Материал: Advanced Imaging of the Abdomen - Jovitas Skucas

GALLBLADDER AND BILE DUCTS

Figure 8.10. Duodenal perforation (arrow) detected 2 days after laparoscopic cholecystectomy. A water-soluble contrast agent was used to perform this study.

studies conclude that morbidity and mortality of laparoscopic cholecystectomy are lower than after an open operation. The most common complication is a bile leak, followed by retained stones, severe bleeding, subhepatic fluid or abscess, and mild pancreatitis (Fig. 8.10). A common duct stricture and retained stones are late complications, often manifesting as cholangitis rather than jaundice.

Because of ease and ready availability, conventional chest and abdomen radiographs should be obtained whenever postlaparoscopic cholecystectomy injury is suspected. They will detect pneumonia and extraluminal gas. Whether they should be followed by CT or US is debatable; either modality detects biliary obstruction and abnormal intraabdominal fluid collections. The definitive study to detect bile duct injury is cholangiography. An ERC can localize a specific site of leakage and detect any underlying strictures. If ERC is unsuccessful or if complete biliary obstruction is encountered, transhepatic cholangiography should define more proximal biliary anatomy. In general, with a major bile duct injury or stricture, percutaneous transhepatic cholangiography is of more value to the surgeon than an endoscopic

approach because it defines the proximal biliary tree anatomy used for reconstruction.

In a setting of localized disruption, including a cystic duct stump leak or extravasation from ducts of Luschka, placement of a biliary stent is often therapeutic.

Bile Duct Injury: Most bile duct injuries manifest during the early postoperative period either as obstructive jaundice or a bile leak. Detection of residual stones or a clip in the bile ducts can be delayed. Most complications can be managed successfully by either ERCP or percutaneously. Biliary leaks are successfully treated by percutaneous biloma drainage combined with either endoscopic or percutaneous transhepatic biliary catheter bypass.

The Bismuth classification is used to describe major bile duct injuries (Fig. 8.11). A preoperative cholangiogram is valuable prior to bile duct injury repair. Subsequent surgical repair is more difficult and is often unsuccessful if a cholangiogram is not obtained preoperatively or the cholangiogram is incomplete.

Common sites for leakage are from a cystic duct stump or from injury to an aberrant bile

Figure 8.11. Bismuth classification of bile duct injuries. In type 1, >2 cm of hepatic duct is intact; in type 2, <2 cm remains; in type 3, little viable hepatic duct is available; and in type 4, the main right and left lobe ducts are involved.

Figure 8.12. Blown cystic duct stump (arrow). The resultant biloma was drained percutaneously.

duct (Fig. 8.12). Some patients have anomalous small right lobe ducts draining directly into the gallbladder (bile ducts of Luschka), and these are torn during a cholecystectomy.Aberrant bile duct leaks are difficult to detect because these aberrant ducts often do not opacify on operative and postoperative cholangiograms. Bile leakage also occurs with inadvertent bile duct laceration. Most bilomas form around the site of leakage; a rare one extends into the lesser sac. Typically a biloma forms within a week or so after surgery. Some bilomas are associated with jaundice. In general, only the symptomatic patient requires additional therapy.

Direct visualization of a leak is by cholan- giography—directly via a T-tube, retrograde, or any other access—or indirectly by detecting a biloma with MRCP, CT cholangiography using an intravenous contrast agent, or US. Contrast enhanced MR cholangiography using MnDPDP or Gd-EOB-DTPA (agents taken up by hepatocytes and excreted into bile ducts) identifies bile duct leaks in these patients (33), although advantages of this technique over other methods of visualizing bile ducts are still debated. Ultrasonography reveals a biloma as a sharply marginated anechoic mass having acoustic enhancement. A hematoma or abscess

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is in the differential diagnosis, although the latter tends to contain a more echoic content.

Biliary scintigraphy is probably more sensitive and more specific than either CT or US in detecting a bile leak. Cholescintigraphy achieves an accuracy of mid-80% in detecting leaks, with CT and US being less sensitive. One can argue that cholescintigraphy should be the first diagnostic modality if a bile leak is suspected but in a number of centers it is relegated to a secondary role. The scintigraphic appearance of a postoperative bile leak is useful for prognosis; if most of the biliary flow is into the duodenum, a perforation will probably resolve without surgical or other intervention.

Occasionally with a small bile leak initial cholescintigraphy is normal, but repeat images obtained after IV morphine reveal a subtle leak. Also, if initial images do not identify a leak, delayed images should be obtained because some small leaks are visualized only several hours later. In spite of these techniques, bile ascites can be difficult to diagnose because of dilution. On the other hand, many small asymptomatic bile leaks are of no clinical significance.

Placement of a biliary drainage catheter, inserted either via an endoscopic approach or percutaneously, is sufficient therapy for most localized bile leaks. Endoscopists insert either an intrabiliary stent or a nasobiliary tube across a leakage site, at times adding a sphincterotomy. Endoscopic placement of a short transpapillary stent without a sphincterotomy is an effective and simple way of equalizing pressures within the bile ducts and duodenum. During percutaneous transhepatic biliary drainage, generally performed when surgical or endoscopic therapy is unsuccessful, side holes are positioned on both sides of a leak.

Among postlaparoscopic cholecystectomy patients referred for therapy of bile leaks to members of the Midwest Pancreaticobiliary Group, most common therapy consisted of sphincterotomy with stent insertion, with biliary leakage healing in 88% of patients (34); percutaneous or surgical drainage of bilomas was required in 32% of patients.

With major bile spill into the peritoneal cavity, immediate reexploration is generally indicated. Bile duct transection or other major injury is usually treated with a Roux-en-Y

GALLBLADDER AND BILE DUCTS

hepaticojejunostomy rather than direct bile duct anastomosis; the latter is associated with subsequent stricture formation, while longterm success rates with a Roux-en-Y hepaticojejunostomy are >80%. Embolization of a biliary leakage site using a percutaneous approach is a potential therapeutic approach.

A clip placed on either the hepatic duct or the common bile duct is the most common cause of acute bile duct obstruction (Fig. 8.13). Obstruction also develops due to inadvertent bile duct cautery or fibrosis for other reasons. Hepatic duct and right hepatic duct necrosis are complications of electrocoagulation. Retained common bile duct stones also result in postoperative obstruction. Some bile duct strictures detected several months after laparoscopic cholecystectomy are associated with a traumatic neuroma, probably induced by prior bile leakage although a thermal injury during cholecystectomy and a resultant fibrous scar may predispose to traumatic neuroma formation.

Initially more proximal bile ducts do not dilate after an obstruction, and CT and US may miss a stricture; scintigraphy, on the other hand, will detect an obstruction. In the presence of a

Figure 8.13. Percutaneous cholangiography in a patient with jaundice after laparoscopic cholecystectomy reveals complete hepatic duct obstruction close to the porta hepatis (arrow). Exploration revealed a metal clip obstructing the hepatic duct. (Courtesy of David Waldman, M.D., University of Rochester.)

bile leak, however, lack of radionuclide activity in the intestines does not imply a more distal bile duct obstruction.

The gold standard for detecting a bile duct obstruction is cholangiography. An MRCP is often a first choice to detect these strictures and any other related complications, such as a leak.

Percutaneous or endoscopic stricture dilation is often a viable option; results are comparable to those of surgical reconstruction. With complete obstruction, such as secondary to a clip placed on the hepatic duct, percutaneous drainage of the obstructed ducts is the initial procedure of choice. On the other hand, with a common bile duct stone or cystic duct leak, a sphincterotomy, stone extraction, and an endoprosthesis are generally preferred.

Cholelithoptysis: Stones are spilled into the peritoneal cavity more often during a laparoscopic cholecystectomy than during an open cholecystectomy. While it was initially believed that no adverse long-term complications follow cholelithoptysis, severe complications requiring a subsequent open surgical procedure have developed. Generally lavage and retrieval of as many stones as possible is attempted after such spill. In fact, open retrieval appears appropriate if several stones or a large stone are lost.

Clips have also been spilled into the peritoneal cavity; their long-term consequence is not known.

Some stones eventually become surrounded by granulation tissue. Or gallstones become encased in a pelvic tumor. Some of these patients present months or even years after a cholecystectomy with intraabdominal infection, abscess, or fistula. Gallstones spilled into the peritoneal cavity have led to bowel obstruction. Stones have eroded into the urinary bladder, eroded through the diaphragm, resulted in an empyema, and have even been expectorated.

At times the specific etiology for such a calculi-induced abscess is suggested by CT or US. Computed tomography shows a gallstone acting as a nidus for surrounding inflammation.

Incomplete Excision: During laparoscopic cholecystectomy the cystic duct is typically transected close to the gallbladder in order to decrease the risk of hepatic duct and common duct injury. This has led to an incomplete cholecystectomy and eventually recurrent cholelithiasis.A bilobed or duplicate gallbladder

is suspected if repeat surgery finds most of the gallbladder still intact in a patient with recurrent symptoms after laparoscopic cholecystectomy.

Other Complications: Tumor seeding from an unsuspected gallbladder carcinoma during cholecystectomy is discussed later in this chapter (see Gallbladder Tumors Malignant Neoplasms).

Imaging studies shortly after a cholecystectomy often detect a pneumoperitoneum. It is of little significance unless it persists.

Major infection is not common after laparoscopic cholecystectomy. Computed tomography should identify any abscesses.

Arterial trauma during surgery leads to false aneurysm formation; subsequent aneurysm rupture into a bile duct results in hemobilia, at times manifesting months after cholecystectomy. The numerous published reports attest that this is not a rare complication. The right hepatic artery is most often involved, although even a renocaval arteriovenous fistula has been reported (35). These aneurysms and hepatic artery-to-bile duct fistulas can be successfully embolized.

Unrecognized bleeding due to trocar insertion has resulted in omental or abdominal wall hematomas.

A draining umbilical sinus tract has developed at a trocar site. Small bowel has herniated through a trocar site and led to an obstruction. Unsuspected bowel injury may occur. Leakage of intestinal content into the peritoneal cavity induces a peritonitis mimicking bile peritonitis. Small bowel necrosis has been reported.

Diaphragmatic injury, even a pneumothorax, has been reported.

Underlying primary adrenal insufficiency can lead to shock, bilateral adrenal hemorrhage, and related complications after laparoscopic cholecystectomy.

Acute Acalculous Cholecystitis

Etiology

The precise etiology of acute acalculous cholecystitis is not known. The reported prevalence varies in the literature, with part of the difficulty being a lack of definition.

Bile stasis and gallbladder inflammation develop secondary to either a chemical or

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ischemic insult. These patients do not have cystic duct obstruction, and usually no stones are present in the gallbladder. Infection from an enteric source may play a role.Acalculous cholecystitis has occurred in association with Vibrio cholera infection, typhoid fever, biliary Ascaris lumbricoides infestation, and even Candida infection following cardiac transplantation.

Cholesterol crystal embolization has been implicated in patients with atherosclerotic vascular disease who develop acalculous cholecystitis. Acalculous cholecystitis develops in young immunosuppressed patients; it is associated with veno-occlusive liver disease. This condition is more common in critically ill patients, those who have had a major traumatic insult, those who are on prolonged bed rest and intensive care, or those who are debilitated.

Diagnosis

Murphy’s sign is difficult to elicit both clinically and sonographically.

The sensitivity and specificity of imaging in detecting acute acalculous cholecystitis are not high. At times the diagnosis is one of exclusion. Computed tomography reveals pericholecystic inflammation, gallbladder wall thickening, and pericholecystic fluid. Gallbladder mucosa tends to enhance with contrast.

Ultrasonography findings of acalculous cholecystitis are similar to those seen with calculous cholecystitis, except for gallstones, and consist of an inconsistent Murphy’s sign, gallbladder wall thickening, and pericholecystic fluid; other occasional findings include gallbladder hydrops, gallbladder sludge, and a striated gallbladder wall. These are rather nonspecific findings, especially in sick patients. Several studies have concluded that these nonspecific US findings are common in intensive care patients and that sonography is of limited value in detecting acalculous cholecystitis (36). On the other hand, acalculous cholecystitis can be excluded when gallbladder US is normal.

Scintigraphy is falsely negative in acute acalculous cholecystitis if radiotracer enters the gallbladder. A high scintigraphic false-positive rate is also found. The gallbladder does not constrict normally to stimulation by cholecystokinin in acalculous cholecystitis, although this is a nonspecific finding, common in postoperative patients.

GALLBLADDER AND BILE DUCTS

Therapy

Acute acalculous cholecystitis is associated with high morbidity and mortality. Many patients developing acalculous cholecystitis are already at high surgical risk. Complications increase with delay in therapy. Percutaneous cholecystostomy using US guidance has evolved as the therapy of choice for these patients.

Laparoscopy has been used as a diagnostic tool for acute acalculous cholecystitis. Such diagnostic laparoscopy can be performed even at the patient’s bedside.

Chronic Cholecystitis

The definition of chronic cholecystitis varies. On one extreme are those who consider the presence of gallbladder stones a sign of chronic cholecystitis; others limit this term to a setting of a small, thick-walled gallbladder wall containing histologic findings of chronic inflammation and fibrosis and no stones. The latter condition is also called chronic acalculous cholecystitis; the problem with this definition is that many gallbladders resected for other conditions in patients with no clinical evidence of disease harbor similar pathologic findings.

Actinomycosis is a rare cause of cholecystitis. Myelofibrosis has presented as chronic cholecystitis.

With the presence of gallstones and an appropriate clinical history, the diagnosis is straightforward. The issue becomes murky when gallstones are absent—a relatively common scenario in clinical practice. Considerable controversy surrounds the clinical and even pathologic diagnosis of chronic acalculous cholecystitis. In fact, some investigators question whether such a disease as chronic acalculous cholecystitis even exists or whether these patients’ symptoms reflect a spectrum of disorders.

Imaging

Ultrasonography in some symptomatic patients reveals a thickened gallbladder wall and no stones, simply sludge, or stones. Without stones, whether these patients should undergo surgery is controversial; a number of postoperative patients are not relieved of their symptoms. A combined endoscopic US and stimulated biliary

drainage procedure has been suggested for these patients. In patients with unremarkable transabdominal US, endoscopic US can reveal gallbladder sludge or stones, or stimulated biliary drainage is positive.

Postcontrast MRI in patients with chronic cholecystitis usually reveals a thickened gallbladder wall, with early mucosal and muscle enhancement in most; stones obviously do not enhance, and the fibrotic subserosa enhances late.

Xanthogranulomatous Cholecystitis

This chronic inflammatory condition is uncommon in the gallbladder and is analogous to xanthogranulomatous pyelonephritis. The presence of chronic infection in a setting of cholelithiasis and bile stasis presumably leads to recurrent inflammation. Also, obstruction and intramural rupture of Rokitansky-Aschoff sinuses appear to play a role. Xanthogranulomatous cholecystitis ranges from a focal condition involving only a portion of the gallbladder wall to diffuse inflammation and fibrosis extending into surrounding tissues. Intramural abscesses and inflammation are eventually replaced by lipidfilled histiocytes, round cells, and other tissue. It has developed after placement of metallic biliary stents. Histology reveals both abscesses and xanthogranulomas, seen as intramural nodules on imaging studies.

Imaging findings are nonspecific in most patients. The gallbladder wall is irregular and thickened, and it blends into adjacent liver parenchyma. Gallstones are common. Computed tomography reveals an intramural hypodense band in about one third of patients (37) or intramural hypodense nodules; similar intramural hypoechoic nodules or bands are found with US. A thickened gallbladder wall ranges from hyperechoic to isoechoic and even hypoechoic compared to liver parenchyma. Chemical shift MR is useful to detect any fat (38). Pericholecystic fluid is an inconsistent finding.

Xanthogranulomatous cholecystitis and gallbladder carcinoma tend to have a similar imaging appearance. Complicating the issue is that patients with xanthogranulomatous cholecystitis are at increased risk of developing a carcinoma. Of interest is that increased serum carbohydrate antigen 19–9 (CA 19–9) levels occur in xanthogranulomatous cholecystitis