Материал: Advanced Imaging of the Abdomen - Jovitas Skucas

Some choledochoceles are treated by simple endoscopic unroofing. Nevertheless, because most choledochal cysts are premalignant, a simple drainage procedure is believed to be insufficient therapy in most patients. A malignancy has developed years after cystenterostomy.

Cyst excision and a hepaticojejunostomy are traditional procedures of choice, with some surgeons preferring a hepaticoantrostomy. The latter anastomosis is believed to be associated with fewer episodes of recurrent cholangitis, although postoperative cholescintigraphy does not differ significantly between the two surgical procedures and thus differences in bile stasis and reflux presumably are not a cause of the more frequent recurrent cholangitis seen after hepaticojejunostomy. An anastomotic bile duct carcinoma is a rare complication.

An unsuspected choledochal cyst is occasionally encountered during laparoscopic cholecystectomy; the underlying anatomy can be studied and a choledochocele diagnosed by either laparoscopic contact US or intraoperative cholangiography.

Findings with Tc-00m-IDA scintigraphy are similar in infants after a Roux-en-Y hepaticojejunostomy and after a hepaticoantrostomy, although the former are more prone to develop recurrent cholangitis.

Caroli’s Disease

In 1958, Caroli observed numerous ectasia-like intrahepatic cysts communicating with the biliary tree (21). This disorder, as described by Caroli, is now believed to be part of the spectrum of congenital hepatic fibrosis. The latter condition is discussed in Chapter 7.

Computed tomography reveals cysts varying in size.At times a central enhancing “dot”is seen postcontrast, representing a portal vein radical, suggesting the diagnosis. With uncomplicated disease, US reveals intrahepatic anechoic cystic structures. Once sludge or stones form in these dilated segments, US identifies hyperechoic, well-marginated foci. As expected, MR reveals these cysts to be hypointense on T1and hyperintense on T2-weighted images. Similar to CT, the central portal vein radical enhances. Occasionally MR identifies septa.

ADVANCED IMAGING OF THE ABDOMEN

To make a diagnosis of Caroli’s disease it is necessary to show that the intrahepatic “cysts” connect to bile ducts, thus distinguishing this entity from polycystic disease. Autosomalrecessive polycystic kidney disease is in the differential diagnosis of Caroli’s disease. Scintigraphy in patients with polycystic kidney disease not uncommonly reveals cholestasis and intrahepatic bile duct dilation, mimicking Caroli’s disease. Thus some type of cholangiogram is generally necessary to differentiate these entities.

An occasional patient is found to have localized dilation of an intrahepatic bile duct without any obstruction. Some of these ducts contain considerable mucinous material and a mucinous cystic neoplasm is often suspected, but resection reveals neither a malignancy nor fibrosis. The term solitary cystic dilation of an intrahepatic bile duct is used to describe this condition. The relationship of such a localised dilation to Caroli’s disease is speculative.

Metachromatic Leukodystrophy

Metachromatic leukodystrophy is primarily in the domain of a neurologist, and the only purpose in mentioning it in a work on the abdomen is that an occasional patient with this lysosomal storage disorder, caused by a deficiency of the lysosomal enzyme arylsulfatase A, has an abnormal gallbladder. A diagnosis is established by detecting deficient leukocyte or fibroblast arylsulfatase A activity. A late-infancy onset is common, although atypical and late onsets have been described. Found worldwide, this condition is considerably more prevalent in certain populations, such as in the Western Navajos with an estimated carrier frequency of 1/25 to 1/50 (22).

Ultrasonography in some children with metachromatic leukodystrophy reveals a diffuse thick, hyperechoic gallbladder wall and a small lumen. A number of these children develop gallbladder papillomatosis. Because gallbladder polyposis is rare in children and has developed before neurologic symptoms of metachromatic leukodystrophy become apparent, discovery of such polyps, often made incidentally, should raise suspicion for this condition. Some children with this condition also develop gallstones. One presented with gastric outlet obstruction due to

GALLBLADDER AND BILE DUCTS

an enlarged gallbladder, treated by percutaneous aspiration, and later developed a gallbladder carcinoma (23).

Trauma

An extrahepatic biliary injury classification scale, devised by the American Association for Surgery of Trauma, is outlined in Table 8.1.

Gallbladder

The most common gallbladder injury due to blunt trauma is contusion; perforation and avulsion are rare. Only occasionally does CT reveal gallbladder wall disruption. A hematoma is identified by CT as focal or diffuse thickening, at times mimicking cholecystitis. Pericholecystic fluid, a poorly defined gallbladder wall, a collapsed gallbladder lumen, and intraluminal blood detected by imaging in a setting of abdominal trauma should suggest gallbladder injury (Fig. 8.6).

Associated intraabdominal trauma is common, often masking underlying gallbladder perforation.

Table 8.1. Surgical biliary injury scale

Grade* Type of injury

IGallbladder contusion Portal triad contusion

IIIComplete gallbladder avulsion Cystic duct laceration/transection

V>50% transection of common hepatic duct >50% transection of common bile duct Combined right and left hepatic duct

injuries

Intraduodenal or intrapancreatic bile duct injury

* Advanced one grade for multiple injuries, up to grade III. Source: Adapted from Moore et al. (24).

Figure 8.6. Sedimentation of blood in gallbladder on T2–weighted MR image results in a hyperintense supernatant fluid. (Source: Burgener FA, Meyers SP, Tan RK, Zaunbauer W. Differential Diagnosis in Magnetic Resonance Imaging. Stuttgart: Thieme, 2002, with permission.)

Bile Ducts

Spontaneous Rupture

Spontaneous bile duct perforation is uncommon and most often is associated with duct obstruction by stones. These perforations range from intrahepatic, to free intraperitoneal, to an encapsulated collection of bile. Aspirated fluid reveals a high bilirubin level. Hepatobiliary scintigraphy detects biliary ascites with a continuing leak.

A cholangiogram, whether performed percutaneously or endoscopically, should be diagnostic if the involved bile duct is visualized. These patients generally undergo surgery, although endoscopic management is also feasible.

Traumatic Bile Leakage

Biliary duct laceration and avulsion are not uncommon with blunt liver trauma. Complete transection of an intrahepatic duct is associated with liver laceration. Rupture of smaller intrahepatic ducts leads to slow bile extravasation, biloma formation tends to be delayed, and imaging findings are rather subtle. At times a subtle injury is not discovered during the initial surgery. Intrapancreatic bile duct injury, including avulsion of this biliary segment, is usually associated with pancreatic trauma. Not all bile

collections after blunt abdominal trauma represent a biloma. An intrahepatic communicating cyst or a choledochal cyst can be confused with a biloma.

Many of these patients undergo CT for suspected trauma to adjacent structures. For subtle bile leakage, however, either direct cholangiography or cholescintigraphy are the imaging modalities of choice. Major extravasation is suspected if scintigraphy reveals intraperitoneal activity greater than in the gastrointestinal tract.

Although not often performed for suspected biliary tract injury, anecdotal reports suggest that MRCP has considerable potential as an alternative to ERCP.

Obstruction

Some patients develop a biliary stricture as a delayed complication to blunt trauma. Whether these are related to a missed focal leak or ischemia is speculation. The suprapancreatic extrahepatic bile ducts are most often involved.

Infection/inflammation

Acute Cholecystitis

Clinical findings in acute cholecystitis range from mild signs and symptoms pointing to a right upper quadrant disorder to a lifethreatening condition. Bacteremia is not common in acute cholecystitis; when present, however, it is associated with increased complications and a higher mortality. An occasional patient develops septic shock and dies within hours of onset of symptoms. Especially in the elderly the differential diagnosis is rather extensive.

Acute cholecystitis appears to be more common than expected after colectomy for ulcerative colitis.

Etiology

Stones

Acute calculus cholecystitis can be defined as inflammation of the gallbladder due to cystic duct obstruction by a gallstone. Infection is an integral part of this condition because without

ADVANCED IMAGING OF THE ABDOMEN

infection, instead of cholecystitis, gallbladder hydrops develops.

Infection

Mentioned here are only the more unusual infections associated with acute cholecystitis. Infection with Ascaris lumbricoides can result in acute cholecystitis. Ultrasonography of a worm in the gallbladder reveals an echogenic structure having nondirectional movements and containing a central anechoic tube.

Tuberculous cholecystitis is rare. The diagnosis is eventually suggested by the pathologist.

In patients with culture positive Salmonella enteric fever, US detected a globular, distended gallbladder in 53%, a positive sonographic Murphy’s sign in 40%, pericholecystic edema or fluid in 40%, gallbladder wall thickening (>4mm) in 34%, intraluminal echoes or sludge in 15%, intramural linear striation in 13%, and mucosal irregularity or sloughing in 6% (25).

A hepatic hydatid cyst rupturing into the gallbladder causing cystic duct obstruction and acute cholecystitis is found in endemic regions. Acute cholecystitis has been associated with Candida albicans infection. Even Vibrio cholerae infection can result in acute cholecystitis.

Other Etiologies

Occasionally acute obstructive cholecystitis is not related to obstruction by gallstones but is secondary to a cystic duct adenoma or other polyp. Anecdotal accounts describe BB shots or other missile fragments leading to acute cholecystitis. An uncommon association exists between acute cholecystitis and hemobilia.

Diagnosis

In general, initial US appears to be more productive than CT in patients with suspected acute biliary disease. Currently, CT does not have a primary role in diagnosing acute cholecystitis; although a number of CT findings have been described, most are nonspecific and some patients with acute cholecystitis have a normalappearing gallbladder. Not uncommon is focal increased CT liver enhancement adjacent to the gallbladder bed, presumably due to increased blood flow from an inflamed gallbladder. Intra-

GALLBLADDER AND BILE DUCTS

hepatic portal vein thrombosis is a complication in some patients with acute cholecystitis; it results in transient hyperdense regions.

Both US and cholescintigraphy achieve similar accuracies of 85% to 90% in patients with suspected acute cholecystitis, and the choice of one over the other varies in different regions of the world. Whether US or cholescintigraphy is the superior diagnostic modality in suspected acute cholecystitis is a matter of opinion. Considerable heat has been generated on this topic. Thus reputable authorities have made statements such as the following (26):

Cholescintigraphy is generally considered to be the study of choice. . . . Although US is sometimes reflexively ordered for the diagnosis of symptomatic biliary disease, the results usually are not specific enough to make the diagnosis of acute cholecystitis.

Ultrasonography

Ideally, an US diagnosis of acute cholecystitis is made by detecting a stone obstructing the cystic duct—a rare finding. More often the sonographic signs suggesting acute cholecystitis are the presence of intraluminal gallstones, gallbladder wall thickening (at times with a threelayered wall appearance), fluid surrounding the gallbladder, and a sonographic Murphy’s sign. Among 69 patients with acute abdominal pain and operated on for acute cholecystitis, preoperative US detected gallbladder wall thickening in 56%, one or more gallstones in 86%, pericholecystic fluid in 14%,gallbladder distention in 46%, and a sonographic Murphy’s sign in 39% (27). Still, US results are not without controversy. In patients with right upper quadrant pain although sensitivity of a sonographic Murphy’s sign is high, specificity is low due to a large number of false positives. Even if presence of gallstones, wall edema and pericholecystic fluid are included, specificity remains rather low, making Murphy’s sign unreliable in distinguishing acute from chronic cholecystitis. Combined use of color velocity imaging (to determine blood flow velocity) and power Doppler US appear to improve both sensitivity and specificity, compared to gray-scale US, in detecting acute cholecystitis.

In most patients with acute cholecystitis, the gallbladder wall thickens diffusely, a nonspecific finding (Table 8.2). Patients with acute viral hepatitis not uncommonly have a

cholecystitis-like clinical presentation and a markedly increased gallbladder wall thickness, as measured by US; in these patients the gallbladder wall reverts to normal once hepatitis clears.

Ultrasonography in an occasional patient with a subhepatic appendix containing an appendicolith suggests cholecystitis with a gallstone.

Occasionally color Doppler US detects gallbladder wall flow in patients with acute cholecystitis, but this is an inconsistent finding.

Magnetic Resonance Imaging

The role of MRI in suspected acute cholecystitis is still evolving. Although MRI accuracy rivals that of US, more ready availability, lower cost, and the simplicity of US ensure its continued use in most institutions.

Most publications deal primarily with T2weighted images, which constitute a basis for MRCP. Findings of acute cholecystitis on T2weighted sequences include the presence of gallstones, a thickened gallbladder wall, and pericholecystic fluid. Among patients with suspected acute cholecystitis, T2-weighted HASTE MRI achieved a 91% sensitivity and 79% specificity in diagnosing acute cholecystitis (28); in those patients who did have acute cholecystitis, HASTE MRI sequences detected a hyperintense pericholecystic signal in 91%, an impressive finding. Gallbladder stones were detected by HASTE MRI in 93% of patients with acute calculus cholecystitis.

Comparing MRCP and US before cholecystectomy, US was superior in evaluating gallbladder wall thickening but MRCP excelled in detecting cystic duct and gallbladder neck calculi and cystic duct obstruction (29).

Gallbladder inflammation leads to increased blood flow, resulting in increased contrast enhancement. Initial enhancement starts at the inner mucosal layer and gradually involves the entire gallbladder wall, findings detected with MR. On immediate postgadolinium images a transient increase in pericholecystic liver enhancement is common in acute cholecystitis patients.

Contrast-enhanced MRI should distinguish between gallbladder wall thickening due to acute cholecystitis and most other conditions listed in Table 8.2; aside from acute cholecysti-