Материал: Advanced Imaging of the Abdomen - Jovitas Skucas

primary sclerosing cholangitis. Also, patients with AIDS cholangitis are more prone to developing superimposed pyogenic cholangitis. Considerable overlap exists between CT and cholangiographic findings.

Tumors

Children with AIDS appear to be at risk for smooth muscle neoplasms. Gallbladder leiomyomas and gallbladder Kaposi’s sarcomas have been reported in HIV-infected children. Some also develop splenic artery calcifications.

Postoperative Changes

Postcholecystectomy

Does the common bile duct dilate after a cholecystectomy? One large study found that, on average, the duct did increase slightly in diameter, although some patients had no significant change (96).

Postcholecystectomy syndrome consists of recurrent biliary-like pain or dyspeptic symptoms. Some patients have sphincter of Oddi dysfunction, a dilated bile duct, or delayed biliary drainage, while others have no objective findings. An increase in bile salt concentration in fasting gastric juice occurs after cholecystectomy, suggesting that duodenogastric reflux may have a role in pathogenesis of this syndrome.

An occasional metal clip applied during cholecystectomy migrates into bile duct lumen and acts as a foreign-body nidus for gallstone formation (Fig. 8.42). Similarly, a suture thread can occasionally be identified in a postcholecystectomy bile duct stone.

Magnetic resonance cholangiopancreatography is evolving into a primary screening study for postcholecystectomy syndrome. Dilated bile ducts, strictures, retained stones, and other related abnormalities are detected. Scintigraphy often shows patent ducts but delayed biliary transit, suggesting liver dysfunction.

Sump Syndrome

Sump syndrome occurs in the presence of distal common bile duct obstruction after a side-to- side choledochoor cholecystoduodenostomy

Figure 8.42. Metal clip encased in a stone (arrow) in a patient with a previous cholecystectomy. (Courtesy of Stephen Laucks, M.D., Hazleton, Pennsylvania.)

(Fig. 8.43). Distal obstruction causes stasis and debris in the distal common bile duct stump, at times associated with cholangitis and even pancreatitis. A sphincterotomy, if feasible, should be curative. Endoscopy via the side-to-side choledocoduodenostomy or even a percutaneous transhepatic approach is occasionally helpful if transpapillary access is not possible.

This syndrome should not develop after a choledochojejunostomy or a hepaticojejunostomy.

Changes After Biliary-Enteric

Anastomoses

Detection of postoperative biliary leaks is discussed in a previous section under complications of therapy for acute cholecystitis. Afferent loop obstruction is covered in Chapter 4.

A cholangiogram, regardless of how it is performed, should be diagnostic of a postoperative bilioenteric stricture (Fig. 8.44), but both ERCP and a percutaneous approach are invasive procedures. Magnetic resonance cholangiopancreatography has evolved into an accurate post-

GALLBLADDER AND BILE DUCTS

Figure 8.43. Sump syndrome. A cholecystoduodenostomy was performed years ago. The distal bile ducts are filled with sludge (arrow).

operative imaging modality to detect these strictures, identify any residual stones, and evaluate dilated ducts. In 34 patients who underwent pancreaticobiliary ductal surgery,

Figure 8.44. Stricture (arrow) and stones (arrowheads) after choledochojejunostomy. The patient had a prior Whipple procedure for a cholangiocarcinoma.

half-Fourier RARE MRCP achieved a 100% sensitivity and 86% to 87% specificity in detecting dilated ducts and choledochoenteric anastomotic strictures (97).

Rarely, cholangitis developing after a hepaticojejunostomy is secondary to reflux of intestinal content from the jejunal limb.

Endoscopic retrograde cholangiopancreatography is feasible after a choledochoduodenostomy but is precluded after a choledochojejunostomy unless the afferent limb is short. Aside from percutaneous cholangiography, MRCP is the procedure of choice to study these bile ducts.

Examination Complications

Endoscopic Retrograde

Cholangiopancreatography

General

A comparison of ERCP complication rates in different centers is a complex task, and most complication studies are difficult to place in perspective. Most endoscopic complications published prior to the early 1990s were anecdotal and tended to underestimate the complications. Since then a number of large, prospective studies have established that mortality and morbidity are directly related to the patient populations studied and the presence of underlying disorders. Thus the complication rate in elderly patients with acute cholangitis is different from that encountered in elective bile duct stone removal. Complication rates for endoscopic sphincterotomy vary with operator experience, indication, amount of manipulation, and degree of duct distention. In general, sphincterotomy complications are higher when the procedure is performed for sphincter of Oddi dysfunction and lower when performed for biliary stone extraction.

Primary ERCP and sphincterotomy complications are bleeding, pancreatitis, perforation, and sepsis. Because ERCP is an endoscopic procedure, the complications of endoscopy in general also occur; these include aspiration,perforation, and the risks of sedation. Endoscopic sphincterotomy complications include intrapapillary contrast extravasation, peri-Vaterian and pericholedochal infiltration, and extraperi-

toneal contrast leakage. The latter presumably involves duodenal perforation.

Suspected post-ERCP complications are best studied with CT. Significant bleeding is an indication for arteriography and, if needed, embolization.

Pancreatitis

Although hyperamylasemia is common after ERCP, only occasionally is clinical pancreatitis evident. Nevertheless, pancreatitis is the most common complication of ERCP. A 5% risk of clinically evident pancreatitis during diagnostic ERCP and up to 10% during therapeutic procedures is probably typical for an experienced endoscopic center. Patients with a normalcaliber common bile duct appear more prone to developing pancreatitis than those with a dilated duct.

Computed tomography is not necessary with suspected mild pancreatitis. With more severe clinical signs and symptoms, CT confirms the diagnosis, identifies any necrosis, and excludes other complications. Computed tomography findings of ERCP-associated pancreatitis are similar to those seen with pancreatitis due to other causes.

Perforation

Perforations are either intraor extraperitoneal in location; the latter is suggested if gas is identified in soft tissues around the papilla of Vater. The clinical relevance of such gas, however, is a complex issue, and soft tissue gas is detected after ERCP in some asymptomatic patients. The amount of gas, identified with CT, does not correlate with the size of a perforation. In fact, some authors do not consider isolated extraperitoneal gas to represent a perforation. At times injected contrast is identified in soft tissues and the procedure is aborted. Most extraperitoneal perforations heal spontaneously, with only a minority progressing to clinically evident infection, sepsis, and abscess.

An intraperitoneal perforation is less common and results in a pneumoperitoneum. Some of these duodenal tears are quite large. Occasionally with a large tear the endoscopist will suddenly visualize the peritoneal cavity and abort the procedure.

ADVANCED IMAGING OF THE ABDOMEN

A guidewire or catheter readily perforates through the bile duct wall, including cystic duct. Most of these perforations close spontaneously.

Post-ERCP CT detection of an abnormal fluid collection generally implies that either percutaneous drainage or surgical correction is necessary. If the clinical or initial CT findings are ambiguous, either a contrast study or follow-up CT should clarify the cause.

A patient developing an acute abdomen after ERCP should be suspected of having either pancreatitis or a perforation. Pancreatitis generally develops several hours after a procedure, while perforations tend to manifest sooner. In most patients CT is the imaging modality of choice to distinguish between these two entities. Whether to perform a water-soluble upper gastrointestinal contrast study to detect a perforation is debatable, but probably is not necessary in most patients. Such a study should be considered only if the results will modify therapy. In a setting of a small perforation, a water-soluble contrast study shortly after ERCP often does not identify a leak, and most patients are managed conservatively.

Other Complications

Over a third of patients develop bacteremia after ERCP (98); Escherichia coli, Morganella morganii, Staphylococcus spp.,and Streptococcus spp. are typical isolates. In spite of bacteremia, septicemia and clinical evidence of infection are uncommon.

Hemorrhage is a relatively common complication after endoscopic sphincterotomy, but most often is self-limiting in scope. Some bleeding can be controlled during endoscopy by sclerotherapy, cautery, epinephrine injection, or balloon tamponade, but extensive arterial bleeding requires either arteriographic embolization or surgical therapy. Hemorrhage can be delayed by 24 to 48 hours after endoscopic sphincterotomy and can be sufficiently brisk to require transfusion.

Endoscopic manipulation of benign and malignant biliary strictures is associated with few complications. Pancreatitis is a possibility. Most bleeding is treated conservatively.

A rare complication of endoscopic sphincterotomy is pneumomediastinum. Portal venous gas is also rare after ERCP and sphincterotomy; presumably intraluminal gas enters

GALLBLADDER AND BILE DUCTS

through mucosal tears. Even fatal hepatic air embolization has developed.

Occasional unexplained prolonged cholestatic jaundice develops after ERCP; presumably it is related to the contrast agent used.

Rarely, a basketed large stone cannot be extracted. Most often such a stone is crushed or a basket wire broken and the crushed stone fragments then extracted.

Percutaneous Cholangiography

Similarly to ERCP, percutaneous transhepatic cholangiography and biliary drainage can result in bacteremia; cholangitis and septicemia are uncommon as long as adequate drainage is maintained.

Significant arterial bleeding does develop during percutaneous transhepatic biliary drainage and stenting. Arterial embolization is required in some.

Perforation of a peri-Vaterian duodenal diverticulum is a rare complication.

Poststenting

An arterioportal fistula is a complication of percutaneous biliary drainage and results in hemobilia. At times transarterial embolization is indicated.

A metallic endoprosthesis eroding through duodenal mucosa can cause bleeding or even duodenal perforation. Most stents migrating distally will pass spontaneously; several have perforated the sigmoid colon. A rare biliary stent migrates proximally into the liver and leads to an abscess.

A long-term complication of biliary stents placed for therapy of benign biliary strictures is obstruction. In one study, primary metallic stent patency decreased from 75% after 12 months to 25% after 36 months (99). Repeat stent occlusions develop due to sludge, stones, or simply mucosal hyperplasia; periodic stent replacement is necessary.

A hunting accident led to buck shot obstructing a biliary prosthesis (100).

Biopsy

Tumor seeding after percutaneous biopsy is discussed in Chapter 7.

A common complication of percutaneous liver biopsy is hemobilia.

References

1.Stabile Ianora AA, Scardapane A, Midiri M, Rotondo A, Angelelli G. [Preand postoperative study of the bile ducts with spiral computerized tomography.] [Italian] Radiol Med 2000;100:152–159.

2.Chopra S, Chintapalli KN, Ramakrishna K, Rhim H, Dodd GD 3rd. Helical CT cholangiography with oral cholecystographic contrast material. Radiology 2000; 214:596–601.

3.Rondeau Y, Soyer P, Meduri B, et al. [MRI cholangiography with rapid spin-echo technique: prospective evaluation of 20 patients.] [French] J Radiol 1998;79: 147–152.

4.Varghese JC, Farrell MA, Courtney G, Osborne H, Murray FE, Lee MJ. Role of MR cholangiopancreatography in patients with failed or inadequate ERCP. AJR 1999;173:1527–1533.

5.Merkle EM, Boll DT, Weidenbach H, Brambs HJ, Gabelmann A. Ability of MR cholangiography to reveal stent position and luminal diameter in patients with biliary endoprostheses: in vitro measurements and in vivo results in 30 patients. AJR 2001;176: 913–918.

6.Savader SJ, Lynch FC, Radvany MG, et al. Singlespecimen bile cytology: a prospective study of 80 patients with obstructive jaundice. J Vasc Intervent Radiol 1998;9:817–821.

7.Sirikci A, Bayram M, Kervancioglu R. Incisional hernia of a normal gallbladder: sonographic and CT demonstration. Eur J Radiol 2002;41:57–59.

8.Ikeda S, Sera Y, Ohshiro H, Uchino S,Akizuki M, Kondo Y. Gallbladder contraction in biliary atresia: a pitfall of ultrasound diagnosis. Pediatr Radiol 1998;28:451– 453.

9.Gilmour SM, Hershkop, M, Reifen R, Gilday D, Roberts EA. Outcome of hepatobiliary scanning in neonatal hepatitis syndrome. J Nucl Med 1997;38: 1279–1282.

10.Rossmuller B, Porn U, Schuster T, Lang T, Dresel S, Hahn K. [Prognostic value of hepatobiliary functional scintigraphy in diagnosis and after-care of biliary atresia.] [German] Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 2000;172:73–79.

11.Saeki M, Honna T, Nakano M, Kuroda T. [Portal hypertension after successful hepatic portoenterostomy in biliary atresia.] [Japanese] Nippon Geka Gakkai Zasshi 1996;97:648–652.

12.Eiberg H, Nielsen IM. Linkage of cholestasis familiaris Groenlandica/Byler-like disease to chromosome 18. Int J Circumpolar Health 2000;59:57–62.

13.Knisely AS. Progressive familial intrahepatic cholestasis: a personal perspective. Pediatr Dev Pathol 2000;3: 113–125.

14.Jacquemin E. [Progressive familial intrahepatic cholestasis and hereditary anomalies. 1. Hepatocellular metabolism of bile acids.] [French] Arch Pediatr 1998;5:45–53.

15.Patriquin H, Lenaerts C, Smith L, et al. Liver disease in children with cystic fibrosis: US-biochemical comparison in 195 patients. Radiology 1999;211:229– 232.

16.Akata D, Akhan O, Ozcelik U, et al. Hepatobiliary manifestations of cystic fibrosis in children: correlation of CT and US findings. Eur J Radiol 2002;41: 26–33.

17.Alonso-Lej F, Rever WB, Pessagno DJ. Congenital choledochal cyst with a report of 2, and an analysis of 94 cases. Int Abstr Surg 1959;108:1–30.

18.Todani T, Watanabe Y, Narusue M, Tabuchi K, Okajima K. Congenital bile duct cysts: classification, operative procedures, and review of thirty-seven cases including cancer arising from choledochal cyst. Am J Surg 1977;134:263–269.

19.Lenriot JP, Gigot JF, Segol P, Fagniez PL, Fingerhut A, Adloff M. Bile duct cysts in adults: a multi-institutional retrospective study. French Associations for Surgical Research. Ann Surg 1998;228:159–166.

20.Kim MJ, Han SJ, Yoon CS, et al. Using MR cholangiopancreatography to reveal anomalous pancreaticobiliary ductal union in infants and children with choledochal cysts. AJR 2002;179:209–214.

21.Caroli J. Couinaud D. Une affection nouvelle sans doute congenitale des voies biliaires: la dilatation kystique uniobaire des canaux hepatiques. Sem Hop 1958;496: 136–142.

22.Holve S, Hu D, McCandless SE. Metachromatic leukodystrophy in the Navajo: fallout of the AmericanIndian wars of the nineteenth century.Am J Med Genet 2001;101:203–208.

23.Simanovsky N, Ackerman Z, Kiderman A, Fields S. Unusual gallbladder findings in two brothers with metachromatic leukodystrophy. Pediatr Radiol 1998;28:706–708.

24.Moore EE, Jurkovich GJ, Knudson MM, et al. Organ injury scaling. VI: Extrahepatic biliary, esophagus, stomach, vulva, vagina, uterus (nonpregnant), uterus (pregnant), fallopian tube, and ovary. J Trauma 1995; 39:1069–1070.

25.Shetty PB, Broome DR. Sonographic analysis of gallbladder findings in Salmonella enteric fever. J Ultrasound Med 1998;17:231–237.

26.Thrall JH, Ziessman HA. Nuclear Medicine. The Requisites. St. Louis: Mosby, 1995.

27.Pinto A, Romano S, Del Vecchio W, et al. [Personal experience in 71 consecutive patients with acute cholecystitis.] [Italian] Radiol Med 2000;99:62–67.

28.Regan F, Schaefer DC, Smith DP, Petronis JD, Bohlman ME, Magnuson TH. The diagnostic utility of HASTE MRI in the evaluation of acute cholecystitis. HalfFourier acquisition single-shot turbo SE. J Comput Assist Tomogr 1998;22:638–642.

29.Park MS,Yu JS, Kim YH, et al. Acute cholecystitis: comparison of MR cholangiography and US. Radiology 1998;209:781–785.

30.Wu CS, Yao WJ, Hsiao CH. Effervescent gallbladder: sonographic findings in emphysematous cholecystitis. J Clin Ultrasound 1998;26:272–275.

31.Ito K, Fujita N, Noda Y, et al. Percutaneous cholecystostomy versus gallbladder aspiration for acute cholecystitis: a prospective randomized controlled trial. AJR 2004;183:193–196.

32.Dinkel HP, Kraus S, Heimbucher J, et al. Sonography for selecting candidates for laparoscopic cholecystectomy: a prospective study. AJR 2000;174:1433–1439.

33.Vitellas KM, El-Dieb A, Vaswani KK, et al. Using con- trast-enhanced MR cholangiography with IV mangafodipir trisodium (Teslascan) to evaluate bile duct leaks after cholecystectomy: a prospective study of 11 patients. AJR 2002;179:409–416.

34.Ryan ME, Geenen JE, Lehman GA, et al. Endoscopic intervention for biliary leaks after laparoscopic cholecystectomy: a multicenter review. Gastrointest Endosc 1998;47:261–266.

35.Di Stasi C, Pedicelli A, Manfredi R, Sallustio G. Renocaval arteriovenous fistula as a complication of laparoscopic cholecystectomy. AJR 2001;176:261–262.

36.Boland GW, Slater G, Lu DS, Eisenberg P, Lee MJ, Mueller PR. Prevalence and significance of gallbladder abnormalities seen on sonography in intensive care unit patients. AJR 2000;174:973–977.

37.Parra JA, Acinas O, Bueno J, Guezmes A, Fernandez MA, Farinas MC. Xanthogranulomatous cholecystitis: clinical, sonographic, and CT findings in 26 patients. AJR 2000;4:979–993.

38.Hatakenaka M, Adachi T, Matsuyama A, Mori M, Yoshikawa Y. Xanthogranulomatous cholecystitis: importance of chemical-shift gradient-echo MR imaging. Eur Radiol 2003;13:2233–2235.

39.Adachi Y, Iso Y, Moriyama M, Kasai T, Hashimoto H. Increased serum CA19–9 in patients with xanthogranulomatous cholecystitis. Hepatogastroenterology 1998;45:77–80.

40.Setiawan MW, Samsi TK, Wulur H, Sugianto D, Pool TN. Dengue haemorrhagic fever: ultrasound as an aid to predict the severity of the disease. Pediatr Radiol 1998;28:1–4.

41.Arai K, Kawai K, Kohda W, Tatsu H, Matsui O, Nakahama T. Dynamic CT of acute cholangitis: early inhomogeneous enhancement of the liver. AJR 2003;181: 115–118.

42.Yoon KH, Ha HK, Lee JS, et al. Inflammatory pseudotumor of the liver in patients with recurrent pyogenic cholangitis: CT-histopathologic correlation. Radiology 1999;211:373–379.

43.Park MS, Yu JS, Kim KW, et al. Recurrent pyogenic cholangitis: comparison between MR cholangiography and direct cholangiography. Radiology 2001;220: 677–682.

44.Geenen DJ, Geenen JE, Jafri FM, et al. The role of surveillance endoscopic retrograde cholangiopancreatography in preventing episodic cholangitis in patients with recurrent common bile duct stones. Endoscopy 1998;30:18–20.

45.Sato M, Watanabe Y, Ueda S, et al. Intrahepatic cholangiocarcinoma associated with hepatolithiasis. Hepatogastroenterology 1998;45:137–144.

46.Cevikol C, Karaali K, Senol U, et al. Human fascioliasis: MR imaging findings of hepatic lesions. Eur Radiol 2003;13:141–148.

47.Ormsby AH, Bauer TW, Hall GS. Actinomycosis of the cholecystic duct: case report and review. Pathology 1998;30:65–67.

48.Ito K, Mitchell DG, Outwater EK. Pancreatic changes in primary sclerosing cholangitis: evaluation with MR imaging. AJR 1999;173:1535–1539.