24DAVID SUTTON

DAVID SUTTON PICTURES

DR. Muhammad Bin Zulfiqar PGR-FCPS III SIMS/SHL

• Fig. 24.2 Small, very dense stones, probably calcium carbonate.

• Fig. 24.3 ' Mixed stones' showing lamination and facets.

• Fig. 24.5 ' Mulberry stones' in gallbladder and bile duct (arrow).

• Fig. 24.6 ' Li my bile' (calcium carbonate sand) on erect film.

• Fig. 24.7 Calcified ('porcelain') gallbladder; the common duct is dilated and contains a large stone (arrow).

• Fig. 24.8 Emphysematous cholecystitis showing (A) gas in the lumen and wall of the gallbladder and (B) a gas-fluid level in the erect posture.

• Fig. 24.9 Gas in biliary tree following endoscopic sphincterotomy (-s). Note overlying benign calcifying breast disease (<-).

• Fig. 24.10 Chronic Ascaris abscess of liver. The worms are seen in contrast against gas in the cavity.

• Fig. 24.11 Large stone (arrow) impacted in the neck of the gallbladder. Note the dense acoustic shadow.

• Fig. 24.12 Multiple small stones (arrows) in the dependent part of the gallbladder. No acoustic shadow.

Fig. 24.13 Acalculous cholecystitis. The gallbladder wall is thickened and reduced in echogenicity.

• Fig. 24.14 (A) Chronic cholecystitis (see text). (B) Inflammatory thickening of the wall of the bile duct seen in transverse section at the level of the bifurcation (arrows).

• Fig. 24.15 Gallbladder polyp fixed to the ventral wall of the gallbladder.

• Fig. 24.16 (A) Calculus obstruction. Note acoustic shadow and the thin rim of bile around the front edge of the stone (arrow). (B) Coronal MIP image of an MR cholangiopancreatogram (MRCP) (TSE 2320/380) showing proximal stenoses (arrow) of the common bile (b) and pancreatic (p) ducts from a cholangiocarcinoma. There is a plastic F5 catheter in situ within the common bile duct which i s not producing any signal artefact. g = gallbladder; L = left. (Courtesy of Dr J. P. R. J enkins.) (C) MR cholangiography showing biliary dilatation due to anastomotic bile duct stricture following liver transplant.

• Fig. 24.16 (A) Calculus obstruction. Note acoustic shadow and the thin rim of bile around the front edge of the stone (arrow). (B) Coronal MIP image of an MR cholangiopancreatogram (MRCP) (TSE 2320/380) showing proximal stenoses (arrow) of the common bile (b) and pancreatic (p) ducts from a cholangiocarcinoma. There is a plastic F5 catheter in situ within the common bile duct which i s not producing any signal artefact. g = gallbladder; L = left. (Courtesy of Dr J. P. R. J enkins.) (C) MR cholangiography showing biliary dilatation due to anastomotic bile duct stricture following liver transplant.

• Fig. 24.18 (A-D) 99 n,Tc-dimethyl-IDA. Serial images at 7 min, 15 min, 80 min and 270 min, showing transit of radioactivity through the liver into the small gut and ascending colon. The gallbladder is not shown, indicating cystic duct obstruction. (Courtesy of Professor E. Rhys Davies.)

• Fig. 24.19 Small cholesterol calculi which float in the erect posture. within a proximal segment of bowel with delayed transit through (A) Prone. (B) Erect.

• Fig. 24.20 Percutaneous cholangiography demonstrating an intrahepatic cholangiopathy of biliary atresia following portoenterostomy. There is some preservation of normal duct morphology but intrahepatic strictures and calculi are features.

• Fig. 24.21 Severe biliary atresia with obliteration of intrahepatic bile ducts. Hyperplastic lymphatics allow some drainage of bile into the constructed portoenterostomy (Kasai procedure). This is the most common type and carries the worst prognosis.

• Fig. 24.22 Fusiform choledochal cyst with a long common channel and associated stricture at the pancreaticobiliary junction.

• Fig. 24.23 CT of a large choledochal cyst with biliary obstruction.

• Fig. 24.24 Caroli's disease with characteristic strictures and segmental

• intrahepatic dilated ducts.

• Fig. 24.25 Biliary obstruction secondary to an acquired 'atresia' in a neonate following a perforated bile duct.

• Fig. 24.26 Characteristic intrahepatic strictures of sclerosing cholangitis.

• Fig. 24.27 Empyema of the gallbladder. The true nature of the fine internal echoes can only be determined by aspiration.

• Fig. 24.28 Cholesterosis, showing fixed mural defects.

• Fig. 24.29 Types of adenomyomatosis. (A) A fundal nodule before and after contraction. (B) Stricture before and after contraction. (C) Rokitansky-Aschoff sinuses.

• Fig. 24.30 (A,B) Fundal nodule of adenomyomatosis before and after gallbladder contraction. Note long cystic duct medial to common bile duct, a congenital anomaly.

• Fig. 24.31 Cholecystogram of phrygian cap resulting from partial septum across the fundus of an otherwise normal gallbladder. This is a normal variant.

• Fig. 24.32 Rokitansky-Aschoff sinuses shown on the after fatty meal film at cholecystography. Stricture is also present.

• Fig. 24.33 Acute suppurative cholangitis. (A) Abscess cavities communicating with dilated ducts following stricture of choledochoenterostomy for malignant disease. (B) After 5 days external drainage via transhepatic tubes, most of the abscess cavities have healed and the ducts are less distended. Biliary sepsis rarely occurs in association with malignant obstruction unless there has been previous intervention.

• Fig. 24.33 Acute suppurative cholangitis. (A) Abscess cavities communicating with dilated ducts following stricture of choledochoenterostomy for malignant disease. (B) After 5 days external drainage via transhepatic tubes, most of the abscess cavities have healed and the ducts are less distended. Biliary sepsis rarely occurs in association with malignant obstruction unless there has been previous intervention.

• Fig. 24.34 Very large gallstone (arrow) in dilated bile duct shown at ERC.

• Fig. 24.35 ' Meniscus' sign of impacted stone (arrow) in bile duct.

• Fig. 24.36 Multiple calculi forming within the common duct following a distal bile duct trauma.

• Fig. 24.37 Correction of a bile leak with surgical drainage via a Roux loop of a sectorial right duct transected at cholecystectomy. The stent demarcates the line of the common bile duct, into which the transected duct had an anomalous insertion which was not recognised at laparoscopic cholecystectomy.

• Fig. 24.38 Benign postcholecystectomy stricture of common duct (arrow). Typical site at level of ligation of cystic duct.

• Fig. 24.39 Stricture of a hepaticojejunostomy.

• Fig. 24.40 Bile duct stricture developing following hepatic resection (A). Recurrent stricturing following biliary reconstruction which was successfully treated by balloon dilatation (B).

• Fig. 24.41 Subcapsular bile leak following blunt liver trauma.

• Fig. 24.42 Percutaneous cholangiography demonstrating a leak from the bile duct following blunt abdominal trauma.

• Fig. 24.43 Characteristic stricturing of sclerosing cholangitis involving the intra- and extrahepatic biliary system.

• Fig. 24.44 Low common bile duct stricture, with characteristic features of extrinsic compression from a pancreatic mass (arrow).

• Fig. 24.45 ' Rat-tail' stricture of common bile duct due to chronic pancreatitis. Note calcification in pancreatic head.

• Fig. 24.46 Ascaris lumbricoides. (A) Ascaris worm in the biliary ducts. (B) Cholecystostomy tube study showing multiple worms extending from common

• bile duct into duodenum. Note associated abscess in right lobe of liver.

• Fig. 24.47 Extrinsic compression along the line of the common duct from choledochal varices secondary to portal vein thrombosis.

• Fig. 24.48 Cholangiocarcinoma of the hilum with a characteristic stricture involving the confluence of the main left and right hepatic ducts

• Fig. 24.49 Papilliferous tumour infiltrating and expanding the common bile duct.

• Fig. 24.50 Direct cholangiography defining the intraductal extension of a biliary cystadenoma of the left liver

Fig. 24.51 ' Double duct' sign. Concomitant strictures of pancreatic duct and bile duct (arrows) diagnostic of carcinoma of head of pancreas.

• Fig. 24.52 Percutaneous cholangiography demonstrating obstruction of the Roux loop following hepaticojejunostomy.

• Fig. 24.53 (A) A fine-needle duct system is used to opacify the ducts and introduce a catheter. (B) An appropriate guide-wire is manipulated through the stricture. (C) A sheath introduction system is then placed into the ducts to allow delivery of the plastic or metallic stent. (D) The sheath is removed and external drainage may be used for the first 24 h if necessary. This will allow subsequent cholangiography to confirm optimum stent deployment and internal drainage.

• Fig. 24.53 (A) A fine-needle duct system is used to opacify the ducts and introduce a catheter. (B) An appropriate guide-wire is manipulated through the stricture. (C) A sheath introduction system is then placed into the ducts to allow delivery of the plastic or metallic stent. (D) The sheath is removed and external drainage may be used for the first 24 h if necessary. This will allow subsequent cholangiography to confirm optimum stent deployment and internal drainage.

• Fig. 24.54 Transhepatic endoprosthesis. (A) A guide-wire has been manipulated through the completely obstructing lesion of the common hepatic duct. (B) An endoprosthesis (arrow) has been positioned through the stricture. (C) Two days later, cholangiography through the external drain (arrow) shows that the prosthesis is functioning (contrast in duodenum) and that the intrahepatic ducts have been decompressed. The external drain is now removed.