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 CHAPTER 41
160. Taylor GA, Atalabi OM, Estroff JA: Imaging of congenital
diaphragmatic hernias. Pediatr Radiol 39(1):1–16, 2009.
161. Terheggen-Lagro SW, Arets HG, van der Laag J, et al: Radiological and
functional changes over 3 years in young children with cystic fibrosis.
Eur Respir J 30(2):279–285, 2007.
162. Terheggen-Lagro S, Truijens N, van Poppel N, et al: Correlation of six
different cystic fibrosis chest radiograph scoring systems with clinical
parameters. Pediatr Pulmonol 35(6):441–445, 2003.
163. Tiddens HA: Chest computed tomography scans should be considered
as a routine investigation in cystic fibrosis. Paediatr Respir Rev
7(3):202–208, 2006.
164. Van Dyke JA, Sagel SS: Calcified pulmonary sequestration: CT
demonstration. J Comput Assist Tomogr 9(2):372–374, 1985.
165. Van Meurs KP, Newman KD, Anderson KD, et al: Effect of
extracorporeal membrane oxygenation on survival of infants with
congenital diaphragmatic hernia. J Pediatr 117(6):954–960, 1990.
166. Veenma DC, de Klein A, Tibboel D: Developmental and genetic aspects
of congenital diaphragmatic hernia. Pediatr Pulmonol 47(6):534–545,
2012.
167. Vu L, Tsao K, Lee H, et al: Characteristics of congenital cystic
adenomatoid malformations associated with nonimmune hydrops and
outcome. J Pediatr Surg 42(8):1351–1356, 2007.
168. Vult von Steyern K, Björkman-Burtscher IM, Geijer M: Radiography,
tomosynthesis, CT and MRI in the evaluation of pulmonary cystic
fibrosis: An untangling review of the multitude of scoring systems.
Insights Imaging 4(6):787–798, 2013.
169. Wagner AL, Szabunio M, Hazlett KS, et al: Radiologic manifestations of
round pneumonia in adults. AJR Am J Roentgenol 170(3):723–726,
1998.
170. Wan YL, Kuo HP, Tsai YH, et al: Eight cases of severe acute respiratory
syndrome presenting as round pneumonia. AJR Am J Roentgenol
182(6):1567–1570, 2004.
171. Weber SA, Ferrari GF: Incidence and evolution of nasal polyps in
children and adolescents with cystic fibrosis. Braz J Otorhinolaryngol
74(1):16–20, 2008.
Chest Imaging in the Pediatric Patient 1189
172. Weinberg PM: Aortic arch anomalies. J Cardiovasc Magn Reson
8(4):633–643, 2006.
173. Weisbrod GL, Chamberlain DW, Tao LC: Pulmonary blastoma, report
of three cases and a review of the literature. Can Assoc Radiol J
39(2):130–136, 1988.
174. Wells TR, Gwinn JL, Landing BH, et al: Reconsideration of the anatomy
of sling left pulmonary artery: The association of one form with
bridging bronchus and imperforate anus. Anatomic and diagnostic
aspects. J Pediatr Surg 23(10):892–898, 1988.
175. White RI, Pollak JS: Pulmonary arteriovenous malformations:
Diagnosis with three-dimensional helical CT—A breakthrough without
contrast media. Radiology 191(3):613–614, 1994.
176. Wick MR, Ritter JH, Humphrey PA: Sarcomatoid carcinomas of the
lung: A clinicopathologic review. Am J Clin Pathol 108(1):40–53,
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177. Wielpütz MO, Eichinger M, Puderbach M: Magnetic resonance imaging
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178. Williams AJ, Schuster SR: Bronchial atresia associated with a
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179. Wilson RD, Hedrick HL, Liechty KW, et al: Cystic adenomatoid
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180. Winters WD, Effmann EL: Congenital masses of the lung: Prenatal and
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181. Wootton-Gorges SL, Stein-Wexler R, Walton JW, et al: Comparison of
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182. Yano Y, Mori M, Kagami S, et al: Inflammatory pseudotumor of the
lung with rapid growth. Intern Med 48(15):1279–1282, 2009.
183. Yasufuku M, Maeda K, Takano Y: Thymopharyngeal duct cyst: An
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809, 2009.
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1198 PART II CT and MR Imaging of the Whole Body
FIG 42-14 Gallstone pancreatitis. The pancreas is enlarged and there
is a peripancreatic fluid collection. The common bile duct (arrow) is
dilated and the wall is thick. Note the tiny stones in the gallbladder and
the thickened gallbladder wall.
FIG 42-15 Suppurative cholangitis caused by gallbladder stone migra-
tion into the common bile duct. Coronal CT shows slightly dilated bile
ducts with severe thickening of the walls of the extrahepatic duct and
gallbladder.
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.
necessary to visualize calcified stones because postcontrast CT masks
them264 (Fig. 42-17). Some stones with mixed composition are isoat-
tenuating to bile or adjacent soft tissue and are therefore difficult to
detect on CT (Fig. 42-18). Pure cholesterol stones are rare but exhibit
low attenuation resembling that of soft tissue (Fig. 42-19) or bile (Fig.
42-20). Stones containing fat or air can be detected because of the
difference in attenuation from bile (Fig. 42-21).
For more accurate detection of intrahepatic ductal stones, thin
section with narrow collimation (<2.5 mm) is necessary. The presence
of bile around a stone results in a ring (bull’s-eye or target sign) or a
crescent of water attenuation between the stone and the bile duct
wall11,14 (Fig. 42-22). A concentrically thickened bile duct wall with
enhancement may be seen around a stone, representing inflamma-
tion and fibrosis due to irritation by the stone. On cholangiograms or
MR cholangiograms, stones are depicted as single or multiple filling
defects (Fig. 42-23). Muddy stones, small fragments of stones, and
gravel are difficult to visualize on CT (see Fig. 42-20), MR, or even
cholangiography.
Bile ducts may not be dilated despite the presence of stones in the
common duct in 24% to 36% of cases12,65 (Fig. 42-24). In acute obstruc-
tion due to stone impaction, the bile duct does not become dilated
until some time has passed. Bile ducts remain dilated after passage of
FIG 42-16 Calcified stone (arrow) in the distal common bile duct.
 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
orifice becomes tight owing to papillitis and papillary edema (see
Fig. 42-13).
Small stones and gravel repeatedly passing through the duodenal
papillary orifice can cause papillitis and eventually papillary steno-
sis.92,359 CT or MRI demonstrates a dilated and thickened bile duct and
an enlarged duodenal papilla164,275 (see Fig. 42-13) but no actual stone
in the bile duct.
The ability to detect a biliary stone by imaging varies depending on
the size, location, and components of the stone.90,142,164,209,275,282 Each
modality has advantages and disadvantages. With CT, detection
depends on the stone’s calcium content and bile duct dilatation. Detec-
tion of stones by MRI is hampered by artifacts caused by pulsation of
the adjacent vessels. During cholangiography, the technique of can-
nulation and bile duct opacification must be optimal for visualization
of small stones.
FIG 42-22 Common bile duct stone with rim calcification (arrow) mim-
icking a bull’s-eye.
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).
Sometimes a stone that is not detected by one imaging modality is
demonstrated by another (Fig. 42-25; see Fig. 42-24). Thus two or
more imaging methods may be necessary for the diagnosis of bile duct
stones.
Cholangitis
Suppurative Cholangitis. Acute suppurative cholangitis is a bacte-
rial infection of the bile ducts occurring mostly in patients with biliary
obstruction caused by either stones or a tumor. Most stones originate
from the gallbladder (Fig. 42-26). The tumor may be a carcinoma of
the bile ducts, head of the pancreas, or ampulla of Vater or (uncom-
monly) a benign tumor.
The bile ducts may be normal or dilated, depending on the cause,
duration, and degree of obstruction. In acute obstruction caused by a
stone, the bile ducts may not be dilated for some time, whereas in
obstruction caused by cancer, the bile ducts are usually dilated.
FIG 42-23 Small stone (arrows) in the common bile duct on MR
cholangiogram.
 CHAPTER 42
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
from the gallbladder. The common bile duct is slightly dilated, and the
wall is thick and enhanced as a concentric ring (arrow). The gallbladder
contains a small stone and its wall is thick and enhanced owing to acute
cholecystitis.
Obstruction of the bile ducts causes bile stasis and a predisposition to
infection. Gram-negative organisms such as E. coli are usually respon-
sible. It is believed that bacteria within the intestinal tract ascend
through the ampulla of Vater; for this reason the disease is also called
ascending cholangitis. Bacterial colonization may also occur through
portal venous bacteremia. The combination of obstruction and colo-
nization leads to cholangitis, but neither obstruction nor colonization
by itself is sufficient to cause disease.223 Patients present with acute
abdominal pain, fever, chills, and sometimes jaundice. In some patients
with bile duct stones or carcinoma along the bile ducts, the initial
symptoms and signs may be similar to those of acute suppurative
cholangitis.
Biliary Tract and Gallbladder 1201
FIG 42-27 Suppurative cholangitis with a common bile duct stone in
a patient with recurrent pyogenic cholangitis. Note concentric thicken-
ing of the bile duct wall with enhancement.
Other than bile duct dilatation, imaging finding are usually
normal.14 The presence of purulent bile may result in increased attenu-
ation of bile (greater than that of water) on CT, but it is usually not
clearly depicted. Depending on the calcium content, stones may be
clearly depicted as calcified high-attenuating foci or as noncalcified
intraluminal material (see Figs. 42-19 and 42-20).
The wall of the bile ducts may be thickened concentrically and dif-
fusely, with dense contrast enhancement (Fig. 42-27; see Fig. 42-26);
this is well delineated with thin-section CT.14 In contrast to periductal-
infiltrating bile duct cancer, the thickness of the bile ducts is uniform
and less than 1 mm. In patients with suppurative cholangitis caused
by a cancer along the bile ducts, a nodular mass or periductal-
infiltrating cholangiocarcinoma is depicted on US, CT (Fig. 42-28),
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.

One complication of suppurative cholangitis is the occurrence of

multiple intrahepatic abscesses, and there may be communication with
the biliary tree. In a fulminating infection of gas-forming organisms,
pneumobilia can be seen on CT.

Recurrent Pyogenic Cholangitis

Incidence. Recurrent pyogenic cholangitis, also known as Orien-
tal cholangitis, Oriental cholangiohepatitis, or intrahepatic pigment
stone disease, is characterized by recurrent attacks of acute bacterial
cholangitis presenting with abdominal pain, fever, chills, and jaun-
dice.33,64,89,269,299 A bile duct stone is an integral part of the disease, and
the symptom complex repeats once or twice a year. The disease is
prevalent in the Far East and Southeast Asia (thus its alternative
names); it occurs infrequently in non-Asians.
The stones in patients with recurrent pyogenic cholangitis are
mainly bilirubinate pigment stones formed in the bile ducts, whereas
the most common stones in Caucasian people are cholesterol stones
in the CBD that originated from the gallbladder.297 Many patients with
recurrent pyogenic cholangitis also have muddy stones or tiny gravel.89
Chronic infection of the biliary tree by C. sinensis or O. viverrini
or inadvertent biliary Ascaris infection is a possible cause of the
disease.209,297 A long-standing partial obstruction due to parasites in the
bile ducts, bile stasis, increased secretion of mucin, or eggs or excreta
of parasites predisposes the patient to form bile duct stones, with the
eggs or debris being the stone’s nidus.209 Alternatively, portal septice-
mia due to poor eating habits and poor nutrition has been proposed
as a cause of bile duct infection and stone formation.57,239 FIG 42-29 Recurrent pyogenic cholangitis. ERCP shows markedly
Pathology and imaging findings. Because of repeated inflamma- dilated intrahepatic bile ducts with rigidity, decreased arborization, right-
tion, the bile duct walls are thickened diffusely owing to inflammatory angle branching, acute tapering, and the “arrowhead” sign. The extra-
cell infiltration and fibrosis. Fibrosis causes the bile ducts to become hepatic duct is also dilated, with proximal narrowing due to segmental
rigid and straight, lacking gentle dichotomous branching (Fig. 42-29). fibrous stricture (arrows). Note the large stones (arrowheads) in the
distal common bile duct.
In severe infection, adjacent hepatic parenchyma is involved, resulting
in cholangiohepatitis.57,64,89,269 Sometimes this inflammation becomes
suppurative and the bile ducts fill with pus. Larger IHDs and extrahe-
patic ducts become dilated because of a stricture of the duodenal peripheral branches164,195,209,220,339 (Fig. 42-30; see Fig. 42-29). Owing to
papilla caused by mechanical irritation and inflammation due to the long-standing inflammation and fibrosis, peripheral bile ducts appear
repeated passage of stones or sharp gravel.209 However, the small IHDs rigid and taper abruptly, producing an “arrowhead” appearance (see
are not dilated because of ductal fibrosis. Thus the biliary tree has a Fig. 42-29).275
“pruned tree” appearance because of the notable dilatation of the Imaging findings include stones, a dilated bile duct, wall thickening,
larger bile ducts, decreased arborization, and nonvisualization of the and duodenal papillary stenosis. Stones are visualized in 70% to 80%
 CHAPTER 42 Biliary Tract and Gallbladder 1203

FIG 42-31 ERCP in a patient with common bile duct obstruction

FIG 42-30 Recurrent pyogenic cholangitis. The extrahepatic ducts and
caused by a passed stone originating from the gallbladder shows simple
lobar and segmental bile ducts are dilated, but the peripheral ducts are
dilatation.
obliterated rapidly. Note multiple small stones in the extrahepatic ducts.
The gallbladder was resected.

of patients in the intrahepatic or extrahepatic ducts or both (see Fig.

42-30).41,208,209 For patients with intrahepatic stones, the lateral segment
of the left hepatic lobe and posterior segment of the right hepatic lobe
are frequent sites of stone lodging.89,209
The characteristic bile duct involvement patterns persist even when
the stone passes into the duodenum. This is true because repeated
passage of stones causes papillitis, fibrosis, and papillary stenosis.
In some cases, bile duct dilatation is limited to the hepatic segmen-
tal or lobar bile ducts. This dilatation occurs as intrahepatic stones
lodge at the branching points of large-caliber bile ducts, causing
mechanical irritation, chronic inflammation, and fibrosis and a resul-
tant stricture209,275 (Fig. 42-31). Frequent sites of focal stricture are the
branching points of the medial and lateral segments of the left hepatic
lobe (Fig. 42-32), posterior segmental duct of the right hepatic lobe,
and bifurcation of the right and left hepatic lobes (see Fig. 42-29).164,209
With acute and chronic inflammation, the wall of the bile duct
becomes thickened. On high-resolution contrast CT, the thickened wall FIG 42-32 Stones in the lateral segmental bile ducts with severe dilata-
is clearly visualized and enhanced (Fig. 42-33). The thickening of the tion due to stricture (arrow).
bile duct in patients with recurrent pyogenic cholangitis is more severe
than in those with acute suppurative cholangitis but less severe than
in patients with periductal-infiltrating cholangiocarcinoma. demonstrate on sonography, CT, cholangiography, and MR cholangi-
During the stage of acute exacerbation, the periductal hepatic ography because the structure of the ampulla-papilla is small, and
parenchyma is enhanced on contrast-enhanced CT, reflecting peri­ papillary stenosis caused by fibrosis cannot be visualized on imaging40
ductal hepatic parenchymal inflammation (cholangiohepatitis) (Fig. (Fig. 42-37).
42-34). Sometimes the hepatic lobe or segments are enhanced in the Complications. Biliary cirrhosis is a possible complication and
arterial phase, probably owing to severe cholangiohepatitis and arterial usually follows long-standing severe, repeated disease.89 Stones at
hyperemia.209 Hepatic abscesses occur as a complication (Fig. 42-35). the lower end of the CBD may cause acute pancreatitis89,204,294 and a
In patients with stricture of the lobar or segmental bile ducts, the cor- choledochoduodenal fistula.89 Intrahepatic cholangiocarcinoma may
responding hepatic lobe or segment becomes atrophic because of long- develop in a stone-harboring bile duct because of long-standing
standing obstruction of the bile ducts.209 Periportal inflammation and inflammation, hyperplasia, and dysplasia.167,186,261 The reported preva-
portal venous encroachment may play an additional role. lence ranges from 1.5% to 11%.167
Duodenal papillitis and papillary stenosis are an integral part of
recurrent pyogenic cholangitis. Impaction of stones and repeated Primary Sclerosing Cholangitis
passage of small stones or sharp gravel through the papillary orifice Incidence. Primary sclerosing cholangitis (PSC) is a chronic cho-
cause irritation, inflammation, edema, fibrosis, and a resultant papil- lestatic liver disease of unknown cause characterized by diffuse inflam-
lary stricture.91,254,272 mation and fibrosis of the biliary tree. PSC is a progressive disease that
A swollen duodenal papilla can be demonstrated on CT (Fig. can lead to obliteration of the bile ducts and subsequently biliary
42-36) and MR cholangiography. Papillary stenosis is difficult to cirrhosis; it may eventually progress to end-stage liver disease and
1204 PART II CT and MR Imaging of the Whole Body
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).
FIG 42-34 Recurrent pyogenic cholangiohepatitis. CT obtained during
the arterial phase shows thickening and enhancement of the bile
ducts (arrows) and stones in the common bile duct. Note the hetero-
geneous enhancement of the hepatic parenchyma and periductal
enhancement.
cholangiocarcinoma. Liver transplantation is the only effective life-
extending treatment for advanced PSC. The disease is much more
common in northern Europe and the United States than elsewhere,
with the age-adjusted incidence in the United States being 1.25 per
100,000 men and 0.54 per 100,000 women10; it is exceedingly rare in
Asian populations. Approximately 70% of the patients are male, and
70% have ulcerative colitis.
Pathology. The pathology of sclerosing cholangitis is character-
ized by a fibrosing inflammation of the biliary tree resulting in diffuse
thickening of the bile duct wall, which if severe enough leads to
obstruction of the lumen.32,236,345 There are alternating areas of focal
narrowing and ductal dilatation.94,197,227 On microscopic examination
there is dense fibrosis, sparse mixed inflammatory cell infiltration, and
a relatively intact epithelium. These findings are nonspecific, and the
diagnosis cannot be based solely on a biopsy specimen.197 Because of
periductal fibrosis, ductal dilatation is not prominent even with high-
degree obstruction. PSC involves the intrahepatic and extrahepatic
ducts. In 20% of patients, the disease is confined to the intrahepatic
and hilar ducts. The gallbladder is involved in 40% of patients.
Imaging findings. Cholangiogram has long been the gold stan-
dard for the diagnosis of PSC. Multiple segmental strictures involving
the intra- and extrahepatic bile ducts are hallmarks of the disease and
characteristic findings (Fig. 42-38). The abnormality is not uniform
along the bile ducts. A normal or less-involved segment alternating
with strictures produces the classic “beaded” appearance (Fig. 42-39).
The length of a stricture can range from 1 to 2 mm to several centi-
meters. When the peripheral bile ducts are obliterated, the bile ducts
have a pruned-tree appearance (see Fig. 42-38). The bile duct wall is
irregular, from a fine brush border to a coarse, shaggy, or nodular
appearance (see Fig. 42-39). Sometimes there are small diverticula.
Thus the combination of short focal strictures and dilatations, beading,
pruning, and mural irregularities are typical for PSC.
MRCP has merit in depicting bile duct involvement patterns of
alternating strictures and dilatations of the entire biliary tree (see
Fig. 42-39).105,145 In addition to the advantage of noninvasiveness, MR
cholangiography can demonstrate abnormal bile ducts proximal to
the completely obstructed segment that cannot be demonstrated by
cholangiography.
 CHAPTER 42 Biliary Tract and Gallbladder 1205

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
thickening (Fig. 42-40) and contrast enhancement (Fig. 42-41) of the
bile duct wall. The thickness varies from 1 to 3 mm. Thus these
imaging techniques are helpful to determine the severity and extent of
disease. In some instances, cholangiographic “beading” can be seen on
contrast-enhanced CT (see Fig. 42-39). Like MRCP, CT has the advan-
tage of being able to visualize an obstructed segment that cannot be
demonstrated on cholangiography.
Other imaging findings include alterations of the hepatic paren-
chyma such as biliary cirrhosis, hepatic segmental atrophy and hyper-
trophy, portal hypertension, a dominant biliary stricture resulting in
obstructive jaundice, calculi in the gallbladder and CBD (25%-30%),
and a complicating cholangiocarcinoma (8%-15%).310
Clinical course. There is an increased incidence of cholangiocar-
cinoma in patients with PSC.310 In a series of patients undergoing liver
transplantation for PSC, 10% were found to have cholangiocarcinoma
in their native livers.129 When the two diseases coexist, the ductal
abnormality of PSC can easily mask the presence of cholangiocarci-
noma.231 Cholangiocarcinoma usually causes more complete obstruc-
tion than PSC (dominant stricture), and there may be markedly dilated
bile ducts proximal to the bile duct segment involved by the cholan-
giocarcinoma. A rapidly progressing segmental stricture and proximal
dilatation on serial images associated with clinical deterioration favor
the presence of cholangiocarcinoma. In this regard, thin-section CT
and MRI are helpful to assess the clinical course.
AIDS Cholangitis. Inflammation of the bile ducts can occur in
patients with acquired immunodeficiency syndrome (AIDS), owing to
an opportunistic infection by cytomegalovirus, Mycobacterium avium-
intracellulare, Candida albicans, Cryptosporidium species, and Klebsi-
ella pneumoniae.35,289 Inflammation may involve the intrahepatic and
extrahepatic ducts as well as the duodenal papillae, resulting in papil-
lary stenosis. Cholangiogram shows irregularities and stricture of the
intrahepatic and extrahepatic bile ducts with associated bile duct dila-
tation. Papillary stenosis often occurs in conjunction with proximal
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).

tissue can also be observed.62,241 CT and sonography may demonstrate

wall thickening of the bile duct and gallbladder. A small nodule may
be seen at the distal end of the CBD, reflecting inflammation and
edema of the papilla of Vater.73

FIG 42-40 Primary sclerosing cholangitis. Sonogram shows the thick-
ened wall of the extrahepatic bile ducts (arrows).
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-
tion of the extrahepatic ducts and without a focal obstructing lesion
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.
FIG 42-42 Clonorchis sinensis in the bile duct. Photomicrograph from
a rabbit liver experimentally infected with C. sinensis shows adult flukes
in the bile duct. Note adenomatous hyperplasia of the mucosa (short
arrows) and periductal fibrosis (long arrows). (Hematoxylin-eosin; ×40.)
reside in the small IHDs. This characteristic pattern of the biliary
tree—apparent on cholangiography, CT, and MR cholangiography—
is not encountered in other bile duct diseases such as cholangitis,
bile duct stone, or tumor.48,49,55,71,72,208,215 Adult flukes in the bile ducts
can be demonstrated on cholangiography (Fig. 42-44) and MR chol-
angiography (Fig. 42-45) as small, linear, elliptical or leaflike filling
defects measuring 2 to 10 mm long.208,215 The worms and their aggre-
gates in the bile duct lumen, in association with the inflammatory
reaction,55,72,208,215 impede contrast opacification of the peripheral ducts
(see Fig. 42-44).
Because of long-standing inflammation and fibrosis, the bile duct
wall is thickened. CT may show the enhancing wall of the bile ducts.
The gallbladder may be distended. In heavy infection the branch ducts
of the tail of the pancreas are dilated, as in the liver.216
Once infection occurs the flukes can live in the biliary tree for
decades. Peripheral intrahepatic dilatation persists for a long time, even
after the flukes are eradicated spontaneously or by the administration
of anthelmintic drugs. Recurrent pyogenic cholangitis and bile duct
stone formation are frequent complications of clonorchiasis. Intra-
ductal inflammation, increased mucin, and mechanical obstruction by
the flukes and their eggs cause bile stasis, which provides a favorable
environment for bacterial infection. The eggs and bacteria serve as nidi
for pigment stone formation.208 A carcinoma may arise from the intra-
hepatic and extrahepatic bile ducts as a complication of long-standing
fluke infection (Figs. 42-46 and 42-47). Chronic inflammatory changes
and adenomatous hyperplasia of the biliary mucosal epithelium may
transform into dysplasia and cholangiocarcinoma.46,53,319
F. hepatica is a trematode that infects cattle and sheep; humans
are accidental hosts. Infection is caused by ingestion of raw aquatic
plants contaminated with metacercariae, which later penetrate the
intestinal wall and migrate through the peritoneal cavity to the liver.
After penetrating Glisson’s capsule, the flukes migrate randomly
through the liver parenchyma (hepatic stage) and enter the bile ducts,
where they mature and release eggs (biliary stage). Hepatic fascioliasis
manifests as clusters of microabscesses, usually in the subcapsular
regions, arranged in a characteristic serpentine fashion resembling
“tunnels and caves”36,121,270,156,281 (Fig. 42-48). A large cystlike necrotic
lesion may also be observed. Imaging findings of biliary fascioliasis
are more or less the same as for clonorchiasis, with bile duct dilata-
tion and intraductal flukes appearing as echogenic foci on ultrasono-
grams and as filling defects on cholangiograms (Fig. 42-49) and MR
cholangiograms.
The intestinal roundworm Ascaris lumbricoides is 15 to 30 cm long
and 3 to 5 mm thick and resides in the human small intestine. Occa-
sionally worms migrate through the papilla of Vater into the biliary
tree, resulting in bile duct obstruction, cholangitis, and pancreatitis.
The long worm is seen as a filling defect on cholangiograms or MR
cholangiograms137,191 (Fig. 42-50).
Bile Duct Strictures
A benign bile duct stricture may affect the intrahepatic or extrahepatic
ducts or both. Common causes of benign strictures are inflammatory
and iatrogenic. PSC and recurrent pyogenic cholangitis are the most
common causes of an inflammatory stricture. An iatrogenic bile duct
injury is most often caused by surgery such as a cholecystectomy, CBD
exploration, T-tube indwelling in the CBD, endoscopic papillotomy, or
liver transplantation.150 A laparoscopic cholecystectomy predisposes to
bile duct injury because the CBD may be mistaken for the cystic duct.
Thermal injury to the bile duct can occur during radiofrequency
 CHAPTER 42 Biliary Tract and Gallbladder 1209

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).

FIG 42-44 Clonorchiasis. Endoscopic retrograde cholangiogram shows

innumerable small elliptical filling defects in the bile ducts, representing
adult Clonorchis sinensis. Filling of the peripheral duct is impeded by
flukes (arrowheads). The intrahepatic ducts are dilated, but the extra-
hepatic bile ducts are not.
FIG 42-46 Clonorchiasis and cholangiocarcinoma of the common
hepatic duct. Endoscopic retrograde cholangiogram shows markedly
dilated intrahepatic bile ducts containing multiple elliptical filling defects
due to adult flukes of Clonorchis sinensis. Arrows point to the segment
of cholangiocarcinoma.

FIG 42-45 Severe clonorchiasis. MRI shows severe dilatation of the

intrahepatic bile ducts up to the periphery of the liver. Adult flukes are
visible in the bile ducts (arrows).
1210 PART II CT and MR Imaging of the Whole Body
FIG 42-47 Peripheral cholangiocarcinoma (arrow) in a patient with clo-
norchiasis, which has caused dilatation of the peripheral bile ducts.
FIG 42-48 Hepatic fascioliasis. CT shows multiple small, clustered,
necrotic lesions in the subcapsular area arranged as “tunnels and
caves.”
FIG 42-49 Biliary fascioliasis. Endoscopic retrograde cholangiogram
shows two elliptical filling defects in the common bile duct representing
adult Fasciola hepatica. (Courtesy Cheol Min Park, MD, Korea University
Medical School, Seoul, Republic of Korea.)
A
B
FIG 42-50 Biliary ascariasis. Endoscopic retrograde cholangiogram
(A) and MRCP (B) show a long convoluted filling defect in the extrahe-
patic ducts representing adult Ascaris lumbricoides. (Courtesy So Yeon
Kim, MD, Ulsan University Medical School, Seoul, Republic of Korea.)
ablation for hepatic tumors173 (Fig. 42-51). Blunt abdominal trauma
may result in injury to the duodenum and extrahepatic bile ducts.
For a biliary stricture with a benign cause, the stenotic segment
shows minimal wall thickening, making it difficult to see on CT or MRI
(Fig. 42-52). The stenotic segment is abrupt and short, measuring less
than 1 cm. In contrast, for periductal-infiltrating cholangiocarcinoma,
the involved bile duct wall is thicker than 2 mm and enhances intensely
after contrast administration.
In PSC, there are multiple sites of stricture and normal or dilated
segments, resulting in a beaded appearance. In recurrent pyogenic
cholangitis, branching points of lobar and segmental bile ducts are
the common sites of stricture; this is where the stones tend to lodge,
causing irritation and inflammation at the branching points, resulting
in fibrosis and stricture. Common sites are the lateral segmental bile
duct of the left hepatic lobe (Fig. 42-53), posterior segmental bile duct
of the right hepatic lobe (Fig. 42-54), and bifurcation of the right and
left hepatic ducts (see Figs. 42-11 and 42-29).
A focal stricture of the CBD occurs in approximately 0.5% of cho-
lecystectomy patients.128 This complication occurs when the cystic duct
is clamped and ligated and the CBD is inadvertently incorporated into
 CHAPTER 42 Biliary Tract and Gallbladder 1211

the ligatures, causing injury.66 Clinical manifestations including jaun-
dice may appear within a week, months, or years, depending on the
severity of the bile duct damage. CT reveals severely dilated IHDs, with
the degree of dilatation depending on the severity of the bile duct
obstruction. At the hepatic hilum there is an abrupt transition from
the dilated bile ducts to the normal extrahepatic ducts, where there is
a short segmental tight stricture (Fig. 42-55). A coronal reconstruction
image better shows the stenotic segment. A biliary stricture caused by
injury to the anastomotic site during liver transplantation typically
occurs at the proximal part of the extrahepatic duct. The degree of
stenosis varies from mild stenosis without bile flow impairment
(Fig. 42-56) to a tight stricture and complete obstruction of bile flow
(Fig. 42-57).
A biliary stricture caused by blunt abdominal trauma occurs in
the suprapancreatic portion of the CBD.352 The CBD is susceptible to
disruption from deceleration injuries, usually at the level of the pan-
creaticoduodenal junction, where it is relatively fixed compared with
the more proximal duct. A delayed common duct stricture has been
reported after blunt abdominal trauma. The injury results in a short
segmental tight stricture with concentric or eccentric involvement and
proximal dilatation.
Neoplasms of the Biliary System
Benign Tumors of the Bile Ducts
Bile duct hamartoma. Bile duct hamartoma, also known as von
Meyenburg’s complex, is a focal disorderly collection of bile ducts and
ductules surrounded by abundant fibrous stroma.60,131 There is usually
a centrally located small cystic lesion lined by a single layer of biliary
epithelium that does not communicate with the biliary tree.256 The
lesions are 0.1 to 1.5 cm in diameter and are scattered diffusely in the
liver parenchyma.
CT shows multiple or innumerable hypoattenuating cystlike
hepatic nodules, typically less than 1.5 cm in diameter, occurring
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
lesions on T2-weighted images (Fig. 42-59). Contrast-enhanced CT or
MRI may show homogeneous enhancement of the lesions256,300,309 (see
Fig. 42-59).
Bile duct adenoma. A solitary adenoma appears as a well-
circumscribed wedgelike mass less than 1 cm in diameter. The gallblad-
der is the most frequent site; these tumors are rare along the bile ducts.
A villous adenoma can occur at the duodenal papilla (Fig. 42-60).
Biliary papillomatosis. Biliary papillomatosis is a papillary or
villous tumor in the intrahepatic or extrahepatic bile ducts showing
cytologic and histologic atypia, though not enough for a diagnosis of
malignancy.268 Papillary fragile tumors are seen on the inner surface of
the biliary tree; there may be multiple tumors or they may spread dif-
fusely along the biliary tree261 (Figs. 42-61 and 42-62). The tumor does
not cause biliary obstruction; although it spreads superficially for a
varying length, it produces a large amount of mucus, resulting in
nonobstructive dilatation of the entire biliary tree.7 This tumor has
great potential for malignant transformation (see Fig. 42-61).261
Biliary cystadenoma and cystadenocarcinoma. Benign and
malignant cystic tumors of bile duct origin can occur in the IHDs of
the liver or rarely in the extrahepatic ducts. These tumors occur in
adults, with a strong middle-aged female predominance. The usually
single tumor is covered by a fibrous capsule and is unilocular or
multilocular, containing mucinous or serous fluid.18 A cystadenoma is
lined by a single layer of cuboidal or tall columnar mucin-producing
cells, and a cystadenocarcinoma is lined by intestinal-type mucosa
(including goblet cells and Paneth cells) associated with varying
degrees of atypia and mitotic activity.18 Benign and malignant compo-
nents may coexist. There is usually no communication between the
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

FIG 42-54 Stricture of bile duct in recurrent pyogenic cholangitis. The

posterior segmental branch of the right hepatic duct is missing (“missing FIG 42-56 Mild bile duct stricture (arrow) at the site of anastomosis
duct” sign; long arrow). Note two stones in the anterior segmental bile after liver transplantation. There are many stones and debris in the bile
duct (short arrows). ducts proximal to the stricture.

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).

parenchyma. Usually the cystic tumor is multiloculated, divided by

FIG 42-58 Biliary hamartomas. CT shows many small cystic lesions
scattered throughout the liver parenchyma.
thin uniform curvilinear septa, and measures 1 mm or less. Sometimes
it is barely visible30,31,52,98,101,189,256,259 (Fig. 42-63). There may be multiple
daughter cysts inside (Fig. 42-64). When the septa are very thin, sonog-
raphy is better than CT or MRI for depicting them. In some cystadeno-
mas, there is no septum or daughter cyst and differentiation from a
simple hepatic cyst is impossible (Fig. 42-65). There may be calcium
deposits in the fibrous capsule or septa. The contents of the cystic
tumor can be serous or mucinous fluid, thus attenuation on CT and
signal intensity on MRI may be different depending on the contents
of the individual loculations (see Fig. 42-64). Papillary areas or polyp-
oid mural nodules in the cyst wall or septa have been reported256 but
are rare with cystadenoma.
A biliary cystadenocarcinoma presents as a single cystic mass
covered by a thick capsule; it contains multiple thick septa, mural
nodules, and polypoid or fungating tumors attached to the cyst wall
or septa213 (Fig. 42-66). Coarse thick septal or capsular calcifications
are more frequent in cystadenocarcinoma189 than in cystadenoma
1214 PART II CT and MR Imaging of the Whole Body

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 42-60 Adenoma of the ampulla of Vater. CT shows a 1-cm mass

(arrow) at the ampulla of Vater that has bulged into the duodenum.

FIG 42-61 Biliary papillomatosis. MRI shows innumerable tiny papillary

tumors in the surface of the dilated intrahepatic bile ducts (arrows). Foci
of carcinoma in situ were found on pathologic examination.
 CHAPTER 42 Biliary Tract and Gallbladder 1215

(Fig. 42-67). The septa and mural nodules are typically enhanced on
contrast-enhanced CT or MRI. Thin or thick septa are clearly visible
on sonography. Various CT attenuation or MR signal intensities are
seen on both T1- and T2-weighted images, depending on the presence
of solid components, hemorrhage, and protein content.256
A cystadenoma arising from the extrahepatic ducts is rare, account-
ing for less than 10% of biliary cystadenomas. The most common
presentation is biliary obstruction and jaundice. As with an intrahe-
patic cystadenoma, an extrahepatic cystadenoma or cystadenocarci-
noma appears as a uniloculated or multiloculated cystic mass with
internal septa and mural nodules in the extrahepatic ducts180,273 (Fig.
42-68). A choledochal cyst, especially a choledochal diverticulum or
choledochocele, can be differentiated based on the presence of septa
or a multiloculated shape. There is no communication between the
cystic tumor and the bile duct.273
Other benign tumors. A plexiform neurofibroma may involve the
biliary tract, forming a branching mass along the intrahepatic and
extrahepatic bile ducts, surrounding the bile ducts and portal
veins, or sometimes forming an intraductal mass159,206 (Fig. 42-69).
Hamartomas, granulosa cell tumors, heterotopic gastric or pancreatic
mucosal rests, and adenomyomas (Fig. 42-70) may appear as intralu-
minal or intramural masses.163 Traumatic neuroma of the bile duct is
not a true neoplasm but a reactive proliferation of pericholangial
nerve tissue caused by cholecystectomy (Fig. 42-71), liver transplanta-
tion, or blunt trauma, resulting in bile duct stricture and proximal
dilatation.134,244,304
Malignant Tumors of the Bile Ducts
Cholangiocarcinoma. Cholangiocarcinoma is the most common
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

and extrahepatic cholangiocarcinoma accounting for 22% to 27% of

FIG 42-65 Biliary cystadenoma. CT shows a unilocular cyst with com-
pression of a segmental bile duct.
cases.262 The majority of cholangiocarcinomas are adenocarcinomas,
regardless of location.151,340 This tumor has a tendency to spread along
the bile duct walls,17 and periductal tissue invasion is common. Mucin
stains are nearly always positive, with mucin production often being
abundant.17,260,340 Predisposing conditions include PSC, biliary para-
sitic diseases such as long-standing C. sinensis or O. viverrini infection,
recurrent pyogenic cholangitis with intrahepatic stones, Thorotrast
exposure, and congenital biliary anomalies such as choledochal cyst
and Caroli’s disease.17,151
Based on growth characteristics, cholangiocarcinomas are classi-
fied as mass-forming, periductal-infiltrating, and intraductal-growing
types210,218,224 (Figs. 42-72 and 42-73). A mass-forming cholangiocarci-
noma arises from the mucosa of the bile ducts, grows into the lumen,
and invades and penetrates the bile duct wall; it thus grows three
dimensionally to a certain size. As the intraluminal tumor occludes the
lumen, the bile duct is obstructed.
In contrast to the mass-forming type, a periductal-infiltrating chol-
angiocarcinoma tends to spread along the bile duct wall and periductal

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
the intact mucosal epithelium.340 Thus the tumor grows longitudi-
nally and extends along the axis of the bile duct like the branch of a
tree.217 The bile duct lumen is diffusely narrowed or completely obliter-
ated. An extrahepatic periductal-infiltrating tumor is characterized
CHOLANGIOCARCINOMA
A of the tumor.
B
C satellite tumors occur owing to the tumor’s propensity to invade the
FIG 42-72 Morphologic classification of cholangiocarcinoma. Tubules
represent bile ducts. Drawings show mass-forming (A), periductal-
infiltrating (B), and intraductal-growing (C) cholangiocarcinomas. (From
Kimura K, et al: Association of gallbladder carcinoma and anomalous
pancreaticobiliary ductal union. Gastroenterology 89:1258–1265, 1985.)
by concentric thickening of the bile duct wall for a variable
length17,210,217,218,340; it does not produce a sizable mass.
Intraductal-growing cholangiocarcinoma grows into the lumen
then spreads superficially along the mucosal layer.122 Tumor cells
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
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
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
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
adjacent peripheral branches of the portal vein.17,210,217,224
The most common appearance of a peripheral intrahepatic chol-
angiocarcinoma on imaging is a well-defined single hypovascular mass
with wavy borders50,54,132,140,210,218,340 (Fig. 42-74). Owing to intrahepatic
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.

reflecting fibrosis; this is helpful in making the distinction from a

FIG 42-75 Multiple intrahepatic cholangiocarcinomas due to
metastases.
and vary in size165,210 (Fig. 42-75). On contrast-enhanced CT or MRI,
thin or thick rimlike enhancement is frequently seen around the
periphery of the tumor on arterial-phase images, and there is gradual
centripetal enhancement on delayed-phase images132,165,316 (Fig. 42-76;
see Figs. 42-74 and 42-75). The entire mass may be enhanced only on
delayed-phase images some hours after contrast administration (Fig.
42-77). These findings reflect the nature of the tumor, which is mainly
desmoplastic. Depending on the cellular and fibrous components, the
central part of the mass may be enhanced homogeneously or hetero-
geneously. Sometimes there is septum-like enhancement.165 Occasion-
ally the hepatic vein traverses the central part of the mass undisturbed.165
Capsular retraction is relatively frequent (see Fig. 42-76).122,165 Bile duct
dilatation peripheral to the tumor is common. However, the bile ducts
may not be dilated even if the tumor arises from one of the IHDs.165,210
On MRI the tumor is hypointense on T1-weighted images and
hyperintense on T2-weighted images (see Fig. 42-76), without a
capsule. Central hypointensity may be seen on T2-weighted images,
metastatic tumor.47,50,119 On dynamic MRI the enhancement pattern is
the same as on dynamic CT.
Hilar and peripheral mass-forming cholangiocarcinomas may
appear the same on imaging, except for the presence of IHD dilata-
tion.51,317 Most hilar cholangiocarcinomas result in obstruction of the
right and left hepatic ducts, and there may be a mass that overrides
and separates the bile ducts.51,123,317
Periductal-infiltrating type. Periductal-infiltrating cholangio-
carcinoma grows along the bile ducts and produces diffuse thickening
of them (Fig. 42-78); it is therefore difficult or impossible to depict the
discrete tumor mass.50,51,120,123,210,218,317 The involved bile duct becomes
narrow for a varying length, resulting in eventual obstruction. The
majority of hilar cholangiocarcinomas are of the periductal-infiltrating
type pathologically, but this type of lesion is not commonly seen in the
periphery of the liver.
On imaging, the involved bile ducts are obliterated or diffusely
narrow, whereas the bile ducts proximal to the cholangiocarcinoma
are dilated210,218 (Fig. 42-79). Nonunion of the right and left hepatic
ducts with or without a visibly thickened wall is a typical finding of
an infiltrating hilar cholangiocarcinoma (see Fig. 42-79).51,123,317 On
cholangiography the lumen may be completely obstructed or markedly
narrowed. A stringlike severely narrowed bile duct may be visualized.120
Hilar cholangiocarcinoma is often associated with lobar or segmental
hepatic parenchymal atrophy, probably because of portal vein invasion
and occlusion and decreased portal flow or because of long-standing
dilatation of the bile ducts and diversion of the portal flow.34,323 There
are combined mass-forming and periductal-infiltrating cholangiocar-
cinomas353 (Fig. 42-80).
Intraductal-growing type. Intraductal tumors are usually nod-
ular or castlike, often spreading superficially along the mucosal surface
and resulting in multiple tumors (papillomatosis or papillary carcino-
matosis) along varying segments of the bile ducts.122,174,200,210,218,219,261
The intraductal-growing type accounts for 8% to 18% of cholangio-
carcinomas.200 The majority of intraductal-growing cholangiocarcino-
mas are papillary adenocarcinomas,174,200,219,353 comprising innumerable
frondlike infoldings of the proliferated columnar epithelial cells and
slender fibrovascular cores.219 Infrequently an intraductal tumor may
be papillotubular or purely tubular. The bile ducts are dilated
1222 PART II CT and MR Imaging of the Whole Body

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.

secondary to incomplete obstruction by tumor, by sloughed tumor

FIG 42-78 Periductal-infiltrating intrahepatic cholangiocarcinoma.
Cancer has spread along the intrahepatic bile ducts (arrows).
debris, or by an excessive amount of mucin.174,219 The lobar or segmen-
tal bile ducts are dilated diffusely, somewhat reminiscent of bronchi-
ectasis in the lung, or aneurysmally, depending on bile duct obstruction
and the amount of mucin production.122
On imaging, the bile ducts of the involved hepatic segment or lobe
are dilated.122 An intraductal tumor can appear as a polypoid mass in
the lumen of the dilated bile ducts (Fig. 42-81). Frequently intraductal
tumors fill multiple segmental or subsegmental bile ducts. The mass is
confined within the bile ducts, leaving the wall of the bile duct intact.
The outer margin of the thickened bile duct wall is smooth and clear.
The tumor may not be seen on imaging when it is small and isoattenu-
ating to the adjacent hepatic parenchyma or when the complex orien-
tation of the dilated bile ducts obscures the presence of the mass. On
ERCP or percutaneous transhepatic cholangiography, the involved
biliary tree is dilated secondary to partial obstruction and there are
filling defects due to the papillary tumors. There may be fine irregulari-
ties, a velvety or serrated contour along the bile ducts, representing the
papillary surface of the tumor.174,219
1224 PART II CT and MR Imaging of the Whole Body

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.

Extrahepatic cholangiocarcinoma. Cholangiocarcinoma can

FIG 42-81 Intraductal-growing papillary neoplasm. CT shows an intra-
ductal polypoid mass (arrow) with bile duct dilatation.
develop in any part of the extrahepatic duct, with 50% to 75% of
reported cases occurring in the upper third of the duct, including the
hepatic hilum, 10% to 25% of cases occurring in the middle third of
the duct, and 10% to 20% of cases occurring in the lower third of the
duct.4,84 Approximately 95% of patients have extrahepatic bile duct
obstruction at the time of diagnosis.79 Involvement of the periductal
lymphatics, nerves, and perineural tissue is frequent.17 Infiltration to
the adjacent arteries and veins and lymph node metastasis are relatively
common.
Mass-forming or nodular type. The tumor forms a nodule that
is usually 1 to 2 cm in diameter210,217,218 (Fig. 42-82). The tumor
obstructs the bile duct lumen, penetrates the wall, and invades the
periductal tissue.340 The tumor mass is usually small at the time of
presentation because the bile ducts are occluded in the early stage of
the disease, and patients present with jaundice. Approximately 25%
of extrahepatic cholangiocarcinomas are of this type. A mass-forming
extrahepatic cholangiocarcinoma can be easily detected on imaging
because the tumor occludes the bile duct, resulting in dilated proximal
 CHAPTER 42 Biliary Tract and Gallbladder 1225

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
should be carefully scrutinized.
Periductal-infiltrating type. This type of tumor constitutes
more than 60% of extrahepatic cholangiocarcinomas. The tumor
appears as a focal or segmental concentric thickening of the extrahe-
patic ducts, with almost complete obstruction of the lumen.210,217,340
The thickened wall (measuring up to 1 cm) is firm and grayish white.340
The extent of the tumor varies, ranging from 0.5 to 6 cm in length; it
may involve all the extrahepatic ducts and extend proximally as far as
the IHDs.
On CT or MRI, the thickened bile ducts can be visualized as an
enhancing ring or spot (Fig. 42-83). It is often difficult to visualize the
lesion on CT or MRI because of the absence of distinct tumor forma-
tion; these imaging studies may show only focal or diffuse thickening
of the bile duct.13,210,217,218 At the site of bile duct obstruction, the tumor
border can be demonstrated as a symmetrically or asymmetrically
thickened bile duct wall, constituting a transition zone.298 On cholan-
giography or MR cholangiography, the involved segment may not be
opacified in cases of complete obstruction, or it may appear to be
stringlike when the lumen is not completely obstructed210 (Fig. 42-84).
Differentiation from acute or recurrent pyogenic cholangitis may
be problematic. The involved bile duct wall is thicker in cases of chol-
angiocarcinoma (usually >1 mm), whereas in cholangitis the bile duct
wall is thinner than 1 mm. Furthermore, the involved segment of the
bile duct is narrowed or obliterated in cholangiocarcinoma but normal
or dilated in cholangitis.
Intraductal-growing type. The intraductal tumor may be pol-
ypoid, sessile, or superficially spreading along the lumen.174,210,217,218
There may also be multiple discrete tumors (papillary cholangiocarci-
nomatosis) along the inner surface of the bile ducts. Usually the tumor
is limited to the mucosa and invades the wall and surrounding tissue
in the very late phase.210,217,218 An intraductal papillary cholangiocarci-
noma is friable and sloughs easily by touching or rubbing at the time
of surgery, or it may slough spontaneously and occlude the bile ducts,
simulating a bile duct stone214 (Fig. 42-85). The bile ducts are dilated
and incompletely obstructed by the tumor itself or by viscous mucin.
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Title: Les mains propres

Essai d'éducation sans dogme

Author: Michel Corday

Release date: August 25, 2023 [eBook #71487]

Language: French

Original publication: Paris: Ernest Flammarion, 1919

Credits: Laurent Vogel and the Online Distributed Proofreading Team

at https://www.pgdp.net (This book was produced from
images made available by the HathiTrust Digital Library.)

*** START OF THE PROJECT GUTENBERG EBOOK LES MAINS

PROPRES ***
 MICHEL CORDAY

Les mains propres

ESSAI D’ÉDUCATION SANS DOGME

PARIS
ERNEST FLAMMARION, ÉDITEUR
26, RUE RACINE, 26

Tous droits de traduction, d’adaptation et de reproduction réservés pour tous les

pays.
Il a été tiré, de cet ouvrage, quinze exemplaires sur papier de
Hollande, tous numérotés.

OUVRAGES DU MÊME AUTEUR

LIBRAIRIE E. FLAMMARION

Dans la même collection :

Vénus ou les Deux Risques.

Les Embrasés.
Sésame ou la Maternité consentie.
Les Frères Jolidan.
Les Demi-Fous.
La Mémoire du cœur.
Mariage de demain.
Les Révélées.
Les Convenus.
Monsieur, Madame et l’Auto.
Plaisirs d’auto.
Les Casseurs de bois.

EN PRÉPARATION :

Les Feux du Couchant.

Les Hauts Fourneaux.

E. GREVIN — IMPRIMERIE DE LAGNY

Droits de traduction et de reproduction réservés pour tous les pays.
Copyright 1919 by Ernest Flammarion.
 A
LA MÉMOIRE
DE
JEAN JAURÈS
 LES MAINS PROPRES

PRÉAMBULE
LE BUT ET LE PLAN

Cet essai s’adresse à ceux qui élèvent leurs enfants en dehors

des dogmes, dans un esprit de libre examen.
Quiconque a entrepris cette tâche en sait les difficultés. Dès
qu’on réfléchit avant d’agir, dès qu’on se demande pourquoi on agit,
dès qu’on ne fait plus une chose uniquement « parce qu’elle se fait »,
tout devient problème.
On a quitté la bonne vieille grande route, si commode, si facile, si
plane, et que le troupeau des générations a suivie. On a devant soi
l’espace en friche, où serpentent quelques pistes indécises, toutes
fraîches. Où est la bonne direction ? Ici, faut-il prendre à droite, à
gauche ? Parfois, on sent l’angoisse du doute. Mais il faut avancer.
Alors, on jette des vues, on s’oriente, on se décide. Et l’on marche,
en entraînant ses petits par la main.
Il faut que l’effort de chaque pionnier serve à ceux qui lui
succéderont. Il faut qu’ils puissent profiter de ses recherches, qu’ils
retrouvent les déterminations qu’il a prises, les directions qu’il a
suivies, l’empreinte de ses pas.
Cet ouvrage n’a pas d’autre but, ni d’autre plan. C’est un
ensemble de modestes solutions aux innombrables problèmes qui
se posent au long de la route. Ce n’est qu’une suite d’opinions. Et on
ne s’en étonnera pas. En effet, qu’est-ce qu’éduquer ? C’est
compléter, fortifier et redresser, par l’influence du milieu, les notions
confuses déposées dans le petit être par l’atavisme et l’hérédité. Or,
nous ne pouvons agir sur l’enfant que par notre exemple, nos
causeries, nos enseignements ; et nous ne faisons alors, en toutes
ces circonstances, qu’imprimer dans la jeune cervelle nos propres
opinions sur toutes choses…
La première partie de cet essai est précisément un exposé des
opinions générales dont nous souhaitons que les enfants soient
pénétrés, plus encore par les entretiens de leurs parents et
l’atmosphère du foyer que par la lecture des livres et les leçons des
maîtres.
La seconde partie est toute d’adaptation.
Quant au titre de cet ouvrage, il est emprunté à l’une de ces vues
morales qui se sont affranchies des anciens dogmes.
 PREMIÈRE PARTIE
OPINIONS

CHAPITRE PREMIER
LE BONHEUR

Quand on se lance, hors de la grande route, hors des chemins

battus, possède-t-on une indication générale sur la direction à
suivre ? La vie humaine a-t-elle une tendance ? Car cette tendance
devrait nous guider. Nous devrions marcher dans son sens.
Oh ! Il ne s’agit pas de rechercher le destin final de l’homme. A
ce sujet, disons-nous simplement que cette planète mourra comme
les autres. Il s’agit de savoir s’il existe une aspiration commune à
tous les êtres depuis qu’ils respirent sur la terre, un signe indicateur
de la vie. Hélas ! La plupart des humains ne se posent même pas la
question. Ils naissent, subsistent, meurent, sans avoir pris
conscience de ce qu’ils ont tenté de réaliser pendant leur vie.
Et pourtant, cette tendance existe. Voyez une rue fréquentée,
vers le soir. Tous les passants courent, se hâtent, se pressent. Or, si
les buts sont différents, le mobile est unique. Obéissant tout droit à
leur instinct débridé ou tenus en lisière par le devoir, cherchant l’utile
ou l’agréable, la hautaine volupté du sacrifice ou le bas plaisir,
regardant le ciel ou la terre, tous aspirent à réaliser leur désir, tous
vont vers leur satisfaction. Oui, tous, malgré des apparences
contraires, malgré de déconcertants détours, tous veulent leur
bonheur.
C’est l’instinct primordial de toute existence. On le surprend chez
le plus infime animalcule dans le champ du microscope. Il fuit la
peine et cherche la joie, c’est-à-dire qu’il fuit le milieu où il souffre et
cherche le milieu où il se plaît. En quoi il obéit bien à la loi de la vie :
car la joie est de la vie accrue, plus intense et plus ardente ; et la
douleur est de la vie diminuée, l’acheminement vers la mort.
Mais qu’est-ce donc que le bonheur ? Ce serait folie d’en donner
une définition applicable à tous les humains, puisque ce milliard et
demi d’êtres sont différents les uns des autres, puisqu’il n’y a pas
deux visages — ni sans doute deux cerveaux — identiquement
semblables. Il y a autant de bonheurs que d’individus.
Mais peu importe qu’on demande ces joies au pouvoir, aux
honneurs, à l’art, aux voyages, aux plaisirs de la table ou de l’amour,
à la conscience de la tâche accomplie, aux sereines recherches du
laboratoire, aux élans de l’altruisme, aux félicités du propriétaire, du
collectionneur, à de modestes travaux manuels, même aux émotions
de la chasse ou de la pêche. Tous ces bonheurs ont des traits
communs. Ils donnent à l’être sa satisfaction, le sens de la plénitude.
Ils portent la vie à sa plus haute tension.
Il existe dans la nature un exemple de cette tendance continuelle
à s’accroître. C’est le végétal. Une plante, une vie humaine
s’efforcent toutes deux d’atteindre leur exubérance totale. Elles
s’élèvent, l’une vers la lumière, l’autre vers le bonheur.
Au surplus, la croissance de l’esprit est toute pareille à celle de la
plante, qui d’abord cherche sa subsistance de toutes parts,
aveuglément, par ses mille racines, dans l’obscurité de la terre, puis,
s’élançant au jour, se nourrit d’éléments plus subtils, obéit à ses
affinités et enfin s’exprime et s’épanouit dans les contours précis de
ses verdures fleuries.
 Si toutes les manifestations d’une existence, actes et pensées,
pouvaient prendre une forme sensible, s’inscrire dans l’espace
comme autant de feuilles et de fleurs, l’ensemble d’une vie complète
apparaîtrait comme un bel arbre, harmonieux, touffu, luxuriant,
étendant ses branches en tous sens, dans un frémissant désir de
s’accroître encore.
Un beau rosier est l’image du bonheur.
Et, de même qu’il y a des végétaux de toutes tailles, du chêne au
brin d’herbe, mais qui tous ont ce caractère commun de remplir leur
ligne, de tendre vers leur complet développement, de même il y a
des vies de toutes envergures, les unes très modestes, les autres
magnifiques, mais qui toutes peuvent être également heureuses,
atteindre leur plein épanouissement. Ce n’est pas une question de
dimension, c’est une question de densité, de plénitude. Une destinée
heureuse, c’est une destinée remplie.
Enfin, de ce point de vue, le but de l’éducation apparaît. Éduquer,
c’est cultiver. C’est favoriser l’expansion de la plante humaine. C’est
la redresser, l’abreuver, l’émonder, la bien exposer, de façon qu’elle
soit forte, saine, qu’elle donne toutes les qualités de l’espèce, qu’elle
atteigne sa plus haute puissance.

Devant la morale du bonheur, une objection se dresse aussitôt.

Mais, dira-t-on, si chacun poursuit son bonheur, uniquement son
bonheur, chacun blessera son voisin, dans cette poursuite. Aussi
faut-il en tracer immédiatement les bornes. Oh ! elles sont indiquées
dans toutes les morales, par la simple loi : « Tu ne nuiras pas. » Il
faut s’arrêter au moment de nuire. Notre bonheur a pour limites le
bonheur du voisin.
Pour reprendre l’analogie avec le monde végétal, un groupe
humain ne doit plus être l’inculte forêt où les arbres s’étouffent
mutuellement. Une société civilisée doit être un jardin, cultivé avec
intelligence, où chaque plante, pour donner toutes ses fleurs et tous
ses fruits, arrête ses frondaisons aux frondaisons voisines.
 Ainsi la plante reste d’un exemple total : monter bien droit, dans
la clarté, s’accroître, s’épanouir, s’orner de fleurs, se répandre en
parfums, donner des fruits, et ne borner son expansion qu’à
l’expansion des autres.
D’ailleurs — et ceci est capital — cette limitation elle-même
apparaît de notre intérêt. Les preuves en abondent.
Il est bien certain que si chacun s’efforçait d’observer cette loi
restrictive, tant de heurts, de drames, de souffrances seraient évités,
que l’état général de l’humanité serait meilleur. Le monde serait plus
agréable à habiter. La vie d’un village est symbolique à cet égard.
Là, par une lente sagesse, tous les habitants sont parvenus à
respecter la terre du voisin. Leur bien se borne au bien d’autrui. Ne
sont-ils pas plus heureux que s’ils dépassaient les limites de leur
propre domaine et débordaient sans cesse sur les domaines
adjacents ? Que de querelles, de luttes, de haines abolies ! Ce serait
la guerre. C’est la paix.
Il y a aussi un fait d’expérience qui, dans l’intérêt de notre propre
bonheur, doit nous détourner de nuire. C’est que, le plus souvent,
tout acte nuisible retombe sur son auteur. La loi d’équilibre, ou de
compensation, joue. Cet acte nuisible fait boomerang. On croit le
projeter contre autrui. Il revient à son point de départ. Le bonheur
conquis sur le voisin n’est plus du bonheur. On l’a payé trop cher. On
lui garde rigueur des remords qu’il éveille. Au fond, nous souffrons
plus du mal que nous faisons que du mal qu’on nous fait.
Enfin, la notion relativement récente, pour ainsi dire scientifique,
de la solidarité, vient encore confirmer qu’il est de notre intérêt de ne
pas nuire. En lésant autrui, nous ne sommes jamais sûrs de ne pas
nous léser nous-mêmes, précisément parce que toutes les cellules
sociales sont dépendantes, solidaires. Quand un point de
l’organisme s’enflamme, tout l’organisme a la fièvre. Tout ce qui nuit
à la collectivité nuit à l’individu. Celui qui, au mépris de la prudence
ou de l’hygiène, jette quelque virus dans la circulation, est-il jamais
sûr que le mal, cheminant à travers le monde, ne viendra pas
frapper l’un des siens ?
 Ainsi, le souci bien compris de notre bonheur même, nous
amène à le borner. Et ceux-là se trompent qui accusent la morale du
bonheur de n’avoir ni sanctions ni freins. Elle les trouve en elle-
même.

Au surplus, la compréhension, le soin de notre propre bonheur,

ne nous détournent pas seulement de nuire, de faire le mal. Ils nous
incitent aussi à faire le bien, car ces lois d’équilibre et de réciprocité
jouent pour le bien comme pour le mal. Faire du bien à autrui, c’est
en faire à soi-même. On fait des heureux pour être heureux. On
reçoit en reflet le bonheur que l’on donne.

Oui, entre la morale religieuse, froide, tranchante, nue, austère,

et la sauvage morale de la force, la morale du browning, il y a place
pour une morale souriante, épanouie, rayonnante, la morale de la
fleur.

Il ne faut point cependant opposer la morale du bonheur aux

morales religieuses. Leur antagonisme est plus apparent que réel. Il
est dans les mots. Qui n’applique en fait la morale du bonheur ?
Il faut, au contraire, considérer cette morale humaine comme le
prolongement des morales divines. Celles-ci tenaient l’homme en
lisière. Elles guidaient ses pas. Elles le jugeaient incapable encore
de marcher seul. Ainsi, la morale chrétienne le maintenait dans le
droit chemin par la crainte de l’enfer et l’espoir du paradis.
La morale du bonheur marque un progrès. Elle correspond à un
état nouveau de civilisation. Elle estime que la créature peut enfin
s’affranchir de tutelle, qu’elle est adulte, qu’elle peut avancer sans
aide, que sa conscience avertie peut éclairer sa conduite.

Les connaissances humaines se présentent comme un tronc

dont trois rameaux ont jailli : art, science, morale. Le premier, l’art, a
donné son élan et ne progresse plus guère ; le deuxième, celui de la
science, vient de se développer prodigieusement ; le troisième, celui
de la morale, végète. Faut-il désespérer qu’il rattrape les deux
autres ?

Il faudrait embellir la vie, la fleurir. N’est-ce pas la tendance

générale des progrès humains ? En effet, quels étaient les instincts
primitifs de l’homme ? Se nourrir, se reposer, se reproduire. Voyez
comme nous avons peu à peu paré, enjolivé ces trois instincts
grossiers ! Du besoin de se nourrir, nous avons fait le délicat plaisir
de la table. Du besoin de se reposer, la volupté du lit. Et le besoin de
se reproduire est devenu l’amour…
Il y a tant à faire, pour embellir la vie, pour l’égayer. Qu’y a-t-il de
plus triste qu’une fête foraine ? Ces musées d’horreur, ces jeux de
massacre, ces manèges bruyants et laids. Ne pourrait-on pas, peu à
peu, couler à des divertissements plus jolis, sans s’écarter du goût
de la foule ? On ne dira jamais assez la tristesse des monuments
publics. Et les magasins ? Pourquoi ne sont-ils pas généralement
plus plaisants aux yeux ? Pourquoi la rôtisserie, la poissonnerie, la
boucherie, ne sont-elles pas toujours décorées de céramiques, de
marbres ? Pourquoi ne pas rechercher un décor qui soit plus joyeux
sans être plus coûteux ? Les tentatives qu’on a faites en ce sens ont
presque choqué. Il semble qu’il y ait quelque chose de sacrilège à
mettre de la grâce, de la beauté, dans le détail de la vie.

Une humanité travaillant pour le bonheur tendrait à encourager

par les plus belles récompenses tous ceux qui collaborent à ce
bonheur, l’artiste, l’inventeur… Et ce ne sont pas les grands héros.

Mettons dans notre vie de la grâce, de l’élégance, de la bonté, de

la poésie, des enthousiasmes, du plaisir. En un mot, cherchons à
l’accroître, à la fleurir, à la faire la plus opulente, la plus luxuriante.
 Ayons aussi des raisons, des buts de vivre. Sans quoi, nous
descendons à la conception la plus misérable, la plus primitive de la
vie, un état inconscient où l’être ne cherche qu’à subsister au jour le
jour.

Candide disait : « Cultivons notre jardin ».

Oui. Représentons-nous chaque existence comme un jardin. Et
voyez, à surface égale, combien les jardins sont différents. L’un est
la brousse, l’autre le paradis. Tout dépend des soins qu’on y donne.

Nous ne pouvons pas prétendre au bonheur absolu, mais nous

devons chercher à l’atteindre par le plus grand nombre de points
possible.
Notre bonheur est enclos dans notre vie, comme la statue dans
le bloc de marbre. C’est à nous de le dégager. Les sculpteurs
praticiens procèdent comme si la statue existait déjà dans sa
gangue de pierre. Ils l’atteignent par des sondages nombreux, qui
s’arrêtent juste à la surface de la future image. Ils la touchent par
points. Nous devons être les praticiens de notre bonheur.

Il faut saisir les beaux instants, c’est-à-dire ceux où l’on est

heureux sans nuire. Et il faut aussi les proclamer, en soi, autour de
soi. On dit plus volontiers : « Quel sale temps ! » que : « Le beau
temps… » Il faut que nos propos soient à l’image de la vie, qui roule
le bon et le mauvais. Ne serait-ce que pour régler notre pensée sur
nos paroles et nous pénétrer de ce sens de l’équilibre.
Il y a d’ailleurs un bonheur dont nous ne prenons pas assez
conscience : l’absence de malheur. Par exemple, que de justes
petites voluptés on se procure à se rendre compte qu’on ne souffre
plus de maux familiers dont on a pâti. Nous n’en jouissons pas.
Nous ne nous disons pas assez : « Quelle chance de ne pas avoir
mal à la tête, mal aux dents ! »
 Au fond, tous nos actes tendent vers l’utile ou l’agréable. Cette
formule en deux mots enferme notre vie. C’est un vase qui la
contient. A nous d’en faire une belle amphore, de l’élargir vers le
haut, d’y mettre toutes les belles fleurs de l’élégance, de l’art, de
l’altruisme.

L’aspect d’une roseraie publique, comme celle de Bagatelle, un

dimanche, où la foule lente, recueillie, discrète, se promène sous les
arceaux de fleurs, apparaît une anticipation, une vision de demain.
 CHAPITRE II
LE TEMPS

La foi dans l’avenir. — La connaissance de l’avenir. — Le présent vaut le passé.

— L’héritage du passé.

Foi dans l’avenir.

Nous aussi, nous croyons à une vie meilleure, à une vie future.
Mais nous ne la garantissons pas dans cet au-delà de la mort que
nul encore n’a sondé d’un regard certain. Notre vie meilleure, c’est
celle de nos descendants. Notre vie meilleure, c’est l’Avenir. Elle
n’est pas dans le ciel. Elle est sur la terre. C’est la vie que nous
forgeons pour ceux qui nous succéderont. Nous y croyons parce que
nous y travaillons, parce qu’elle est le prolongement de notre vie.
Voilà l’acte de foi qui doit nous soutenir au cours de notre existence.
Cette vie meilleure, nous ne l’attendons pas dans la résignation,
sous le joug des dogmes. Nous la préparons, nous apportons notre
humble pierre à l’édifice, dans le courage et l’allégresse.

Devant les vagues monstrueuses, stupides et magnifiques qui se

jettent et se brisent contre la jetée, je pense que les hommes ont
dompté les forces extérieures de la nature et qu’ils n’ont pas encore
dompté les forces intérieures, c’est-à-dire celles qui sont en eux : la
colère, la haine, la méchanceté, celles qui les poussent à nuire, à
tuer… Ils ont asservi les flots, les vents, la foudre ; ils n’ont point
encore refréné leurs instincts barbares.
 Mais qui donc aurait osé prédire aux premiers hommes ces
victoires sur la nature déchaînée ? Et qui peut assurer que les
hommes futurs ne couronneront pas cette victoire, en l’achevant sur
eux-mêmes ?

Dans les grandes maladies qui frôlent la mort, les êtres se

montrent souvent si beaux, si grands, si délicats, si exquis, si
touchants, qu’ils dévoilent une humanité supérieure.
Ils montrent ce qu’ils auraient pu être, ce qu’ils auraient été s’ils
avaient pu se libérer de toutes les entraves qui les retenaient de
montrer le meilleur d’eux-mêmes.
On dirait qu’au seuil de la mort ils voient l’avenir des hommes et
déjà le réalisent.

J’entends des gens dire que nous avons la même mentalité que
l’homme des cavernes, que la morale n’a pas fait de progrès,
parallèlement à la science et sous son influence.
Est-ce bien sûr ? Et surtout s’est-il écoulé assez de temps pour
que ces progrès nous soient sensibles ? Les phénomènes
d’évolution, ceux qui ont sculpté la surface de la terre, ceux qui ont
peu à peu réalisé l’être humain, sont tellement lents, exigent tant de
milliers d’années !
Les notions acquises depuis quelques siècles seulement
modifient peut-être l’esprit de l’homme. Mais l’empreinte n’est pas
encore assez profonde pour que nous discernions ce relief nouveau.
Prenez en exemple la conception de l’infini, la conception qu’il y
a des astres derrière les astres, qu’il n’y a pas de limites à l’espace.
Elle est récente, puisque les anciens voyaient un univers borné,
voûté. Elle est fille de l’astronomie moderne. Or, cette notion de
l’infini, de notre terre perdue comme un grain de boue, comme une
cellule isolée d’un organisme immense, cette notion n’est-elle pas
pour nous montrer la petitesse, la vanité de nos querelles, de nos
luttes, et par conséquent pour améliorer peu à peu la morale ? Ne