Материал: Advanced Imaging of the Abdomen - Jovitas Skucas

GALLBLADDER AND BILE DUCTS

eter can be detected. One should keep in mind, however, that blood clots, gas, and polyps have a similar appearance.

Intravenous Cholangiography

Intravenous cholangiography also detects bile duct stones, and some have reported a detection rates approaching 100%. These are exceptional results. More typical is a 50% sensitivity and over 95% specificity.

Therapy

The Presurgical Patient

The imaging approach to a precholecystectomy patient suspected of harboring choledocholithiasis remains controversial. Gastroenterologists and surgeons tend to take opposite views, depending on their relative expertise. Typically, if a patient is first seen by a gastroenterologist, preoperative ERC is obtained and, if stones are identified, endoscopic sphincterotomy and stone extraction are performed. Some surgeons, on the other hand, regardless of whether an open or laparoscopic cholecystectomy is contemplated, prefer to explore extrahepatic bile ducts during surgery. Some surgeons believe that the morbidity and mortality for surgical therapy of choledocholithiasis are comparable to or lower than that with endoscopic sphincterotomy. At times a combined laparoscopic and endoscopic procedure is preferred.

One therapeutic approach with suspected biliary stones is to divide patients into lowand high-risk groups. Low-risk patients undergo endoscopic US to confirm the presence of stones, followed by surgery. High-risk patients, on the other hand, undergo ERCP and sphincterotomy. Such an approach should be modified for individual expertise; also, the availability of MRCP modifies the strategy employed.

In patients with common bile duct and hepatic duct stones, endoscopic sphincterotomy and basket extraction achieve complete stone clearance in up to 90%; adding lithotripsy raises the success rate. Small stones tend to pass spontaneously after sphincterotomy. Most stones smaller than about 1cm can be retrieved with either a basket or a balloon. Larger stones are

usually fragmented, and the fragments are then extracted. Most stones proximal to a stricture, on the other hand,are difficult to extract and the stricture must first be dilated.

Endoscopic papillary balloon dilation is performed by some endoscopists instead of a sphincterotomy; whether the risk of complications is less after balloon dilation is not clear.

Endoscopic common bile duct cannulation is often not feasible in patients with a previous Billroth II gastric resection due to an excessively long afferent loop. Nevertheless, successful ERCP has been achieved in patients with a Billroth II anastomosis and even in an occasional patient with a Roux-en-Y reconstruction. A percutaneous transhepatic approach to sphincterotomy and stone extraction is an occasional alternative.

Intraoperative Imaging

A number of patients with choledocholithiasis and failed preoperative endoscopic stone extraction undergo a conventional open cholecystectomy and common bile duct exploration. Occasionally during an open cholecystectomy a surgeon encounters a stone impacted in the distal common bile duct that cannot be removed by stone forceps, basket, or catheter. Previous surgical practice was to perform a transduodenal sphincterotomy, but some surgeons elect to leave the stone in place,insert a T-tube,and then have a radiologist extract the stone through the T-tube tract. After a T-tube is in place and the bile ducts decompressed, many of these socalled impacted stones float free. Such an approach is also feasible during laparoscopic cholecystectomy.

One approach to managing common bile duct stones is to perform endoscopic US in the operating suite before laparoscopic cholecystectomy in patients at high risk of choledocholithiasis. Ultrasonography is also feasible during laparoscopy by introducing a transducer probe through one of the trocar sites. Extrahepatic bile ducts are readily visualized, and both common bile duct and cystic duct stones are detected. The sensitivity and specificity approach 100% for stone detection; the surgical approach is then modified accordingly. In addition, intraoperative US potentially also detects gallbladder polyps and adenomyomato-

sis, although the specificity and sensitivity are not established.

Laparoscopic US can rival laparoscopic cholangiography in stone detection, although the latter procedure better defines the anatomy, and these examinations are complementary. Ultrasonography is more difficult to perform and is limited in visualizing the intrapancreatic portion of the common bile duct. Also, although laparoscopic US detects most bile duct stones, it does not detect subtle anomalous biliary ducts. A practical problem in applying published results is that technically excellent operative cholangiographic and sonographic study quality are difficult to achieve; in many institutions radiologists control neither the choice of operative radiographic equipment used nor the technical factors employed.

If during a laparoscopic cholecystectomy imaging reveals unsuspected stones, one option is to approach them with postoperative ERCP, at which time most bile ducts can be cleared of stones. On the other hand, if expertise with laparoscopic bile duct exploration is available, these patients undergo laparoscopic ductal stone clearance rather than an open procedure. The common bile duct can be explored either via a choledochotomy and T-tube insertion or through a transcystic duct choledochoscope— technically difficult procedures that prolong surgical time. In experienced hands, however, choledocholithiasis is successfully managed with primary laparoscopic choledochotomy and stone extraction. Laparoscopic transcystic common bile duct exploration or choledochotomy are easier if the cystic duct and common bile duct are dilated.

One alternative for patients with an abnormal laparoscopic cholangiogram is to thread a double-lumen catheter through the cystic duct and into the duodenum. The catheter allows postoperative cholangiography and also assists postoperative endoscopic sphincterotomy and stone extraction.

Intraoperative choledochoscopic electrohydraulic lithotripsy has been performed for a stone impacted in the distal common bile duct, but limited data are available for this procedure.

The High-Risk Patient

Extracorporeal lithotripsy is an alternative for surgically high-risk patients with choledo-

ADVANCED IMAGING OF THE ABDOMEN

cholithiasis. Such lithotripsy was more in vogue a number of years ago and is currently performed in only a limited number of centers, mostly in Europe. Stones are visualized by US. Complete stone clearance has been achieved in 80% to 90% of patients. Some patients require several sessions, and subsequent endoscopic fragment extraction may be necessary. One consideration is that in some patients with successful lithotripsy, stones eventually recur.

Intracorporeal contact lithotripsy using an electrohydraulic or laser lithotriptor has had limited application. Specialized equipment is required for each technique. Nevertheless, percutaneous transhepatic or retrograde cholelithotripsy is an option in some high-risk patients or with complex stones. It is performed under local anesthesia, an access tract dilated, and stones fragmented using choledochoscopic lithotripsy. Any residual fragments are removed either through a transhepatic route or endoscopically. The electrohydraulic and laser approaches have similar success rates, morbidities, and hospitalization times. An alternate technique in a patient with failed endoscopic stone therapy is percutaneous transhepatic calculi extraction using occlusion catheters and Dormia baskets (91); balloon dilation of the papilla is generally also performed. In a difficult situation, a motor-driven basket can fragment a stone. Even the Angiojet thrombectomy device has been used to clear impacted intrahepatic debris (92).

Biliary Dyskinesia

The term biliary dyskinesia is used to describe abnormal bile duct function when an anatomic cause has been excluded. Also called acalculous biliary colic, initially it was applied mostly to sphincter of Oddi spasm. A separate entity, cystic duct syndrome, has been introduced. Both represent a paradoxical response to bile flow. Thus instead of the gallbladder constricting, sphincter of Oddi dilating and bile flowing into the duodenum, the sphincter remains in spasm when cholecystokinin is injected.

Ultrasonography suggests that instead of constricting, in some patients the gallbladder initially relaxes in response to a fatty meal, followed by a marked constriction. Such

GALLBLADDER AND BILE DUCTS

bimodal gallbladder response differs from the simple unimodal constriction of most normal gallbladders.

Cholescintigraphy is often the imaging procedure of choice in identifying these conditions. The diagnosis, however, should be made cautiously and only after excluding more obvious diagnoses.

Fistula

Cholecystoand choledochoenteric fistulas develop primarily to the duodenum and stomach but occasionally involve small bowel and colon. About two thirds of these are choledochoduodenal, followed by cholecystoduodenal, cholecystocholedochal, and the least common being cholecystocolonic fistula; the vast majority of these fistulas are caused by biliary calculi, and a small minority are due to malignancies and, rarely, peptic ulcer disease.

Among duodenal fistulas most involve the duodenal bulb. Some of the incriminating gallstones cause gallstone ileus, although smaller gallstones pass through the gastrointestinal tract without obstructing (gallstone ileus is discussed in Chapters 3 and 4). Pneumobilia is a variable finding. Many of these patients do not have signs and symptoms of acute cholecystitis, although a past history of biliary stones or recurrent biliary tract infection is not uncommon.

A cholecystocolic fistula induces diarrhea. Cholangitis is not common. The diagnosis can be established with a barium enema, although some of these fistulas produce sufficient colonic distortion that a barium enema even suggests a colon carcinoma. Biliary scintigraphy identifies a cholecystocolic fistula by direct transverse colon visualization without significant small bowel activity.

In an occasional patient with a cholecystocutaneous fistula, gallstones pass through the fistula. At times an adjacent abscess develops. These external fistulas are best studied with fistulography. Detection of internal fistulas by imaging is problematic; the claimed detection rates with CT and MRI vary considerably.

Bronchobiliary fistulas are rare. Many of these are sequelae of prior hydatid cyst surgery; a rare one is secondary to a hepatocellular carcinoma.

Gallbladder Torsion/Volvulus

Some authors use the terms torsion and volvulus interchangeably. To maintain accuracy, volvulus should be reserved for gallbladder torsion with lumen obstruction.

The gallbladder fundus is encased by peritoneum, which occasionally is rather lax, thus allowing the gallbladder to twist around the elongated mesentery.A twist occludes either bile outflow, blood flow, or both, and volvulus ensues. Clinically, gallbladder volvulus mimics acute cholecystitis and is a cause of acute abdominal pain. At times gallbladder volvulus suggests acute appendicitis. Neglected gallbladder volvulus evolves to perforation, bile peritonitis, and spill of any gallstones into the peritoneal cavity. Spilled bile is often infected, thus further compounding gallbladder perforation.

Laparoscopic cholecystectomy for torsion and volvulus has been performed. Initial laparoscopic gallbladder decompression and detorsion aid subsequent cholecystectomy.

Gallbladder Hydrops

Gallbladder hydrops develops secondary to gallbladder distention due to cystic duct obstruction in the absence of infection. In some patients the gallbladder is palpable.

Vascular Lesions

Hemobilia

Hemobilia signifies hemorrhage into bile duct lumen. These patients present with upper gastrointestinal bleeding, abdominal pain is common, and, obstructive jaundice develops due to intraductal blood clots. Hemobilia originating in the gallbladder has led to malignant hypertension (93). Hemobilia is a rare cause of pancreatitis.

Causes of hemobilia are rather extensive (Table 8.8). A coagulopathy, often part of endstage liver cirrhosis, is a somewhat neglected diagnosis of spontaneous hemobilia.An eroding umbilical venous catheter is a cause for these fistulas (Fig. 8.40). Trauma and resultant vascu-

Table 8.8. Etiologies of hemobilia

Trauma

Liver biopsy (Pseudo)aneurysm

Hepatic artery Cystic artery

Superior pancreaticoduodenal artery

Arterioportal fistula

Neoplasm

Hepatocellular carcinoma

Liver metastases

Gallbladder carcinoma

Vasculitis

Polyarteritis nodosa

Lupus vasculitis

Coagulopathy

Coagulopathy due to end-stage cirrhosis

Idiopathic thrombocytopenic purpura

Infection

Septic emboli

Ascariasis

Gallstone eroding into an artery

Iatrogenic

Figure 8.40. Splenic vein-to-bile duct fistula due to umbilical catheter erosion. Contrast was injected into the umbilical catheter.

ADVANCED IMAGING OF THE ABDOMEN

lar-to-bile duct fistula are common causes of hemobilia. Even small hepatocellular carcinomas result in hemobilia. Hemobilia due to metastases, on the other hand, is uncommon.

Endoscopy detects bleeding from the ampulla of Vater.

Blood increases bile attenuation 30 to 50HU. Blood clots form eventually and, having a higher specific gravity than bile, tend to settle into a dependent position in the gallbladder or bile ducts. Clotted blood appears as cast-like bile duct and gallbladder defects.

Ultrasonography reveals gallbladder blood clots as intraluminal masses. Blood within dilated bile ducts is hyperechoic. Aneurysms adjacent to bile ducts are detected with Doppler US; if needed, CT or selective hepatic arteriography provides confirmation.

Technetium-99m–red blood cell scintigraphy in a patient bleeding into intrahepatic bile ducts results in early gallbladder activity.

Arteriography identifies a source of uncontrolled bleeding in most patients, and transcatheter arterial embolization should arrest bleeding in most. Rarely, operative ligation of a bleeding vessel or even major liver resection is necessary.

Eventual gallbladder ischemia is a presumed common pathway for some of the cholecystitides. Ischemic cholecystitis can be induced by arterial chemoembolization of a hepatocellular carcinoma (94).

Gallbladder edema, congestion, and multiple small-vessel thrombi develop after crack cocaine use.

Bile duct ischemia is uncommon except in a setting of feeding vessel ligation or intravascular chemotherapy. Some secondary sclerosing cholangitis presumably is ischemic in origin.

Crack cocaine use leads to small-vessel thrombi, gallbladder wall edema and eventual ischemia.

Varices

Gallbladder varices develop in a setting of portal vein thrombosis. These dilated veins bypass a locally thrombosed portal vein segment and drain into intrahepatic portal vein branches. They probably do not interfere with gallbladder function. Children with portal hypertension due to extrahepatic portal vein obstruction also develop gallbladder varices.

GALLBLADDER AND BILE DUCTS

Gallbladder varices are recognized by both CT and US, with CT arterial portography identifying communication with intrahepatic portal vein branches. Ultrasonography reveals these varices as tortuous, dilated vessels in the gallbladder wall.

Patients with portal vein cavernous transformation develop bile duct varices as part of venous collaterals; some of these varices exert sufficient pressure on the bile duct lumen to induce cholestasis. Angiography outlines the underlying vascular anatomy, and cholangiography defines these serpiginous extraluminal defects.

Pericholecystic Fluid

Collections

Fluid around the gallbladder is common both in acute cholecystitis and in such conditions as pancreatitis, gallbladder torsion, ascites, adjacent abscess, and hematoma. Superficially, pericholecystic fluid mimics gallbladder wall edema, but this fluid does not enclose the entire gallbladder and does not enhance with contrast.

Cholangitis

Acquired immunodeficiency syndrome patients develop cholestatic liver enzyme abnormalities. Many of these patients have infection with an unusual organism, but some have no source for cholangitis and direct HIV infection is postulated.

Acquired immunodeficiency syndrome cholangitis, at times called AIDS cholangiopathy and AIDS-related sclerosing cholangitis, is detected with cholangiography (Fig. 8.41). Mild abnormalities found with direct cholangiography tend to be missed by other imaging modalities. Neoplastic disease, on the other hand, is better detected with CT.

Imaging reveals mild to moderate multiple strictures involving both intraand extrahepatic bile ducts. Bile duct wall outline tends to be irregular. The overall appearance is similar to that seen in sclerosing cholangitis, although it is possible to differentiate with imaging between AIDS-associated cholangitis and primary sclerosing cholangitis; in AIDS cholangitis papillary stenosis is relatively common, and a number of these patients develop gallbladder and cystic duct involvement—findings not seen in

Immunosuppression

Acquired Immunodeficiency

Syndrome

Cholecystitis

A number of opportunistic infections are implicated in acute acalculous cholecystitis in acquired immunodeficiency syndrome (AIDS) patients. Ultrasonography reveals a distended gallbladder, no calculi, and a thickened gallbladder wall—nonspecific findings.

Not all HIV-infected patients with right upper quadrant symptoms have cholecystitis. Ultrasonography in patients undergoing inter- leukin-2 therapy reveals gallbladder wall thickening and intramural and pericholecystic fluid (95); the severity of these findings is related to interleukin-2 dose, and both symptoms and US abnormalities resolve after the end of therapy.

Cholecystectomy in AIDS patients often does not improve symptom and is associated with a high mortality.

Figure 8.41. Acquired immunodeficiency syndrome (AIDS) cholangitis. The bile ducts contain mild strictures and a slight irregular outline is evident, findings similar to mild primary sclerosing cholangitis.