Книги по МРТ КТ на английском языке / Advanced Imaging of the Abdomen - Jovitas Skucas

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-

Table 8.2. Causes of diffuse gallbladder wall thickening

Local conditions

Acute cholecystitis

Chronic cholecystitis

Hepatitis

Associated with portal hypertension

Portal vein thrombosis

Acute viral hepatitis

AIDS cholangitis

Systemic disorders

Hypoalbuminemia

Renal failure

Ascites

Chemotherapy

Severe congestive heart failure

Graft-versus-host disease

tis, other conditions show minimal gallbladder wall enhancement and pericholecystic liver enhancement.

Scintigraphy

Cholescintigraphy with Tc-99m-HIDA or one of the other IDA derivatives assesses gallbladder function. For this test to be valid, however, reasonably normal hepatic uptake and excretion is necessary. Cholescintigraphy results are not meaningful in a setting of severe hepatocellular dysfunction or common bile duct obstruction. The test should also be interpreted with caution after sphincterotomy because some of these patients have gallbladder nonvisualization even without acute cholecystitis. Likewise, gallbladder nonvisualization is found in patients with cystic fibrosis and in a setting of a choledochal cyst.

Several hours of fasting are normally required before cholescintigraphy is performed; otherwise, resultant gallbladder contraction prevents radiotracer and bile flow into the gallbladder, thus leading to a false-positive test. One disadvantage of cholescintigraphy is that it generally requires several hours to perform this test, a fact accentuated by ultrasonographers.

Gallbladder ejection fraction is measured during cholecystokinin cholescintigraphy and by US. In most institutions an ejection fraction of <35% is considered abnormal, although this limit varies depending on injection method used. In general, a normal gallbladder ejection fraction excludes dysfunction. Both scintigra-

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phy and US are reproducible techniques in studying gallbladder contraction, but these two tests are not directly interchangeable.

A fatty meal induces gallbladder emptying, and, in general, a standardized liquid fatty meal results in good intraindividual reproducibility of gallbladder emptying; there is, however, considerable interindividual variability. Aside from CCK-dependent effects, other mechanisms probably are involved in gallbladder emptying. Gallbladder US in young, nulliparous women reveals fasting volume and postprandial ejection fractions to be slightly greater during the luteal phase than during the follicular phase. Gallbladder volume roughly doubles during pregnancy and then decreases postpartum. Gallbladder motility and gallbladder ejection fraction are significantly impaired in late pregnancy.

Gallbladder visualization during cholescintigraphy (or oral cholecystography) essentially excludes acute cholecystitis. Normally nonvisualization is defined as a lack of gallbladder activity up to 4 hours after radiotracer administration.

Some patients have increased tracer activity in liver parenchyma adjacent to the gallbladder—the pericholecystic rim sign. This activity is associated with acute cholecystitis in most but not all patients and is believed to be secondary to increased blood flow to parenchyma adjacent to an inflamed gallbladder. It is not to be confused with tracer within the gallbladder.

What is the significance of gallbladder nonvisualization but the presence of a pericholecystic rim sign? Morphine-augmentation is helpful in visualizing the gallbladder in some and thus excluding acute cholecystitis, although even then there are false-positives.

Gallbladder contractility is decreased in patients with a prior vagotomy. Likewise, the gallbladder does not contract normally in patients with achalasia or those on octreotide therapy.

Gallbladder contraction before injecting Tc-99m-IDA allows subsequent tracer material to accumulate within the gallbladder and decreases the number of false-positive results. A common drug used to stimulate gallbladder contraction is cholecystokinin-octapeptide (CCK-8). It is used selectively; for instance, in some institutions patients who have been fasting for 24 hours or longer are pretreated

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with CCK while others are not. Slow infusion of a physiologic dose of CCK-8 results in more complete gallbladder emptying than a bolus injection.

If the gallbladder is not visualized in 60 to 90 minutes, often 0.04mg/kg morphine sulfate is injected IV and additional images are obtained for 30 to 60 minutes. Intravenous morphine increases sphincter of Oddi pressure and thus bile accumulates within the gallbladder. If the gallbladder still does not visualize during morphine-augmented cholescintigraphy, in the appropriate clinical setting a diagnosis of acute cholecystitis is reasonable. If, on the other hand, the gallbladder is not visualized within an initial 90 minutes but is observed after morphine, abnormal gallbladder function should be suspected.

A variant of the above technique is to combine cholecystokinin pretreatment together with morphine augmentation. Imaging is performed in patients after Tc-99m-BrIDA until gallbladder activity is identified or up to 90 minutes postinjection; if no gallbladder is identified, a second dose of BrIDA is followed by morphine sulfate.

Gallbladder scintigraphy can be performed using indium-111–labeled autologous white blood cells. Labeled white blood cells accumulate within the gallbladder wall in acute cholecystitis. In some patients, however, delayed imaging is required, thus delaying the diagnosis.

Perforated Cholecystitis

Neglected cholecystitis evolves into gallbladder perforation. Most perforations are walled-off and result in pericholecystic fluid or a right upper quadrant abscess, a common location being between the gallbladder and adjacent liver. Free perforation into the peritoneal cavity results in bile peritonitis, while an occasional perforation into the liver evolves into a liver abscess.

Chronic perforations have evolved into a cholecystocutaneous or cholecystoenteric fistula, and even a cholecystogastric fistula (Fig. 8.7). Some cholecystoenteric fistulas are secondary to gallstones eroding into the gut (discussed in Chapter 4).

Detection of gallbladder perforation is not straightforward. Adherent omentum, fat, or

adhesions often mask a recent perforation. Computed tomography visualizes only about half of gallbladder wall defects, and US even less. Pericholecystic fluid and gallbladder wall thickening are often the only pertinent imaging findings.

Gangrenous Cholecystitis

Gangrenous cholecystitis is a sequela of either calculus or acalculus cholecystitis.

Computed tomography and US reveal similar findings. The gallbladder wall is irregular and thick. Sloughed gallbladder mucosa is seen as thin intraluminal linear echoes parallel to the gallbladder wall and a striated wall edema pattern seen with US should suggest gangrenous cholecystitis. Often inflammation extends to surrounding structures. A sonographic Murphy’s sign is less often elicited in these patients than with more conventional acute cholecystitis.

Color Doppler US reveals no flow within a thickened gallbladder wall in acute necrotizing cholecystitis.

Occasionally a thin rim of increased scintigraphic activity, a rim sign, is seen adjacent to the gallbladder fossa, a sign associated with gallbladder wall gangrene. The presence of a

Figure 8.7. Spontaneous cholecystocutaneous fistula (arrow) secondary to cystic duct obstruction by a stone.

rim sign, together with subsequent gallbladder visualization after administration of morphine, does occur with gallbladder gangrene. The rim sign should be distinguished from tracer activity in adjacent liver parenchyma.

Empyema/Abscess

Empyema, consisting of an obstructed, pusfilled gallbladder lumen, leads to marked gallbladder distention. Ultrasonography shows a markedly distended, hyperechoic sludgecontaining gallbladder. Computed tomography reveals this pus-filled gallbladder content to have greater attenuation than bile. At times a frank abscess is identified (Fig. 8.8).

Laparoscopic cholecystectomy is difficult in the setting of gallbladder empyema and many of these patients undergo conventional cholecystectomy.

Emphysematous Cholecystitis

Emphysematous cholecystitis is a severe form of acute cholecystitis manifesting with gas (not air) in the gallbladder lumen, wall, bile ducts, or pericholecystic tissues, and no abnormal communication between the biliary tree and gastrointestinal tract. It develops if gas-forming bacteria predominate as the infectious organism. Diabetes mellitus is a common underlying condition. Some of these patients do not appear systemically ill, and unless imaging suggests the condition, conservative therapy may be initially

Figure 8.8. Salmonella cholecystitis resulting in a gallbladder abscess (arrow). The abscess was drained percutaneously. (Courtesy of Georgine DeMarino, M.D., University of Iowa.)

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initiated. Nevertheless, mortality is about 15%. Gallstones are absent in some of these patients. In some, a superimposed pneumoperitoneum suggests a perforation. Rarely, simultaneous emphysematous pyelonephritis and emphysematous cholecystitis develop.

The diagnosis is straightforward with conventional radiography and CT, revealing gas in the gallbladder lumen, wall, or pericholecystic tissues (Fig. 8.9). Ultrasono-graphy can miss emphysematous cholecystitis due to gallbladder nonvisualization; intramural gas can be confused with gas within the bowel. If the gallbladder is identified, US reveals highly reflective echoes from nondependent gallbladder wall segments. Exten-sive gas mimics gallbladder wall calcifications. Ultrasonography in one patient revealed gas bubbles rising within the gallbladder and floating to the surface, an appearance called effervescent gallbladder

(30).

Cholescintigraphy may or may not detect cystic duct obstruction in these patients.

Although successful percutaneous gallbladder drainage has been performed in these patient, most are managed surgically.

Eosinophilic Cholecystitis

Histologically, eosinophilic cholecystitis consists of a transmural eosinophilic infiltrate. It is associated with allergic conditions, parasites, hypereosinophilic syndromes, and even with calculous acute cholecystitis. Tissue infiltration with eosinophils and eosinophilic granulomas occurs in necrotizing granulomatous vasculitis involving the gallbladder; similar features are found in allergic granulomatous angiitis of Churg and Strauss.

Therapy

In Pregnancy

Traditionally, a pregnant woman with acute cholecystitis has undergone an open cholecystectomy, although a laparoscopic cholecystectomy is feasible. If warranted, cholangiography is performed.

A pneumoperitoneum is induced during a typical laparoscopic cholecystectomy; gasless laparoscopic cholecystectomy has been performed in pregnant women.

A

Ultrasonography-guided percutaneous cholecystostomy may have a role in pregnancy; biliary decompression is maintained during pregnancy and an elective cholecystectomy performed after delivery.

Percutaneous Cholecystostomy/Aspiration

Does percutaneous transhepatic gallbladder drainage have a role in patients with acute suppurative cholecystitis? A common indication for percutaneous cholecystostomy is in a high surgical risk patient with suspected acute cholecystitis. Ultrasonography is commonly used for guidance. Following successful cholecystostomy most patients improve, the exception being those who have either transmural gallbladder inflammation or gangrene.

Gallbladder aspiration is an alternate procedure to percutaneous cholecystostomy in some patients. In a comparison, 82% of gallbladder aspirations and 100% of percutaneous cholecystostomies were technically successful (31); viscid sludge or pus prevented aspiration through a 21-gauge needle in some patients. Complications are more common with percutaneous cholecystostomy than aspiration. A typical scenario is US-guided percutaneous gallbladder drainage followed by laparoscopic cholecystectomy several days later, after clinical

Figure 8.9. Emphysematous cholecystitis. Radiograph (A) and CT

(B) in two different patients. Gas is present in the gallbladder wall and lumen (arrow). Pneumobilia was identified on other images.

improvement. Inflammation subsides after drainage and the cystic duct often becomes patent, as shown by cholescintigraphy performed after percutaneous gallbladder drainage.

In general, for most patients with acute acalculous cholecystitis a percutaneous cholecystostomy is curative; in the presence of stones, however, a percutaneous cholecystostomy simply provides drainage and an eventual definitive procedure is necessary in most patients.

Open Cholecystectomy

This is not the place to discuss the relative merits and indications of open versus laparoscopic cholecystectomy. Rather, the emphasis here is on the role of imaging. In general, selective rather than routine intraoperative cholangiography is performed. Intraoperative fluoroscopic cholangiography is becoming more popular than static images. A fluoroscopic study can be performed faster than a comparable static study; whether the information obtained with a fluoroscopic image is sufficient is debatable. Quality control of intraoperative images remains a problem.

The indications for intraoperative cholangiography continue to be debated by surgeons. Risk factors correlating with presence of chole-

docholithiasis include history of jaundice, pancreatitis, hyperbilirubinemia and hyperamylasemia. Other criteria whether to perform intraoperative cholangiography include dilated bile ducts on preoperative US and unclear US findings.

Laparoscopic Cholecystectomy

Compared to open cholecystectomy, laparoscopic cholecystectomy requires a longer operative time, but it leads to less pain, a shorter hospitalization, and earlier recovery, and it is associated with a lower morbidity.

Cirrhosis is generally considered a relative contraindication for laparoscopic cholecystectomy.

Extensive adhesions surrounding the gallbladder make laparoscopic cholecystectomy more difficult. Neither CT nor US can reliably detect these adhesions although MRI may have a role. Nonvisualization of the gallbladder on drip infusion cholangio-graphy appears to have value in predicting extensive adhesions, but this study is rarely performed.

Imaging

Laparoscopic cholecystectomy achieves the same end result as an open cholecystectomy, yet with the former procedure surgeons generally prefer a more specific preoperative diagnosis concerning the presence or absence of bile duct stones; although these stones are readily detected by operative cholangiography, their removal during laparoscopic cholecystectomy is problematic and is one of the causes of conversion to an open cholecystectomy. The luxury of T-tube insertion if bile duct stones are detected and their later removal via the T-tube tract by interventional radiologists is not a viable option during laparoscopic cholecystectomy.

Preoperative US aids in predicting whether intraoperative difficulties are encountered. Preoperative US detection of gallbladder wall thickening was found to be the most sensitive and pericholecystic fluid the most specific indicator of a difficult laparoscopic cholecystectomy and the possible need for conversion to laparotomy (32).

Is ERC necessary prior to routine laparoscopic cholecystectomy? Prior to laparoscopic cholecystectomy, ERC not only detects bile duct

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stones but also outlines any anomalous biliary anatomy. If stones are found, a sphincterotomy and stone extraction are then performed. Patients having normal biliary US and normal liver function tests have a >95% negative ERC rate, and for these patients preoperatively ERC appears unnecessary. Some surgeons thus argue that endoscopic sphincterotomy prior to laparoscopic cholecystectomy should be reserved only for seriously ill patients or a suspected malignancy, because laparoscopic transcystic duct exploration can be successful in over 90% of cholecystectomies and is safe. Even if laparoscopic cystic duct exploration is not successful, then either open choledochotomy or postoperative endoscopic sphincterotomy is considered.

The role of operative cholangiography during laparoscopic cholecystectomy is not settled and depends, in part, on whether preoperative imaging is performed. Some surgeons obtain it almost routinely, while others use it selectively. The study is safe and adds little to patient morbidity, but it does prolong surgery. A learning curve exists in performing successful intraoperative cholangiography. A success rate of over 90% can be achieved. Digital C-arm fluoroscopy is a useful guide for intraoperative cholangiography. In general, laparoscopic cholangiography and, if needed, common bile duct exploration obviate a need for a later second procedure such as endoscopic sphincterotomy in patients with retained stones.

Intraoperative cholangiography detects biliary tract complications, and often conversion to an open laparotomy can be performed to repair a visualized injury. Such conversion results in earlier detection of injuries and fewer subsequent procedures to correct the injury.

Operative cholangiography performed primarily to detect bile duct stones is discussed later (see Biliary Stones).

Complications

General: Complications occur during laparoscopic cholecystectomy, with postoperative complication rates of 4% to 6% being typical. Initially, after the introduction of laparoscopic cholecystectomy, bile duct injuries were more common than during the previous open cholecystectomy era. Nevertheless, most recent

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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

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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.