Professional Documents
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160. Taylor GA, Atalabi OM, Estroff JA: Imaging of congenital 172. Weinberg PM: Aortic arch anomalies. J Cardiovasc Magn Reson
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161. Terheggen-Lagro SW, Arets HG, van der Laag J, et al: Radiological and 173. Weisbrod GL, Chamberlain DW, Tao LC: Pulmonary blastoma, report
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162. Terheggen-Lagro S, Truijens N, van Poppel N, et al: Correlation of six 174. Wells TR, Gwinn JL, Landing BH, et al: Reconsideration of the anatomy
different cystic fibrosis chest radiograph scoring systems with clinical of sling left pulmonary artery: The association of one form with
parameters. Pediatr Pulmonol 35(6):441–445, 2003. bridging bronchus and imperforate anus. Anatomic and diagnostic
163. Tiddens HA: Chest computed tomography scans should be considered aspects. J Pediatr Surg 23(10):892–898, 1988.
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166. Veenma DC, de Klein A, Tibboel D: Developmental and genetic aspects of cysti fibrosis lung disease. J Thorac Imaging 28(3):151–159, 2013.
of congenital diaphragmatic hernia. Pediatr Pulmonol 47(6):534–545, 178. Williams AJ, Schuster SR: Bronchial atresia associated with a
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1198 PART II CT and MR Imaging of the Whole Body
A B
FIG 42-17 A, Heavily calcified left intrahepatic stones (arrows) are seen on precontrast CT. B, The stones
are not clearly delineated on postcontrast CT because the adjacent liver parenchyma enhances.
CHAPTER 42 Biliary Tract and Gallbladder 1199
A
A
B
B
FIG 42-18 Innumerable small intrahepatic stones in a patient with
recurrent pyogenic cholangitis. Because attenuation of the stones and FIG 42-20 Common bile duct stone (arrow) with water attenuation on
liver is similar, CT (A) shows several weakly calcified intrahepatic stones CT (A) and cholangiogram (B).
(arrows), whereas many stones are visible on cholangiogram (B).
FIG 42-19 Common bile duct stone with soft tissue attenuation
(arrow). FIG 42-21 Common bile duct stone (arrow) containing air presenting
with the “Mercedes-Benz” sign.
1200 PART II CT and MR Imaging of the Whole Body
a stone through the papilla of Vater because the duodenal papillary Sometimes a stone that is not detected by one imaging modality is
orifice becomes tight owing to papillitis and papillary edema (see demonstrated by another (Fig. 42-25; see Fig. 42-24). Thus two or
Fig. 42-13). more imaging methods may be necessary for the diagnosis of bile duct
Small stones and gravel repeatedly passing through the duodenal stones.
papillary orifice can cause papillitis and eventually papillary steno-
sis.92,359 CT or MRI demonstrates a dilated and thickened bile duct and Cholangitis
an enlarged duodenal papilla164,275 (see Fig. 42-13) but no actual stone Suppurative Cholangitis. Acute suppurative cholangitis is a bacte-
in the bile duct. rial infection of the bile ducts occurring mostly in patients with biliary
The ability to detect a biliary stone by imaging varies depending on obstruction caused by either stones or a tumor. Most stones originate
the size, location, and components of the stone.90,142,164,209,275,282 Each from the gallbladder (Fig. 42-26). The tumor may be a carcinoma of
modality has advantages and disadvantages. With CT, detection the bile ducts, head of the pancreas, or ampulla of Vater or (uncom-
depends on the stone’s calcium content and bile duct dilatation. Detec- monly) a benign tumor.
tion of stones by MRI is hampered by artifacts caused by pulsation of The bile ducts may be normal or dilated, depending on the cause,
the adjacent vessels. During cholangiography, the technique of can- duration, and degree of obstruction. In acute obstruction caused by a
nulation and bile duct opacification must be optimal for visualization stone, the bile ducts may not be dilated for some time, whereas in
of small stones. obstruction caused by cancer, the bile ducts are usually dilated.
A B
FIG 42-24 Small stone in the common bile duct. Intraductal sonogram discloses a stone (A), but there is
no stone visible on cholangiogram (B).
CHAPTER 42 Biliary Tract and Gallbladder 1201
A B
FIG 42-25 Small stones in the common bile duct (arrows) are visualized on MR cholangiogram (A) but not
on cholangiogram (B).
FIG 42-26 Acute suppurative cholangitis caused by a stone originating FIG 42-27 Suppurative cholangitis with a common bile duct stone in
from the gallbladder. The common bile duct is slightly dilated, and the a patient with recurrent pyogenic cholangitis. Note concentric thicken-
wall is thick and enhanced as a concentric ring (arrow). The gallbladder ing of the bile duct wall with enhancement.
contains a small stone and its wall is thick and enhanced owing to acute
cholecystitis.
Other than bile duct dilatation, imaging finding are usually
normal.14 The presence of purulent bile may result in increased attenu-
Obstruction of the bile ducts causes bile stasis and a predisposition to ation of bile (greater than that of water) on CT, but it is usually not
infection. Gram-negative organisms such as E. coli are usually respon- clearly depicted. Depending on the calcium content, stones may be
sible. It is believed that bacteria within the intestinal tract ascend clearly depicted as calcified high-attenuating foci or as noncalcified
through the ampulla of Vater; for this reason the disease is also called intraluminal material (see Figs. 42-19 and 42-20).
ascending cholangitis. Bacterial colonization may also occur through The wall of the bile ducts may be thickened concentrically and dif-
portal venous bacteremia. The combination of obstruction and colo- fusely, with dense contrast enhancement (Fig. 42-27; see Fig. 42-26);
nization leads to cholangitis, but neither obstruction nor colonization this is well delineated with thin-section CT.14 In contrast to periductal-
by itself is sufficient to cause disease.223 Patients present with acute infiltrating bile duct cancer, the thickness of the bile ducts is uniform
abdominal pain, fever, chills, and sometimes jaundice. In some patients and less than 1 mm. In patients with suppurative cholangitis caused
with bile duct stones or carcinoma along the bile ducts, the initial by a cancer along the bile ducts, a nodular mass or periductal-
symptoms and signs may be similar to those of acute suppurative infiltrating cholangiocarcinoma is depicted on US, CT (Fig. 42-28),
cholangitis. and MRI.
1202 PART II CT and MR Imaging of the Whole Body
A B
FIG 42-28 A and B, Acute suppurative cholangitis caused by carcinoma of the common hepatic duct (arrow
in B). Note the dilated bile ducts and concentric thickening of the wall in A.
A B
FIG 42-33 Recurrent pyogenic cholangitis. A, Cholangiogram shows severe dilatation and acute peripheral
tapering of the intrahepatic bile ducts with the “arrowhead” sign. There are multiple large stones in the
extrahepatic duct. B, CT shows a dilated common bile duct and stones within it. Note the thickened wall of
the common bile duct (arrows).
A B
FIG 42-35 A, Multiple liver abscesses (arrows) in a patient with recurrent pyogenic cholangitis. B, In addition
to the liver abscesses (arrows), note the small stone in the dilated segmental bile duct (arrowhead).
A B
FIG 42-36 Axial (A) and coronal (B) CT shows a markedly enlarged ampulla of Vater containing a stone that
is bulged into the duodenum (arrow in B).
Sonography and contrast-enhanced CT and MRI may show noma.231 Cholangiocarcinoma usually causes more complete obstruc-
thickening (Fig. 42-40) and contrast enhancement (Fig. 42-41) of the tion than PSC (dominant stricture), and there may be markedly dilated
bile duct wall. The thickness varies from 1 to 3 mm. Thus these bile ducts proximal to the bile duct segment involved by the cholan-
imaging techniques are helpful to determine the severity and extent of giocarcinoma. A rapidly progressing segmental stricture and proximal
disease. In some instances, cholangiographic “beading” can be seen on dilatation on serial images associated with clinical deterioration favor
contrast-enhanced CT (see Fig. 42-39). Like MRCP, CT has the advan- the presence of cholangiocarcinoma. In this regard, thin-section CT
tage of being able to visualize an obstructed segment that cannot be and MRI are helpful to assess the clinical course.
demonstrated on cholangiography.
Other imaging findings include alterations of the hepatic paren- AIDS Cholangitis. Inflammation of the bile ducts can occur in
chyma such as biliary cirrhosis, hepatic segmental atrophy and hyper- patients with acquired immunodeficiency syndrome (AIDS), owing to
trophy, portal hypertension, a dominant biliary stricture resulting in an opportunistic infection by cytomegalovirus, Mycobacterium avium-
obstructive jaundice, calculi in the gallbladder and CBD (25%-30%), intracellulare, Candida albicans, Cryptosporidium species, and Klebsi-
and a complicating cholangiocarcinoma (8%-15%).310 ella pneumoniae.35,289 Inflammation may involve the intrahepatic and
Clinical course. There is an increased incidence of cholangiocar- extrahepatic ducts as well as the duodenal papillae, resulting in papil-
cinoma in patients with PSC.310 In a series of patients undergoing liver lary stenosis. Cholangiogram shows irregularities and stricture of the
transplantation for PSC, 10% were found to have cholangiocarcinoma intrahepatic and extrahepatic bile ducts with associated bile duct dila-
in their native livers.129 When the two diseases coexist, the ductal tation. Papillary stenosis often occurs in conjunction with proximal
abnormality of PSC can easily mask the presence of cholangiocarci- duct stricture. Tiny polypoid intraductal defects due to granulation
1206 PART II CT and MR Imaging of the Whole Body
A B
FIG 42-37 Papillary stenosis due to repeated passage of stones. A, ERCP shows dilatation of the extrahe-
patic ducts. There is normal contraction of the sphincter of Oddi at the end of the common bile duct (arrow).
B, CT shows a normal-sized duodenal papilla (arrow).
A B
FIG 42-38 Primary sclerosing cholangitis. A, ERCP shows multisegmental or diffuse narrowing and proximal
dilatation of the intra- and extrahepatic bile ducts. Peripheral ducts have a “pruned tree” appearance.
B, Contrast-enhanced CT shows diffuse thickening of the wall of the intra- and extrahepatic bile ducts
(arrows). Also note thickening of the gallbladder wall.
CHAPTER 42 Biliary Tract and Gallbladder 1207
B C
FIG 42-39 Primary sclerosing cholangitis. A, MR cholangiogram shows innumerable foci of focal or seg-
mental narrowing or dilatation of the intrahepatic bile ducts, with a “beaded” appearance and obliteration of
the extrahepatic duct (arrow). B and C, CT shows peripheral bile duct narrowing and dilatation, with scattered
segments of peripheral duct dilatation. Note obliteration of the lumen of the extrahepatic duct due to severe
thickening of the wall (arrow in C).
Parasitic Diseases
Biliary parasitic diseases include clonorchiasis, opisthorchiasis, fascio-
liasis, and ascariasis. These diseases are prevalent in East and Southeast
Asia but rare in the United States and Western Europe. C. sinensis and
O. viverrini are human liver flukes acquired through ingestion of raw
freshwater fish harboring metacercariae; Fasciola hepatica is a sheep
liver fluke and humans are infected accidentally. Adult flukes live in the
bile ducts and produce a mechanical obstruction, mucosal inflamma-
tion, adenomatous hyperplasia, and periductal fibrosis (Fig. 42-42).
Infection with C. sinensis and O. viverrini produces diffuse and
uniform dilatation of the peripheral IHD, with no or minimal dilata-
FIG 42-40 Primary sclerosing cholangitis. Sonogram shows the thick- tion of the extrahepatic ducts and without a focal obstructing lesion
ened wall of the extrahepatic bile ducts (arrows). along the bile ducts208,215 (Fig. 42-43). This occurs because the flukes
1208 PART II CT and MR Imaging of the Whole Body
A B
FIG 42-41 A and B, Primary sclerosing cholangitis involving segmental intrahepatic bile ducts and extrahe-
patic ducts, with thickening of the bile duct wall and intense enhancement (arrow in B). The gallbladder wall
is also thickened and enhanced.
A B
FIG 42-43 Mild clonorchiasis infection. A and B, CT shows mild dilatation of the peripheral intrahepatic bile
ducts, without dilatation of the central duct (arrow in B).
B
FIG 42-50 Biliary ascariasis. Endoscopic retrograde cholangiogram
FIG 42-48 Hepatic fascioliasis. CT shows multiple small, clustered, (A) and MRCP (B) show a long convoluted filling defect in the extrahe-
necrotic lesions in the subcapsular area arranged as “tunnels and patic ducts representing adult Ascaris lumbricoides. (Courtesy So Yeon
caves.” Kim, MD, Ulsan University Medical School, Seoul, Republic of Korea.)
the ligatures, causing injury.66 Clinical manifestations including jaun- the more proximal duct. A delayed common duct stricture has been
dice may appear within a week, months, or years, depending on the reported after blunt abdominal trauma. The injury results in a short
severity of the bile duct damage. CT reveals severely dilated IHDs, with segmental tight stricture with concentric or eccentric involvement and
the degree of dilatation depending on the severity of the bile duct proximal dilatation.
obstruction. At the hepatic hilum there is an abrupt transition from
the dilated bile ducts to the normal extrahepatic ducts, where there is Neoplasms of the Biliary System
a short segmental tight stricture (Fig. 42-55). A coronal reconstruction Benign Tumors of the Bile Ducts
image better shows the stenotic segment. A biliary stricture caused by Bile duct hamartoma. Bile duct hamartoma, also known as von
injury to the anastomotic site during liver transplantation typically Meyenburg’s complex, is a focal disorderly collection of bile ducts and
occurs at the proximal part of the extrahepatic duct. The degree of ductules surrounded by abundant fibrous stroma.60,131 There is usually
stenosis varies from mild stenosis without bile flow impairment a centrally located small cystic lesion lined by a single layer of biliary
(Fig. 42-56) to a tight stricture and complete obstruction of bile flow epithelium that does not communicate with the biliary tree.256 The
(Fig. 42-57). lesions are 0.1 to 1.5 cm in diameter and are scattered diffusely in the
A biliary stricture caused by blunt abdominal trauma occurs in liver parenchyma.
the suprapancreatic portion of the CBD.352 The CBD is susceptible to CT shows multiple or innumerable hypoattenuating cystlike
disruption from deceleration injuries, usually at the level of the pan- hepatic nodules, typically less than 1.5 cm in diameter, occurring
creaticoduodenal junction, where it is relatively fixed compared with throughout both lobes of the liver256 (Fig. 42-58). MRI shows tiny
FIG 42-51 Bile duct stricture caused by thermal injury during radiofre- FIG 42-53 Tight stricture (arrow) at the left hepatic duct in a patient
quency ablation for hepatocellular carcinoma. CT shows severe dilata- with recurrent pyogenic cholangitis. Note stones in the left hepatic duct
tion of the posterior segmental bile ducts abutting the necrotic nodule. proximal to the stricture site.
A B
FIG 42-52 Bile duct stricture due to recurrent pyogenic cholangitis and fibrosis. A, Cholangiogram shows
a tight stricture at the bifurcation (arrow). Note several stones in the extrahepatic duct. B, CT shows tight
narrowing and wall thickening at the bifurcation (arrow).
1212 PART II CT and MR Imaging of the Whole Body
hypointense lesions on T1-weighted images and strongly hyperintense varying length, it produces a large amount of mucus, resulting in
lesions on T2-weighted images (Fig. 42-59). Contrast-enhanced CT or nonobstructive dilatation of the entire biliary tree.7 This tumor has
MRI may show homogeneous enhancement of the lesions256,300,309 (see great potential for malignant transformation (see Fig. 42-61).261
Fig. 42-59). Biliary cystadenoma and cystadenocarcinoma. Benign and
Bile duct adenoma. A solitary adenoma appears as a well- malignant cystic tumors of bile duct origin can occur in the IHDs of
circumscribed wedgelike mass less than 1 cm in diameter. The gallblad- the liver or rarely in the extrahepatic ducts. These tumors occur in
der is the most frequent site; these tumors are rare along the bile ducts. adults, with a strong middle-aged female predominance. The usually
A villous adenoma can occur at the duodenal papilla (Fig. 42-60). single tumor is covered by a fibrous capsule and is unilocular or
Biliary papillomatosis. Biliary papillomatosis is a papillary or multilocular, containing mucinous or serous fluid.18 A cystadenoma is
villous tumor in the intrahepatic or extrahepatic bile ducts showing lined by a single layer of cuboidal or tall columnar mucin-producing
cytologic and histologic atypia, though not enough for a diagnosis of cells, and a cystadenocarcinoma is lined by intestinal-type mucosa
malignancy.268 Papillary fragile tumors are seen on the inner surface of (including goblet cells and Paneth cells) associated with varying
the biliary tree; there may be multiple tumors or they may spread dif- degrees of atypia and mitotic activity.18 Benign and malignant compo-
fusely along the biliary tree261 (Figs. 42-61 and 42-62). The tumor does nents may coexist. There is usually no communication between the
not cause biliary obstruction; although it spreads superficially for a cystic tumor and the bile ducts.
A biliary cystadenoma appears as a solitary cystic mass possessing
a well-defined fibrous capsule containing clear fluid. The fibrous
capsule may not be evident when the mass is covered by the liver
A B
FIG 42-55 Iatrogenic stricture of the common hepatic duct after cholecystectomy. A, CT shows intrahepatic
bile duct dilatation and abrupt stricture at the confluence of the rigid hepatic duct (arrow). B, Cholangiogram
shows complete obstruction at the bifurcation (arrow).
CHAPTER 42 Biliary Tract and Gallbladder 1213
A B
C
FIG 42-57 Bile duct stricture at the site of anastomosis in a liver transplant patient. A and B, CT shows
fibrous thickening of the anastomosis site (arrow) between the dilated intrahepatic ducts and the extrahepatic
duct. C, ERCP shows the tight stricture at the anastomosis site (arrow).
A B
C
FIG 42-59 Biliary hamartomas (von Meyenburg’s complex). A, T2-weighted image shows innumerable tiny
high-signal-intensity nodules and cystic lesions in the liver. On T1-weighted (B) and gadolinium-enhanced (C)
images, the number of lesions is markedly decreased, suggesting that many of the nodules are enhanced
and isoattenuating to the liver parenchyma.
(Fig. 42-67). The septa and mural nodules are typically enhanced on Other benign tumors. A plexiform neurofibroma may involve the
contrast-enhanced CT or MRI. Thin or thick septa are clearly visible biliary tract, forming a branching mass along the intrahepatic and
on sonography. Various CT attenuation or MR signal intensities are extrahepatic bile ducts, surrounding the bile ducts and portal
seen on both T1- and T2-weighted images, depending on the presence veins, or sometimes forming an intraductal mass159,206 (Fig. 42-69).
of solid components, hemorrhage, and protein content.256 Hamartomas, granulosa cell tumors, heterotopic gastric or pancreatic
A cystadenoma arising from the extrahepatic ducts is rare, account- mucosal rests, and adenomyomas (Fig. 42-70) may appear as intralu-
ing for less than 10% of biliary cystadenomas. The most common minal or intramural masses.163 Traumatic neuroma of the bile duct is
presentation is biliary obstruction and jaundice. As with an intrahe- not a true neoplasm but a reactive proliferation of pericholangial
patic cystadenoma, an extrahepatic cystadenoma or cystadenocarci- nerve tissue caused by cholecystectomy (Fig. 42-71), liver transplanta-
noma appears as a uniloculated or multiloculated cystic mass with tion, or blunt trauma, resulting in bile duct stricture and proximal
internal septa and mural nodules in the extrahepatic ducts180,273 (Fig. dilatation.134,244,304
42-68). A choledochal cyst, especially a choledochal diverticulum or
choledochocele, can be differentiated based on the presence of septa Malignant Tumors of the Bile Ducts
or a multiloculated shape. There is no communication between the Cholangiocarcinoma. Cholangiocarcinoma is the most common
cystic tumor and the bile duct.273 malignant tumor arising from the epithelium of the bile ducts. It is
much less common than hepatocellular carcinoma, accounting for 5%
to 30% of all primary hepatic malignancies.290 The peak age is in the
sixth to seventh decades. Hilar cholangiocarcinoma is the most
common lesion, accounting for 53% to 67% of cases, with peripheral
intrahepatic cholangiocarcinoma accounting for 6% to 25% of cases
FIG 42-62 Biliary papillomatosis. Cholangiogram shows multiple small FIG 42-63 Biliary cystadenoma. CT shows a large oval cyst containing
flat papillary tumors along the proximal extrahepatic duct. barely visible septa and small daughter cysts.
A B
FIG 42-64 Biliary cystadenoma. A and B, CT shows curvilinear thin septa and daughter cysts. The attenu-
ation value of cysts differs depending on the hemorrhage and protein content.
1216 PART II CT and MR Imaging of the Whole Body
A B
C D
FIG 42-66 Biliary cystadenocarcinoma. CT (A), MRIs (B and C), and a sonogram (D) show a large unilocular
cyst containing thick septa and multiple daughter cysts and solid components. Note the thick irregular
capsule.
CHAPTER 42 Biliary Tract and Gallbladder 1217
A B
C
FIG 42-67 Biliary cystadenocarcinoma. Sonogram (A), CT (B), and MRI (C) show an oval unilocular cyst
containing a solid mass with an irregular surface. Note the punctate calcific focus and thick irregular wall
(arrows in B).
1218 PART II CT and MR Imaging of the Whole Body
A B
C
FIG 42-68 Cystadenoma of the extrahepatic duct. Sonogram (A), MR cholangiogram (B), and cholangiogram
(C) show an ovoid cystic lesion producing balloon-like expansion of the extrahepatic duct. Note the thin wall
between the cyst and the bile duct (arrow in A); there is no communication between them. (Courtesy Dong
Ho Lee, MD, Kyung Hee University Medical School, Seoul, Republic of Korea.)
CHAPTER 42 Biliary Tract and Gallbladder 1219
A B
FIG 42-69 Neurofibroma of the bile ducts in a patient with neurofibromatosis. CT (A) and MR cholangiogram
(B) show an intraductal mass (arrow) causing obstruction of the right and left hepatic ducts. (Courtesy Jun
Woo Lee, MD, Pusan National University Medical School, Pusan, Republic of Korea.)
A B
FIG 42-70 Adenomyoma of the distal common bile duct. A, CT shows a well-marginated mass in the ampul-
lary region (arrow). B, Cholangiogram shows a mass between the common bile duct and duodenum (arrows).
A B
FIG 42-71 Traumatic neuroma of the common bile duct after cholecystectomy. Coronal CT (A) and MR
cholangiogram (B) show an eccentric mass in the common bile duct at the site of resection of the cystic
duct (arrow). (Courtesy Yong Yeon Jeong, MD, Chonnam University Medical School, Guangju, Republic of
Korea.)
1220 PART II CT and MR Imaging of the Whole Body
tissue.210,218,224,260,340 Occasionally a substantial tumor extends beneath by concentric thickening of the bile duct wall for a variable
the intact mucosal epithelium.340 Thus the tumor grows longitudi- length17,210,217,218,340; it does not produce a sizable mass.
nally and extends along the axis of the bile duct like the branch of a Intraductal-growing cholangiocarcinoma grows into the lumen
tree.217 The bile duct lumen is diffusely narrowed or completely obliter- then spreads superficially along the mucosal layer.122 Tumor cells
ated. An extrahepatic periductal-infiltrating tumor is characterized are confined to the mucosal layer and do not invade deep to the
submucosal layer. In contrast to mass-forming and periductal-
infiltrating cholangiocarcinomas, the bile duct lumen is not completely
CHOLANGIOCARCINOMA obstructed.210,218
The prognosis of mass-forming and periductal-infiltrating chol
angiocarcinomas is generally unfavorable; intraductal-growing
cholangiocarcinoma has a much better prognosis after surgical resec-
tion.140,210,295,349 Precise information about tumor location, extent,
growth pattern, and staging is mandatory for optimal treatment plan-
ning and for a prediction of prognosis. Surgical resection should be
individually tailored depending on the morphologic type and the stage
A of the tumor.
Peripheral intrahepatic and hilar cholangiocarcinomas.
Intrahepatic cholangiocarcinomas include peripheral and hilar chol-
angiocarcinomas. The vast majority of peripheral cholangiocarci
nomas are the mass-forming type, whereas the majority of hilar
cholangiocarcinomas are the periductal-infiltrating type.50 Clinically,
intrahepatic peripheral cholangiocarcinoma usually presents with
nonspecific abdominal symptoms, whereas hilar cholangiocarcinoma
B
presents with jaundice because of large bile duct obstruction.
Mass-forming type. A mass-forming intrahepatic cholangiocar-
cinoma is usually sizable, and the tumor does not cause clinical symp-
toms in its early stages. Grossly the tumor is firm and whitish gray
because of abundant fibrous stroma.17 The margin is well circum-
scribed and wavy or lobulated. There may be central necrosis.290 Satel-
lite tumors, especially around the main tumor, are common. These
C satellite tumors occur owing to the tumor’s propensity to invade the
FIG 42-72 Morphologic classification of cholangiocarcinoma. Tubules adjacent peripheral branches of the portal vein.17,210,217,224
represent bile ducts. Drawings show mass-forming (A), periductal- The most common appearance of a peripheral intrahepatic chol-
infiltrating (B), and intraductal-growing (C) cholangiocarcinomas. (From angiocarcinoma on imaging is a well-defined single hypovascular mass
Kimura K, et al: Association of gallbladder carcinoma and anomalous with wavy borders50,54,132,140,210,218,340 (Fig. 42-74). Owing to intrahepatic
pancreaticobiliary ductal union. Gastroenterology 89:1258–1265, 1985.) metastasis via the portal vein, satellite or daughter nodules are frequent
A B
C D
FIG 42-73 Mode of spread of cholangiocarcinoma. Drawings show mucosal (A), mass-forming (B), periductal-
infiltrating (C), and intraductal-growing (D) cholangiocarcinoma.
CHAPTER 42 Biliary Tract and Gallbladder 1221
A B
FIG 42-74 Peripheral cholangiocarcinoma. A, CT during the arterial phase shows a lobulated mass with a
well-enhancing periphery and a heterogeneously enhancing center. Note a small satellite tumor (arrow).
B, CT during the delayed phase shows the same mass, but it appears much smaller because of gradual
enhancement from the periphery.
A B
C
FIG 42-76 MRI of peripheral cholangiocarcinoma. There is a well-defined lobulated mass with a dimple at
the surface (arrow). The mass is of low signal intensity on the T1-weighted image (A) and of high signal
intensity on the T2-weighted image (B). The central part is enhanced in the equilibrium phase (C), reflecting
the presence of massive fibrosis.
CHAPTER 42 Biliary Tract and Gallbladder 1223
A B
C D
FIG 42-77 Contrast enhancement of peripheral cholangiocarcinoma. T1-weighted images before gadolinium
administration (A) and immediately (B), 5 minutes (C), and 3 hours (D) after gadolinium injection. In the arte-
rial phase the peripheral part is enhanced. In the delayed phase the central part is gradually enhanced and
eventually greatly enhanced.
A B
FIG 42-79 A and B, Periductal-infiltrating cholangiocarcinoma involving the intra- and extrahepatic ducts.
Note the ill-defined mass involving the right and left hepatic ducts (arrows in A) and the encircling and
thickening of the extrahepatic ducts (arrows in B), obliterating the lumen of the bile duct.
A B
FIG 42-80 A and B, Combined mass-forming and periductal-infiltrating cholangiocarcinoma showing a
large ill-defined irregular mass (arrows) involving the hilum of the liver and wall thickening along the extra-
hepatic duct.
A B
FIG 42-82 Nodular or mass-forming cholangiocarcinoma of the distal common bile duct (arrow) on CT
(A) and cholangiogram (B).
A B
FIG 42-83 Periductal-infiltrating cholangiocarcinoma. Axial (A) and coronal (B) CT images show concentric
thickening of the common hepatic duct (arrow in A) involving the upper half of the extrahepatic duct (arrow
in B).
bile ducts.13,123 However, because the mass is usually small, images opacified in cases of complete obstruction, or it may appear to be
should be carefully scrutinized. stringlike when the lumen is not completely obstructed210 (Fig. 42-84).
Periductal-infiltrating type. This type of tumor constitutes Differentiation from acute or recurrent pyogenic cholangitis may
more than 60% of extrahepatic cholangiocarcinomas. The tumor be problematic. The involved bile duct wall is thicker in cases of chol-
appears as a focal or segmental concentric thickening of the extrahe- angiocarcinoma (usually >1 mm), whereas in cholangitis the bile duct
patic ducts, with almost complete obstruction of the lumen.210,217,340 wall is thinner than 1 mm. Furthermore, the involved segment of the
The thickened wall (measuring up to 1 cm) is firm and grayish white.340 bile duct is narrowed or obliterated in cholangiocarcinoma but normal
The extent of the tumor varies, ranging from 0.5 to 6 cm in length; it or dilated in cholangitis.
may involve all the extrahepatic ducts and extend proximally as far as Intraductal-growing type. The intraductal tumor may be pol-
the IHDs. ypoid, sessile, or superficially spreading along the lumen.174,210,217,218
On CT or MRI, the thickened bile ducts can be visualized as an There may also be multiple discrete tumors (papillary cholangiocarci-
enhancing ring or spot (Fig. 42-83). It is often difficult to visualize the nomatosis) along the inner surface of the bile ducts. Usually the tumor
lesion on CT or MRI because of the absence of distinct tumor forma- is limited to the mucosa and invades the wall and surrounding tissue
tion; these imaging studies may show only focal or diffuse thickening in the very late phase.210,217,218 An intraductal papillary cholangiocarci-
of the bile duct.13,210,217,218 At the site of bile duct obstruction, the tumor noma is friable and sloughs easily by touching or rubbing at the time
border can be demonstrated as a symmetrically or asymmetrically of surgery, or it may slough spontaneously and occlude the bile ducts,
thickened bile duct wall, constituting a transition zone.298 On cholan- simulating a bile duct stone214 (Fig. 42-85). The bile ducts are dilated
giography or MR cholangiography, the involved segment may not be and incompletely obstructed by the tumor itself or by viscous mucin.
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DANCE ON STILTS AT THE GIRLS’ UNYAGO, NIUCHI
I see increasing reason to believe that the view formed some time
back as to the origin of the Makonde bush is the correct one. I have
no doubt that it is not a natural product, but the result of human
occupation. Those parts of the high country where man—as a very
slight amount of practice enables the eye to perceive at once—has not
yet penetrated with axe and hoe, are still occupied by a splendid
timber forest quite able to sustain a comparison with our mixed
forests in Germany. But wherever man has once built his hut or tilled
his field, this horrible bush springs up. Every phase of this process
may be seen in the course of a couple of hours’ walk along the main
road. From the bush to right or left, one hears the sound of the axe—
not from one spot only, but from several directions at once. A few
steps further on, we can see what is taking place. The brush has been
cut down and piled up in heaps to the height of a yard or more,
between which the trunks of the large trees stand up like the last
pillars of a magnificent ruined building. These, too, present a
melancholy spectacle: the destructive Makonde have ringed them—
cut a broad strip of bark all round to ensure their dying off—and also
piled up pyramids of brush round them. Father and son, mother and
son-in-law, are chopping away perseveringly in the background—too
busy, almost, to look round at the white stranger, who usually excites
so much interest. If you pass by the same place a week later, the piles
of brushwood have disappeared and a thick layer of ashes has taken
the place of the green forest. The large trees stretch their
smouldering trunks and branches in dumb accusation to heaven—if
they have not already fallen and been more or less reduced to ashes,
perhaps only showing as a white stripe on the dark ground.
This work of destruction is carried out by the Makonde alike on the
virgin forest and on the bush which has sprung up on sites already
cultivated and deserted. In the second case they are saved the trouble
of burning the large trees, these being entirely absent in the
secondary bush.
After burning this piece of forest ground and loosening it with the
hoe, the native sows his corn and plants his vegetables. All over the
country, he goes in for bed-culture, which requires, and, in fact,
receives, the most careful attention. Weeds are nowhere tolerated in
the south of German East Africa. The crops may fail on the plains,
where droughts are frequent, but never on the plateau with its
abundant rains and heavy dews. Its fortunate inhabitants even have
the satisfaction of seeing the proud Wayao and Wamakua working
for them as labourers, driven by hunger to serve where they were
accustomed to rule.
But the light, sandy soil is soon exhausted, and would yield no
harvest the second year if cultivated twice running. This fact has
been familiar to the native for ages; consequently he provides in
time, and, while his crop is growing, prepares the next plot with axe
and firebrand. Next year he plants this with his various crops and
lets the first piece lie fallow. For a short time it remains waste and
desolate; then nature steps in to repair the destruction wrought by
man; a thousand new growths spring out of the exhausted soil, and
even the old stumps put forth fresh shoots. Next year the new growth
is up to one’s knees, and in a few years more it is that terrible,
impenetrable bush, which maintains its position till the black
occupier of the land has made the round of all the available sites and
come back to his starting point.
The Makonde are, body and soul, so to speak, one with this bush.
According to my Yao informants, indeed, their name means nothing
else but “bush people.” Their own tradition says that they have been
settled up here for a very long time, but to my surprise they laid great
stress on an original immigration. Their old homes were in the
south-east, near Mikindani and the mouth of the Rovuma, whence
their peaceful forefathers were driven by the continual raids of the
Sakalavas from Madagascar and the warlike Shirazis[47] of the coast,
to take refuge on the almost inaccessible plateau. I have studied
African ethnology for twenty years, but the fact that changes of
population in this apparently quiet and peaceable corner of the earth
could have been occasioned by outside enterprises taking place on
the high seas, was completely new to me. It is, no doubt, however,
correct.
The charming tribal legend of the Makonde—besides informing us
of other interesting matters—explains why they have to live in the
thickest of the bush and a long way from the edge of the plateau,
instead of making their permanent homes beside the purling brooks
and springs of the low country.
“The place where the tribe originated is Mahuta, on the southern
side of the plateau towards the Rovuma, where of old time there was
nothing but thick bush. Out of this bush came a man who never
washed himself or shaved his head, and who ate and drank but little.
He went out and made a human figure from the wood of a tree
growing in the open country, which he took home to his abode in the
bush and there set it upright. In the night this image came to life and
was a woman. The man and woman went down together to the
Rovuma to wash themselves. Here the woman gave birth to a still-
born child. They left that place and passed over the high land into the
valley of the Mbemkuru, where the woman had another child, which
was also born dead. Then they returned to the high bush country of
Mahuta, where the third child was born, which lived and grew up. In
course of time, the couple had many more children, and called
themselves Wamatanda. These were the ancestral stock of the
Makonde, also called Wamakonde,[48] i.e., aborigines. Their
forefather, the man from the bush, gave his children the command to
bury their dead upright, in memory of the mother of their race who
was cut out of wood and awoke to life when standing upright. He also
warned them against settling in the valleys and near large streams,
for sickness and death dwelt there. They were to make it a rule to
have their huts at least an hour’s walk from the nearest watering-
place; then their children would thrive and escape illness.”
The explanation of the name Makonde given by my informants is
somewhat different from that contained in the above legend, which I
extract from a little book (small, but packed with information), by
Pater Adams, entitled Lindi und sein Hinterland. Otherwise, my
results agree exactly with the statements of the legend. Washing?
Hapana—there is no such thing. Why should they do so? As it is, the
supply of water scarcely suffices for cooking and drinking; other
people do not wash, so why should the Makonde distinguish himself
by such needless eccentricity? As for shaving the head, the short,
woolly crop scarcely needs it,[49] so the second ancestral precept is
likewise easy enough to follow. Beyond this, however, there is
nothing ridiculous in the ancestor’s advice. I have obtained from
various local artists a fairly large number of figures carved in wood,
ranging from fifteen to twenty-three inches in height, and
representing women belonging to the great group of the Mavia,
Makonde, and Matambwe tribes. The carving is remarkably well
done and renders the female type with great accuracy, especially the
keloid ornamentation, to be described later on. As to the object and
meaning of their works the sculptors either could or (more probably)
would tell me nothing, and I was forced to content myself with the
scanty information vouchsafed by one man, who said that the figures
were merely intended to represent the nembo—the artificial
deformations of pelele, ear-discs, and keloids. The legend recorded
by Pater Adams places these figures in a new light. They must surely
be more than mere dolls; and we may even venture to assume that
they are—though the majority of present-day Makonde are probably
unaware of the fact—representations of the tribal ancestress.
The references in the legend to the descent from Mahuta to the
Rovuma, and to a journey across the highlands into the Mbekuru
valley, undoubtedly indicate the previous history of the tribe, the
travels of the ancestral pair typifying the migrations of their
descendants. The descent to the neighbouring Rovuma valley, with
its extraordinary fertility and great abundance of game, is intelligible
at a glance—but the crossing of the Lukuledi depression, the ascent
to the Rondo Plateau and the descent to the Mbemkuru, also lie
within the bounds of probability, for all these districts have exactly
the same character as the extreme south. Now, however, comes a
point of especial interest for our bacteriological age. The primitive
Makonde did not enjoy their lives in the marshy river-valleys.
Disease raged among them, and many died. It was only after they
had returned to their original home near Mahuta, that the health
conditions of these people improved. We are very apt to think of the
African as a stupid person whose ignorance of nature is only equalled
by his fear of it, and who looks on all mishaps as caused by evil
spirits and malignant natural powers. It is much more correct to
assume in this case that the people very early learnt to distinguish
districts infested with malaria from those where it is absent.
This knowledge is crystallized in the
ancestral warning against settling in the
valleys and near the great waters, the
dwelling-places of disease and death. At the
same time, for security against the hostile
Mavia south of the Rovuma, it was enacted
that every settlement must be not less than a
certain distance from the southern edge of the
plateau. Such in fact is their mode of life at the
present day. It is not such a bad one, and
certainly they are both safer and more
comfortable than the Makua, the recent
intruders from the south, who have made USUAL METHOD OF
good their footing on the western edge of the CLOSING HUT-DOOR
plateau, extending over a fairly wide belt of
country. Neither Makua nor Makonde show in their dwellings
anything of the size and comeliness of the Yao houses in the plain,
especially at Masasi, Chingulungulu and Zuza’s. Jumbe Chauro, a
Makonde hamlet not far from Newala, on the road to Mahuta, is the
most important settlement of the tribe I have yet seen, and has fairly
spacious huts. But how slovenly is their construction compared with
the palatial residences of the elephant-hunters living in the plain.
The roofs are still more untidy than in the general run of huts during
the dry season, the walls show here and there the scanty beginnings
or the lamentable remains of the mud plastering, and the interior is a
veritable dog-kennel; dirt, dust and disorder everywhere. A few huts
only show any attempt at division into rooms, and this consists
merely of very roughly-made bamboo partitions. In one point alone
have I noticed any indication of progress—in the method of fastening
the door. Houses all over the south are secured in a simple but
ingenious manner. The door consists of a set of stout pieces of wood
or bamboo, tied with bark-string to two cross-pieces, and moving in
two grooves round one of the door-posts, so as to open inwards. If
the owner wishes to leave home, he takes two logs as thick as a man’s
upper arm and about a yard long. One of these is placed obliquely
against the middle of the door from the inside, so as to form an angle
of from 60° to 75° with the ground. He then places the second piece
horizontally across the first, pressing it downward with all his might.
It is kept in place by two strong posts planted in the ground a few
inches inside the door. This fastening is absolutely safe, but of course
cannot be applied to both doors at once, otherwise how could the
owner leave or enter his house? I have not yet succeeded in finding
out how the back door is fastened.