white. at the head of the pancreas, the common bile duct meets the pancreatic duct, and they exit into the second part of the duodenum, forming the hepatopancreatic ampulla (ampulla of Vater)

divided into 3 regions: fundus, body, and neck

bile produced by the left and right portions of the liver travel through the right and left hepatic ducts (1-2 mm in diameter). These two ducts join to form the common hepatic duct the common hepatic duct lies anterior to the portal vein and to the right of hepatic artery the common hepatic duct descends roughly 3 cm before the cystic duct (3-4 cm long) from the gallbladder joins it from the right

Adenomyomatosis one of the many causes for gallbladder wall thickening pathologically, it is identified by proliferation of the gallbladder mucosa with diverticular outpuochings known as Rokitansky-Aschoff sinuses typically cholesterol deposits are seen within the gallbladder wall and cause a comet tail artifact

the common bile duct passes posterior to the first portion of the duodenum. It then descends via a groove on the superolateral portions of the posterior head of the pancreas sometimes traveling through the pancreas head. The four

Causes of GB wall thickening biliary causes include: -acute cholecystitis, gall bladder carcinoma, polyps, as well as adenomyomatosis

nonbiliary causes include: -CHF, hepatitis, pancreatitis as well as AIDs cholangiopathy

Acute Acalculous Cholecystitis represents inflammation of the gallbladder in the absence of demonstrated calculi the disease process is distinct from the calculous variety, in which the primary initiating event is believed to be obstruction of the cystic duct typically occurs as a secondary event in patients who are hospitalized and acutely ill from another cause

Pathophysiology at least 3 mechanisms a. systemic mediators of inflammation and trauma b. biliary stasis c. generalized or localized ischemia in turn, the mechanisms often result in functional or secondary mechanical obstruction of the cystic duct from inflammation and bile viscosity Sonographic signs compatible with acalculous cholecystitis

gallbladder wall thickening mucosal irregularity luminal distention increased bile density (biliary sludge) intramural or intraluminal gas intraluminal hemorrhage localized pericholecystic fluid collections inflammatory infiltration of pericholecystic fat indistinctiveness of the liver-gallbladder interface

Acute Cholecystitissonographic criteria for acute cholecystitis -a thickened gallbladder wall (normal GB wall- 3mm thick this appearance is neither sensitive nor specific for an inflammatory process

Case -patient is a 72-year old woman who presents with nausea and vomiting

75-80% of gallstones are of the cholesterol type 10-25% of gallstones are bilirubinate of either black or brown pigment in Asia, pigmented stones predominate, although recent studies have shown an increase in cholesterol stones in the Far East

Porcelain Gallbladder has been termed calcifying cholecystitis, cholecystopathia chronic calcaria, or calcified gallbladder are 5 times more common in women than in men most often considered a sequel of lowgrade chronic inflammation some have postulated that it is secondary to intramural hemorrhage or an imbalance in calcium metabolism

Complications biliary colic- 56 % acute cholecystitis- 36 % acute pancreatitis- 4 % choledocholithiasis- 3 % gall bladder cancer- 0.3 % cholangitis- 0.2 %

Gall Stones

appear as single or multiple filling defects within the gallbladder and are densely calcified, rim calcified, laminated, or have a central nidus of calcification

Cholelithiasis is the pathologic state of stones or calculi within the gallbladder lumen

associated with chronic gallbladder inflammation and gall stones in 95 % of cases it appears as an echogenic arc with dense posterior shadowing

Carcinoma of the Gallbladder the most common primary hepatobiliary carcinoma the fifth most common malignancy of the GI tract predominantly affects older persons with long-standing cholecystolithiasis GB epithelial tumors tend to behave similarly to other GI adenocarcinomas GB tumors occur in the fundus in 60 % of patients, in the body in 30 %, and neck 10 % early lymphatic spread occurs to the retroperitoneal, right celiac, and pancreaticoduodenal nodes direct invasion of the liver, extrahepatic biliary ducts, and duodenum, and colon occurs intraperitoneal seeding may occur

stones also may present as a soft-tissue density or a lucent filling defect within the bile. Some stones may contain air most gallstones have no signal on MRI and present as signal void-filling defects within the gallbladder

on T2-weighted sequences where signalvoid stones are contrasted against highsignal bile on T1 weighted sequences, bile usually shows a homogenous low signal

Ultrasound findings GB wall thickening single or multiple intraluminal mass extraluminal mass extending to the liver polyps larger than 1 cm in diameter Extraluminal mass extending to the liver this often is accompanied by a large mass replacing the GB fossa the mass often is complex with areas of necrosis visible this is the most common manifestation of GB carcinoma, accounting for 40-65 % of GB carcinomas

signal-void stones also may be apparent on T1-weighted images high signal may be seen occasionally on T2-weighted images within stones that contain bile within clefts stones with high fatty acid content may demonstrate high signal on T1-weighted images

US shows echogenic mass adherent to gallbladder fundus (arrows). CT shows enhancing mass within the gallbladder (arrows) with involvement of the liver (arrow head)

Porcelain gallbladder along with distention and filled with sludge and calculi

3-Left inferior lateral subsegment 4a-Left superior medial subsegment 4b-Left inferior medial subsegment 5-Right inferior anterior subsegment 6-Right inferior posterior subsegment 7-Right superior posterior subsegment 8-Right superior anterior subsegment

Bacterial (Pyogenic) Abscess 80-85 % of all abscesses are bacterial in origin bacteria gain access to liver via the portal or biliary system. Possible causes are iatrogenic, biliary disease, diverticular disease, trauma, and inflammatory bowel disease E. coli and anaerobes are the two most common offending agents in pyogenic abscess most pyogenic abscesses occur in the right lobe


unique in having a dual blood supply - 75 % originating from the portal venous system and -25 % arising from the hepatic artery the hepatic veins are responsible for drainage of filtered blood from the liver into the IVC 3 Functional Lobes right left caudate the right and left lobes are further divided into 2 segments each: -the anterior and posterior segments of the right lobe -the medial and lateral segments of the left lobe Segments

Radiogrpahic Findings (US) heterogenous, rounded masses with irregular, thickened walls and poor peripheral definition fluid and debris inside the abscess can create internal echoes gas-containing lesion also has acoustic shadowing CT

heterogenous lesion with irregular margin (arrowhead) and possible peripheral enhancement internal septations or papillary projections 20 % contain gas

Amebic Abscess trnasmitted by fecal-oral route the organism, E. histolytica, first infects the colon, then gains access to the liver via portal venous system patients generally present with right upper quadrant pain

1-Caudate lobe 2-Left superior lateral subsegment

Radiographic Findings (US & CT) indistinguishable from bacterial abscess. Tends to be peripheral in location

CT Findings

Diffuse Hepatic Disease CirrhosisCauses alcohol alpha 1-antitrypsin postnecrotic (hepatitis) metabolic disease: Wilson, hemochromatosis, glycogen storage disease congestive heart failure Pathology hepatocyte necrosis fibrosis nodular regeneration Radiographic Findings

generally non specific including: a peripherally based, round or oval low density lesion which often demonstrates a peripheral rim of slightly higher attenuation the peripheral rim will often enhance with contrast administration


Echinococcal Abscess dogs are the main intermediate hosts of hydatid disease eggs get ingested, hatch in the stomach and duodenum, travel to the liver via portal venous drainage, encyst in the liver and grow slowly the cysts can exert mass effect on the surrounding liver and biliary system. The right lobe of the liver is most frequently involved the cysts can rupture into the pleural cavity, peritoneal cavity, alimentary canal, or biliary tree, causing profound shock, peritonitis, and anaphylaxis

of advanced necrosis liver surface nodularity contracted liver with ascites atrophy of the posterior segments (VI, VII) of the right lobe enlarged caudate lobe (I) and lateral segments (II, III) of the left lobe prominent umbilical vein irregular enhancement

Radiographic Findings (US)

US- advanced cirrhotic liver appears to be nodular, irregular, and contracted with relatively enlarged caudate lobe (C) and lateral segment (L) of the left lobe. Fatty infiltration and fibrosis give a coarse echotexture of the liver parenchyma

double-layered cyst, classic double-line sign, water lily sign, racemose

Contrast CT: areas of fibrosis and regeneration may become isodense to parenchyma. The surface of the liver may be very nodular in cirrhosis

Diffuse Fatty Infiltration a reversible process in which t