Материал: Advanced Imaging of the Abdomen - Jovitas Skucas

Внимание! Если размещение файла нарушает Ваши авторские права, то обязательно сообщите нам

499

GALLBLADDER AND BILE DUCTS

49.Loftus EV Jr, Sandborn WJ, Tremaine WJ, et al. Primary sclerosing cholangitis is associated with nonsmoking: a case-control study. Gastroenterology 1996;110: 1496–1502.

50.Vitellas KM, El-Dieb A, Vaswani KK, et al. MR cholangiopancreatography in patients with primary sclerosing cholangitis: interobserver variability and comparison with endoscopic retrograde cholangiopancreatography. AJR 2002;179:399–407.

51.Ito K, Mitchell DG, Outwater EK, Blasbalg R. Primary sclerosing cholangitis: MR imaging features. AJR 1999;172:1527–1533.

52.Revelon G, Rashid A, Kawamoto S, Bluemke DA. Primary sclerosing cholangitis: MR imaging findings with pathologic correlation. AJR 1999;173:1037–1042.

53.Collett JA, Allan RB, Chisholm RJ, Wilson IR, Burt MJ, Chapman BA. Gallbladder polyps: prospective study. J Ultrasound Med 1998;17:207–211.

54.Yoshimitsu K, Honda H, Jimi M, et al. MR diagnosis of adenomyomatosis of the gallbladder and differentiation from gallbladder carcinoma: importance of showing Rokitansky-Aschoff sinuses. AJR 1999;172: 1535–1540.

55.Yoshimitsu K, Honda H, Shinozaki K, et al. Helical CT of the local spread of carcinoma of the gallbladder: evaluation according to the TNM system in patients who underwent surgical resection. AJR 2002;179: 423–428.

56.Paquet KJ. Appraisal of surgical resection of gallbladder carcinoma with special reference to hepatic resection. J Hepato Biliary Pancreatic Surg 1998;5:200–206.

57.Winston CB, Chen JW, Fong Y, Schwartz LH, Panicek DM. Recurrent gallbladder carcinoma along laparoscopic cholecystectomy port tracks: CT demonstration. Radiology 1999;212:439–444.

58.Stephen MR, Farquharson MA, Sharp RA, Jackson R. Sequential malt lymphomas of the stomach, small intestine, and gall bladder. J Clin Pathol 1998;51:77–79.

59.Tamada K,Ueno N,Tomiyama T,et al. Characterization of biliary strictures using intraductal ultrasonography: comparison with percutaneous cholangioscopic biopsy. Gastrointest Endosc 1998;47:341–349.

60.Park M-S, Kim TK, Kim KW, et al. Differentiation of extrahepatic bile duct cholangiocarcinoma from benign stricture: Findings at MRCP versus ERCP. Radiology 2004;233:234–240.

61.Alcaraz MJ, De la Morena EJ, Polo A, Ramos A, De la Cal MA, Gonzalez Mandly A. A comparative study of magnetic resonance cholangiography and direct cholangiography. Rev Esp Enferm Dig 2000;92:427– 438.

62.Kim MJ, Mitchell DG, Ito K, Outwater EK. Biliary dilatation: differentiation of benign from malignant causes—value of adding conventional MR imaging to MR cholangiopancreatography. Radiology 2000;214: 173–181.

63.Nagakawa T, Ohta T, Kayahara M, et al. A new classification of Mirizzi syndrome from diagnostic and therapeutic viewpoints. Hepatogastroenterology 1997; 44:63–67.

64.Redston MS, Wanless IR. The hepatic von Meyenburg complex: prevalence and association with hepatic and renal cysts among 2843 autopsies. Mod Pathol 1996;9: 233–237.

65.Kim YW, Park YK, Park JH, et al. A case with intrahepatic double cancer: hepatocellular carcinoma and cholangiocarcinoma associated with multiple von Meyenburg complexes. Yonsei Med J 1999;40:506– 509.

66.Tozawa K, Akita H, Kusada S, et al. Testicular metastases from carcinoma of the bile duct: a case report. Int J Urol 1998;5:106–107.

67.Lee JW, Han JK, Kim TK, et al. Computed tomography features of intraductal intrahepatic cholangiocarcinoma. AJR 2000;175:721–725.

68.Soyer P, Pelage JP, Zidi SH, Boudiaf M, Rymer R. Portal vein invasion by intrahepatic peripheral cholangiocarcinoma: a rare cause of portal hypertension. AJR 1998;171:1413–1414.

69.Maetani Y, Itoh K, Watanabe C, et al. MR imaging of intrahepatic cholangiocarcinoma with pathologic correlation. AJR 2001;176:1499–1507.

70.Yoon KH, Ha HK, Kim CG, et al. Malignant papillary neoplasms of the intrahepatic bile ducts: CT and histopathologic features. AJR 2000;175:1135–1139.

71.Braga HJ, Imam K, Bluemke DA. MR imaging of intrahepatic cholangiocarcinoma: use of ferumoxides for lesion localization and extension. AJR 2001;177: 111–114.

72.Matsuo S, Shinozaki T, Yamaguchi S et al. Intrahepatic cholangiocarcinoma with extensive sarcomatous change: report of a case. Surg Today 1999;29:560–563.

73.Lieser MJ, Barry MK, Rowland C, Ilstrup DM, Nagorney DM. Surgical management of intrahepatic cholangiocarcinoma: a 31–year experience. J Hepato Biliary Pancreatic Surg 1998;5:41–47.

74.Tanaka N, Yamakado K, Nakatsuka A, Fujii A, Matsumura K, Takeda K. Arterial chemoinfusion therapy through an implanted port system for patients with unresectable intrahepatic cholangiocarcinoma -initial experience. Eur J Radiol 2002;41:42–48.

75.Chang WH, Kortan P, Haber GB. Outcome in patients with bifurcation tumors who undergo unilateral versus bilateral hepatic duct drainage. Gastrointest Endosc 1998;47:354–362.

76.Golfieri R, Giampalma E, Muzzi C, et al. [Unresectable hilar cholangiocarcinoma: combined percutaneous and radiotherapeutic treatment.] [Italian] Radiol Med 2001;101:495–502.

77.Fukuda T, Iwanaga S, Sakamoto I, et al. Computed tomography of neural plexus invasion in common bile duct carcinoma. J Comput Assist Tomogr 1998;22: 351–356.

78.Lim HS, Jeong YY, Shen YL, Kang HK, Cho CK. CT and MRI findings of primary non-Hodgkin’s lymphoma of the common bile duct mimicking cholangiocarcinoma. AJR 2004;182:1608–1609.

79.Maes M, Depardieu C, Dargent JL, et al. Primary lowgrade B-cell lymphoma of MALT-type occurring in the liver: a study of two cases. J Hepatol 1997;27:922–927.

80.Wenzel DJ, Gaede JT, Wenzel LR. Intrabiliary colonic metastasis mimicking primary biliary neoplasia. AJR 2003;180:1029–1032.

81.Deenitchin GP, Yoshida J, Chijiiwa K, Tanaka M. Complex cystic duct is associated with cholelithiasis. HPB Surg 1998;11:33–37.

82.Garcia Molina FJ, Garcia Gil JM, Fernandez Mena J, Navarro Freire F. Computerized tomographic assess-

500

ADVANCED IMAGING OF THE ABDOMEN

ment of the composition of gallstones. Rev Esp Enferm Dig 1998;90:851–862.

83.Tsai HM, Lin XZ, Chen CY, Lin PW, Lin JC. MRI of gallstones with different compositions. AJR 2004;182: 1513–1519.

84.Hellstern A, Leuschner U, Benjaminov A, et al. Dissolution of gallbladder stones with methyl tert-butyl ether and stone recurrence: a European survey. Dig Dis Sci 1998;43:911–920.

85.Soto JA, Alvarez O, Munera F, Velez SM., Valencia J, Ramirez N. Diagnosing bile duct stones: comparison of unenhanced helical CT, oral contrast-enhanced CT cholangiography, and MR cholangiography. AJR 2000; 175:1127–1134.

86.Kim KH, Kim W, Lee HI, Sung CK. Prediction of common bile duct stones: its validation in laparoscopic cholecystectomy. Hepatogastroenterology 1997;44: 1574–1579.

87.Hunt DR. Common bile duct stones in non-dilated bile ducts? An ultrasound study. Australas Radiol 1996;40: 221–222.

88.Kim TK, Kim BS, Kim JH, et al. Diagnosis of intrahepatic stones: superiority of MR cholangiopancreatography over endoscopic retrograde cholangiopancreatography. AJR 2002;179:429–434.

89.Kondo H, Kanematsu M, Shiratori Y, et al. MR cholangiography with volume rendering: receiver operating characteristic curve analysis in patients with choledocholithiasis. AJR 2001;176:1183–1189.

90.Soto JA, Barish MA, Alvarez O, Medina S. Detection of choledocholithiasis with MR cholangiography: comparison of three-dimensional fast spin-echo and singleand multisection half-Fourier rapid acquisition with relaxation enhancement sequences. Radiology 2000;215:737–745.

91.Zorger N, Manke C, Lenhart M, Volk M, Link J, Feuerbach S. [Percutaneous transpapillary extraction of biliary calculi for symptomatic choledocholithiasis

after unsuccessful endoscopic treatment.] [German] Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 2001;173:92–96.

92.Loehr SP, Hamilton C, Gargan K, Gilliam J. Use of the Angiojet thrombectomy device to facilitate removal of impacted intrahepatic ductal debris. AJR 2002;179: 370–372.

93.Seguin P, Le Bouquin V, Campion JP, Malledant Y. [Hemobilia of gallbladder origin manifesting as malignant hypertension.] [French] Presse Med 1998;27:913.

94.De Diego A, Santos L,Vaquero J, et al. [Ischemic cholecystitis caused by arterial chemoembolization of hepatocellular carcinoma.] [Spanish] Rev Esp Enferm Dig 1999;91:74–75.

95.Premkumar A, Walworth CM, Vogel S, et al. Prospective sonographic evaluation of interleukin-2–induced changes in the gallbladder. Radiology 1998;206:393– 396.

96.Feng BX, Song QM. Does the common bile duct dilate after cholecystectomy—sonographic evaluation in 234 patients. AJR 1995;165:859–861.

97.Tang Y, Yamashita Y, Arakawa A, et al. Pancreaticobiliary ductal system: value of half-Fourier rapid acquisition with relaxation enhancement MR cholangiopancreatography for postoperative evaluation. Radiology 2000;215:81–88.

98.Barragan Casas JM, Hernandez Hernandez JM, Garcinuno Jimenez MA, et al. Bacteremia caused by digestive system endoscopy. Rev Esp Enferm Dig 1999;91:105–116.

99.Gabelmann A, Hamid H, Brambs HJ, Rieber A. Metallic stents in benign biliary strictures: long-term effectiveness and interventional management of stent occlusion. AJR 2001;177:813–817.

100.Maroy B. [An odd hunting accident: acute obstruction of a biliary prosthesis caused by a buck shot.] [Letter] [French] Gastroenterol Clin Biol 1996;20:123.

9

Pancreas

Technique

Computed Tomography

Techniques and terminology used with computed tomography (CT) are discussed in Chapter 7. Intrapancreatic structures and peripancreatic vessels are better visualized with helical CT than with conventional CT. Multislice CT images both soft tissues and vessels and, if desired, provides three-dimensional (3D) views. Some authors use the term pancreatic phase, defined as 40 to 70 seconds after the start of intravenous contrast infusion.

A typical multislice CT technique consists of a biphasic (pancreatic phase and portal venous phase) thin slice study of the upper abdomen. An additional arterial phase is useful for identifying adjacent blood vessels and detecting hypervascular tumors. In general, a higher contrast dose and faster injection rate result in greater and earlier parenchymal enhancement.

Computed tomography angiography can depict secondary arterial branches such as the pancreaticoduodenal arcades and dorsal pancreatic artery. Three-dimensional volume rendering appears superior to maximum intensity projection (MIP) and shaded surface display (SSD) in evaluating these vessels (1).

Ultrasonography

The use of bowel hypotonia combined and gastroduodenal distention with water (a technique

called hydrosonography) aids in visualizing the pancreas. After ingesting water with simethicone, followed by patient rotation, the pancreatic tail was visualized by ultrasonography (US) in 79% of patients, compared to 7% in controls (2).

Endoscopic US provides better resolution of structures in the pancreatic head than conventional US. Especially with small lesions, endoscopic US can guide percutaneous biopsy and aspiration cytology. Most endoscopic US of the pancreas is performed either transgastric or transduodenal. Color Doppler US of the pancreas is feasible using an endoscopic approach.

Intraductal US probes using up to 30-MHz transducers are being developed. A probe inserted through the ampulla into the pancreatic duct can image structures up to 20 to 30mm in diameter. The portal vein and other adjacent larger veins are readily visualized.

Carbon dioxide bubbles mixed with heparinized saline and injected into the celiac artery are a potential intraarterial contrast agent when imaging the pancreas. Such US, termed sonographic angiography, appears useful when evaluating pancreatic vascularity; pancreatic ductal cancers show no or mild enhancement, while islet cell tumors and serous cystadenomas reveal strong enhancement. This specialized technique is better suited for endoscopic US rather than transabdominal US. Currently the literature on sonographic angiography is rather limited.

501

502

The pancreas can be imaged through subcostal and umbilical laparoscopic ports. A fluidfilled stomach acts as an acoustic window, although resolution of pancreatic lesions is improved by using a higher frequency transducer directly from the lesser sac.

Magnetic Resonance Imaging

Magnetic resonance (MR) techniques useful in evaluating the pancreas are T1and T2weighted sequences, arterial and venous phase postcontrast images, magnetic resonance cholangiopancreatography (MRCP), and magnetic resonance angiography (MRA). Fatsuppression improves image conspicuity (MRCP is discussed in more detail below; see Pancreatography). The term hydrospiral CT has been used for helical CT of the pancreas when using pharmacologic bowel paralysis and water distention of the stomach and duodenum.

Normal pancreas is isoto slightly hyperintense to liver on T1-weighted images and hypointense to surrounding fat. It becomes hyperintense on T1-weighted fat-suppression images. It is isoto hyperintense to liver on T2-weighted images. The extracellular gadolinium chelates enhance normal pancreatic parenchyma homogeneously. Because most tumor vascularity differs from normal tissue vascularity, postcontrast pancreatic-phase or equilibrium-phase imaging was initially often employed, with pancreatic ductal cancers tending to be hypointense and islet cell tumors hyperintense on these images. Currently, with further advances in technique, fat-suppressed preand postcontrast arterial phase T1weighted images are commonly employed.

In normal individuals, the pancreatic arterial phase occurs at about 15 seconds from the start of contrast injection, the parenchymal phase at 25 seconds, the portal phase at 60 seconds, and the equilibrium phase at about 100 seconds. In distinction to the liver, which receives most of its blood supply from the portal vein and thus enhances maximally during the portal phase, maximal pancreatic enhancement is during the late arterial-to-pancreatic phase. After intravenous (IV) bolus of gadopentetate dimeglumine in patients with no pancreatic malignancies, the best pancreatic images are obtained

ADVANCED IMAGING OF THE ABDOMEN

15 seconds after the arrival of contrast in the abdominal aorta (3); the peripancreatic vessels, on the other hand, are best seen at 25 seconds or later.

Short sequences that minimize artifacts are necessary in pancreatic MRI. A typical study for tumor detection consists of an oral contrast agent to outline the gastrointestinal tract and preand postgadolinium images. With state- of-the-art MR units, fat-suppressed, single breath-hold spoiled gradient echo (SGE) sequences are often used. Combining fat suppression and oblique imaging improves visualization of both normal pancreas and abnormalities, compared with conventional axial and axial fat-suppressed T1-weighted imaging; oral barium aids as a duodenal contrast marker in differentiating pancreatic head from adjacent bowel.

Endoscopic MRI uses an endoscope with a small radiofrequency coil attached to the tip. After endoscopic tip placement in the duodenum, the patient is placed in an MR unit and appropriate images are obtained. Preliminary results suggest that the pancreatic duct is well defined, tumors in the pancreatic head are identified, and even portal vein invasion is detected (4).

Uptake of the manganese MR contrast agent (Mn-DPDP) is evident by a normal pancreas, which becomes hyperintense on T1 postcontrast images, while signal intensity of many lesions is unchanged. As a result, lesion conspicuity is increased. Further study is needed to define the role of this contrast agent, which persists in the pancreas considerably longer than gadolinium.

Pancreatography

Endoscopic

Endoscopic retrograde pancreatography (ERP) is the current approach to direct pancreatic duct visualization.

Transgastric pancreatography using endoscopic US for guidance has been attempted. This technique has a possible role after failed endoscopic retrograde cholangiopancreatography (ERCP), although MR pancreatography appears more appropriate.

503

PANCREAS

Percutaneous

One alternative is percutaneous pancreatography performed under US guidance, followed by contrast injection into the pancreatic duct under fluoroscopic control. With a previously unsuccessful ERP, this technique occasionally appears worthwhile if the pancreatic duct is dilated due to chronic pancreatitis or pancreatic carcinoma.

Computed Tomography

Similar to the bile ducts, CT multiplanar reformatted imaging using minimum intensity projections of selected tissue volume thicknesses reduces partial volume effects and makes a normal pancreatic duct visible. In particular, multiplanar images combined with 0.5-mm or thinner axial images during the arterial phase aid in evaluating the pancreatic duct (5); current techniques allows visualization of the main pancreatic duct in over 90% of patients and accessory pancreatic duct in about half, but not

the side branches.

 

 

In

distinction to

MR pancreatography,

CT

pancreatography

detects

pancreatic

calcifications.

Magnetic Resonance

Magnetic resonance cholangiopancreatography is discussed in more detail in Chapter 8. By selecting appropriate heavily weighted T2 pulse sequences, nonflowing fluid appears bright against a darker background. Magnetic resonance pancreatography relies on this property of bile and pancreatic fluid being hyperintense on T2-weighted images. The main pancreatic duct is readily identified, but normal secondary branches are visualized incompletely. Images resemble those obtained with ERCP, with a number of publications concluding that detection of pancreatic duct abnormalities is similar to ERCP. It is a noninvasive procedure, no contrast is injected into the ducts, and thus no complications are encountered. It can be performed with a mid-strength [0.5-tesla (T)] magnet. Magnetic resonance pancreatography achieves sensitivities of >80% and specificities >90% in detecting pancreatic duct stenosis, obstruction, and dilation.

Secretin stimulation of pancreatic secretions improves MR visualization of a nondilated main

pancreatic duct (6); no gross improvement is evident once the pancreatic duct is dilated. Secretin stimulated MRCP can be used to measure pancreatic duct flow rates and changes in duodenal fluid volume, findings indicative of pancreatic exocrine function (7), yet whether secretin administration is of value in a setting of chronic pancreatitis as a test of pancreatic function is arguable.

Oral contrast agents such as iron gluconate, iron oxide, and barium sulfate reduce background noise and make interpretation easier.

Pancreatic duct caliber should be measured with caution on MR images; partial volume averaging of an adjacent splenic vein makes the duct appear wider with some MR sequences. If needed, T2-weighted spin-echo (SE) sequences are used to differentiate a pancreatic duct (high signal intensity fluid) from flowing blood (signal void). Magnetic resonance pancreatography overestimates duct stenoses. Secretin in a dose of 1 clinical unit/kg stimulates pancreatic exocrine secretions, distends the pancreatic duct transiently, and improves pancreatic duct visualization.

Pancreatoscopy

Instruments for direct visualization of the pancreatic duct mucosa are becoming available. Currently described are thin fiberscopes several millimeters in diameter and pancreatoscopes, which are inserted either via an ERCP cannula or are free-standing. Their primary role is in visualizing and defining lesions involving the main pancreatic duct.

Scintigraphy

2-[18F]-fluoro-deoxy-D-glucose positron emission tomography (FDG-PET) appears useful in assessing indeterminate CT findings for suspected pancreatic carcinoma. The primary future interest in PET will probably be in tumor uptake. For example, if levodopa (L-dopa) is labeled with carbon 11 in the b position, the radioactive carbon label follows L-dopa through decarboxylation to dopamine, and significant uptake occurs in a pancreatic glucagonoma and gastrinoma (8); on the other hand, with C 11 in the L-dopa carboxyl group, it is eliminated from tissue as CO2 during decarboxylation and little C-11 uptake occurs.

504

Biopsy

Both solid and cystic pancreatic tumors are routinely biopsied on an outpatient basis using US guidance, the tumor etiology is established, and few complications are encountered. As an alternative, aspiration using endoscopic US as a guide achieves high diagnostic accuracy in evaluating pancreatic tumors.

The most common complication associated with fine-needle aspiration is acute pancreatitis.

The presence of a trained cytopathologist is a prerequisite to interpreting fine-needle aspiration biopsies.

Congenital Abnormalities

Several systems are in use for classifying congenital pancreatic duct anomalies. A common scheme is to subdivide anomalies into migration and fusion. The most common is fusion failure between the dorsal and ventral pancreatic ducts (pancreas divisum).

Migration variations include pancreatic rests, which are formed by incomplete migration of the prepancreatic anlage. As a result, pancreatic tissue remains in stomach wall, duodenum, and other structures. Likewise,failure of full rotation of the prepancreatic buds results in an annular pancreas.

In some patients it is difficult to predict whether a detected congenital anomaly is indeed responsible for a particular clinical problem.

Agenesis

Complete agenesis of the pancreas is incompatible with life. Partial agenesis is rare, with either the ventral or dorsal segment failing to develop. This congenital anomaly is associated with polysplenia and intrathoracic anomalies. Agenesis of the dorsal segment results in only the head of the pancreas being present; CT and MR show this segment as an oval mass. Many of these patients also have diabetes mellitus, presumably because of islet cell agenesis, which normally are predominantly located in the body and tail of the pancreas.

The uncinate process is either absent or hypoplastic in patients with intestinal nonrota-

ADVANCED IMAGING OF THE ABDOMEN

tion, presumably secondary to incomplete pancreatic primordial ventral bud rotation.

Pancreas Divisum

Pancreatography and immunohistochemical staining of pancreatic polypeptide identify two types of dorsal and ventral duct fusion (Fig. 9.1):

(1) one-point fusion at the junction of main duct and accessory pancreatic duct, and (2) twopoint fusion not only at the primary duct junction site but also at a second site. Abnormal embryologic fusion (or lack of fusion) of the ventral and dorsal primordia causes pancreas divisum.

Pancreas divisum is the most common congenital anomaly of the pancreas, with autopsy studies showing about a 6% prevalence. Some consider pancreas divisum to be an innocuous congenital variant, while others believe that it is associated with a higher prevalence of pancreatitis. The frequency of pancreas divisum in patients with pancreatitis is significantly higher than in a general population. If found in several family members, is this hereditary pancreatitis in a setting of familial pancreas divisum? Pancreatitis in this patient population often is focal and limited to a dorsal distribution. It is often technically difficult in these patients to cannulate the dorsal pancreatic duct (duct of Santorini); nevertheless, some endoscopy centers have achieved a high success rate and have become referral centers for this procedure.

Pancreas divisum does not appear to predispose to an anomalous pancreaticobiliary duct union.

Pancreas divisum is generally detected by pancreatography. At times CT identifies distinct ventral and dorsal pancreatic ducts (Fig. 9.2). Occasionally CT suggests pancreas divisum by an indistinct mass in the head of the pancreas.

An MRCP detects about half the pancreas divisum anomalies. Secretin administration appears to aid in this detection.

The prevalence of both acute relapsing pancreatitis and chronic pancreatitis appears to decrease following minor papilla sphincterotomy and resultant accessory duct decompression. At times stenting of the dorsal pancreatic duct relieves symptoms.

Источник: https://tut-files.ru/previewfile/161921