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384 J. Silberzweig
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A,B
FIGURE 31-14. Inferior vena cava
stenosis following liver transplantation. (A).
Marked focal stenosis at the upper inferior
arrow
vena cava anastomosis (
stenosis was treated with percutaneous
balloon angioplasty.
). (B). The
or surgical anastomotic revision. Most nonanastomotic
strictures are due to bile duct ischemia. Percutaneous
stents and dilation can be used in the management of
nonanastomotic strictures that develop within 3 months
after transplantation in the absence of pretransplantation
primary sclerosing cholangitis, ductopenic rejection,
cytomegalovirus infection, or hepatic artery thrombo-
63–65
sis.
Nonanastomotic biliary leaks that are not at the T-tube
site are associated with hepatic artery thrombosis in 89%
of cases.
66
These leaks are usually hilar or intrahepatic.
Bile leaks can be treated with percutaneous biliary decompression and drainage. If hepatic artery thrombosis
is present, the outcome is poor despite drainage. In some
liver-transplant recipients, biloma drainage can prevent
the need for retransplantation or prolong graft survival
until a donor liver becomes available.
Acute transplant rejection
Acute transplant rejection cannot be reliably detected by
radiologic methods. Biopsy of the graft with histologic
examination remains the standard for detecting hepatic
graft rejection.
50
nancy. The estimated prevalence of malignancy in OLT
patients is increased 100-fold compared with that of agematched populations. Most of these malignancies are
non-Hodgkin’s lymphoma or squamous cell skin can-
67
cer.
■ Spleen
The spleen contributesto theremoval ofcellular elements
from the circulating blood. Abnormal and aged er ythrocytes, abnormal granulocytes, normal and abnormal
platelets, and cellular debris are cleared by the spleen. The
spleen also has an immunologic function. Patients who
have had a splenectomy are at increased risk for overwhelming bacterial infection.
68,69
Pathologic conditions that may be evaluated and
treated with splenic arteriography and embolization include splenic trauma, splenic artery aneur ysms, and hypersplenism. Splenic artery embolization may be performed before elective open or laparoscopic splenectomy
to minimize operative blood loss.
Posttransplant malignancy
Transplant recipients undergoing immunosuppressive
therapy are at increased risk of developing malig-
Trauma
The spleen is the most frequently injured abdominal
organ in patients with blunt abdominal trauma.
70
Splenic
Liver and Spleen 385
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injury may manifest immediately after trauma or become
apparent several days or weeks later. Conventional operative treatment of splenic injury consists of splenectomy.
Partial splenectomy and splenorrhaphy have been successful in preserving splenic tissue and function.
71
Nonoperative management of blunt splenic trauma that includes observation and bed rest has been used as an
alternative to laparotomy. The rationale for this treatment method is that many splenic injuries are not actively
bleeding at the time of laparotomy; however, a failure of
nonoperative management carries the risk of hemodynamic instability necessitating blood transfusion and urgent laparotomy. Reports demonstrated a 31 to 48% failure rate of nonoperative management.
72,73
The aggressive use of arteriography and splenic artery
embolization in cases of splenic injury has improved significantly the rate of splenic salvage with nonoperative
management.
74,75
In most trauma centers, abdominal CT
is used for the initial identification of splenic injury in
hemodynamically stable patients. CT also is used for follow-up evaluation of splenic injury in patients who undergo nonoperative management. Findings indicative of
splenic injury by CT include intraparenchymal hematomas, subcapsular hematomas, an irregular splenic outline, and hemoperitoneum. Indications for splenic arteriography vary by trauma center. At some trauma centers,
arteriography is performed in all cases of splenic injury
identified by CT, whereas at other centers arteriography
is performed only in cases in which there is the presence
of an intraparenchymal contrast collection hyperdense
with respect to the surrounding parenchyma.
The angiographic findings in splenic trauma may be
subtle and vary with the severity of injury. Splenic arteriography often may show a mottled parenchymal blush,
which should not be confused with contusion or laceration. Cases of extremely fine punctate extravasations (Seu-
rat spleen) do not represent a significant sign of bleeding
and therefore do not require embolization.
74
The presence of splenic hematomas may result in an
inhomogeneous parenchymal phase with splaying of
smaller splenic artery branches. Overall spleen size may
appear normal or enlarged. Extravasations resulting
from splenic injury often are coarse, irregular, blotchy
swirls of contrast material that may not appear to originate from a specific arterial branch. This finding has
been called the “starry night” appearance and may involve a portion of or the entire spleen (Fig. 31-15). This
appearance has been attributed to pooling and leaking of
blood from the fragmented sinusoids.
76
Other angiographic findings include well-defined arterial pseudoaneurysms, arterial extravasation, arterial or venous branch
occlusion, and arteriovenous shunting (Fig. 31-16).
A B
FIGURE 31-15. Splenic trauma. (A). Abdominal computed to-
mography image shows splenic injury (
vehicle accident. (B). Splenic arteriogram shows a “starry night”
pattern. (C) Coil embolization of the splenic artery was performed. (Courtesy of S. Sclafani)
arrow
) following a motor-
C
386 J. Silberzweig
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A B
FIGURE 31-16. Splenic injury with arteriovenous shunting. This patient was involved in a motor-vehicle accident 6 months
before the arteriogram was taken. (A) Arterial phase shows the splenic injury with arteriovenous shunting. P, portal vein. The
massive shunting resulted in portal hypertension. (B). Venous phase of the splenic arterial injection shows opacification of
esophageal varices (
arrow
).
Discrete pseudoaneurysms arising from intrasplenic or
other smaller branches can be treated with selective coil
embolization. An alternative to selective splenic artery
branch embolization is main splenic artery embolization.
If extravasation of contrast material is seen within or
extended beyond the spleen, the proximal splenic artery
just distal to the dorsal pancreatic artery is occluded with
coils. Embolization is performed in the proximal splenic
artery between the origin of the dorsal pancreatic branch
and the next most distal pancreatic branch. Several coils
can be packed into the splenic artery to accelerate occlusion. Occlusion of the splenic artery with coils lowers the
distal perfusion pressure without causing ischemia and
tissue infarction.
Splenic artery aneurysms
Although visceral artery aneurysms are rare, nearly half
of all visceral artery aneur ysms occur in the splenic artery. The incidence of splenic artery aneurysms is less
than 1 in 1000 in the general population. Splenic artery
aneurysms occur twice as frequently in women as in men.
Most splenic artery aneur ysms are present in the main
trunk of the splenic artery (Fig. 31-17). Splenic arter y
aneurysms frequently are multiple. The etiology of
splenic artery aneurysms is medial degeneration with
superimposed atherosclerosis. Predisposing conditions
include atherosclerosis, pregnancy, and portal hyperten-
77,78
sion.
splenic artery aneurysm are usually absent, but patients
may present with pain in the left upper quadrant. Calcifi-
Specific symptoms related to the presence of a
cation in the aneurysm wall is reported in as many as two
thirds of patients. Causes of pseudoaneurysms of the
splenic artery include pancreatitis (Fig. 31-18), infection,
surgery, and trauma.
Splenic artery aneurysms may rupture, embolize, or
thrombose. The most frequent complication is aneurysm
rupture, which occursin about10% ofpatients.
77–79
There
is an increased risk of splenic artery aneurysm rupture in
pregnant women or women of childbearing age.
79
Calcified aneurysms also rupture, although less frequently.
Splenic artery aneurysms typically rupture into the peritoneal cavity or rarely into the gastrointestinal tract, spleen,
or pancreas.
80
Because of the high mortality from rupture, all symptomatic splenic arter y aneurysms should be resected.
Asymptomatic aneurysms exceeding 2.5 cm in diameter
should be treated.
81
The conventional treatment has
been surgical ligation or excision of the aneursym with or
without splenectomy. Patients at increased surgical risk
can be treated with percutaneous transarterial emboliza-
82,83
tion.
If the aneurysm arises from the main splenic
artery, the “sandwich” embolization technique is used. A
nest of embolization coils is placed distal and proximal to
the aneur ysm with the purpose of excluding it from the
circulation.
Hypersplenism
Hypersplenism refers to overactivity of splenic function
leading to accelerated removal of any or all of the circulating cellular elements of the blood. Typical features of
Liver and Spleen 387
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A B
FIGURE 31-17. Splenic artery aneurysm. (A). Abdominal computed to-
arrow
mogram shows a large aneurysm (
mural thrombus. (B). Arteriography. (C). Coil embolization of the splenic
artery proximal and distal to the aneurysm was performed. (Courtesy of
B. Kanner)
hypersplenism include splenomegaly, anemia, leukope-
84
nia, and thrombocytopenia.
Surgical splenectomy is the
traditional therapy for hypersplenism; however, partial
splenic embolization is an accepted alternative to surgical
splenectomy.
85
Several diseases have been treated by partial splenic
embolization as an alternative to splenectomy. Partial
splenic embolization has been useful in the treatment of
hypersplenism related to idiopathic thrombocytopenic
purpura, portal hypertension, and thalassemia. Partial
splenic embolization has been used for the treatment of
hypersplenism in children.
84
Embolization is performed with the catheter positioned in the distal splenic artery beyond the pancreatic
and gastric branches. Gelfoam pledgets or polyvinyl alcohol particles may be used. The goal is to reduce splenic
) of the splenic artery containing
perfusion by 70 to 80%. The procedure often is performed in a staged manner over several weeks to reduce
the risk of complication from excessive infarction of
splenic tissue. Patients are given broad-spectrum antibiotics before the procedure. Postembolization pain, fever,
and leukocytosis are expected to be present for several
days after the procedure. The spleen shrinks markedly
over 3 to 4 months after the embolization procedure,
with improvement in platelet and leukocyte count. The
results of partial splenic embolization are long lasting in
most patients. Repeat embolization may be necessary if
less than 50% of the splenic volume is embolized initially.
Complications of partial splenic artery embolization
include splenic rupture, pancreatitis, pneumonia,
splenic abscess formation, and overwhelming sepsis.
These major complications can occur with excessive
C
388 J. Silberzweig
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A B
C
splenic devascularization. Inadvertent nontarget embolization to the liver, stomach, or pancreas can occur. Transient respiratory complications, such as pleural effusion
and atelectasis, commonly occur and are related to the
extent of embolization and the size of the spleen.
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J.J. TrambertTheBiliary Tree and Pancreas
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32
■■■
The Biliary Tree and Pancreas
JONATHAN J. TRAMBERT
Radiological evaluation and percutaneous transcatheter
intervention in the pancreas and biliary tree constitute a
substantial subset of gastrointestinal radiology and intervention. The anatomic proximity of the pancreas and
biliary tree and the fact that disease in one area often has
a profound effect on the other make it logical to consider
both in the same chapter.
■ Biliary Tree
Percutaneous radiological evaluation and intervention
are usually sought in a patient with suspected obstructive
jaundice. Before percutaneous procedures are undertaken in the bile duct, as much information as possible
should be obtained from the clinical history and physical
examination. Noninvasive studies should be obtained to
confirm the presence of an obstruction and to evaluate
for any related findings that could significantly affect the
safety and feasibility of the percutaneous intervention.
Workup
The clinical background can yield much useful information. For example, the onset of jaundice associated with
pain usually is due to an acute mechanical obstruction
such as acute choledocholithiasis or acute pancreatitis.
Painless jaundice usually is associated with malignant obstruction.
Imaging studies
If obstructive jaundice is clinically suspected, ultrasound
should be one of the initial imaging studies. It is nonin-
vasive, it is excellent for detecting bile duct distentsion
(Fig. 32-1), and it can yield information about the state
of the liver parenchyma. At times, in addition to the
intrahepatic bile ducts, the pancreas and distal bile ducts
can be evaluated. Ultrasound also can yield information
about the presence of ascites, which is extremely relevant
when planning percutaneous interventions, as will be
discussed later.
Computerized tomography (CT) is also valuable, especially if it is performed with intravenous contrast (Fig.
32-2). Although slightly less sensitive to intrahepatic bile
duct dilation than ultrasound, CT yields additional important information that is often difficult to obtain with ultrasound (e.g., the cause of distal bile duct obstruction, the
presence of liver metastases or primary tumors elsewhere
in the body that may be metastatic to the liver). CT is also
less operator dependent than ultrasound, although it is
more expensive andthe use of intravenous contrastmakes
it slightly more invasive.
Cholescintigraphy with hepatic 2,6-dimethyliminodeacetic acid (HIDA) and related agents is sometimes useful for assessing biliary tract functional status. A mechanical obstruction usually is associated with the absence of
radionuclide activity in the bowel even on delayed images.
Magnetic resonance (MR) imaging and MR cholangiography hold promise for the noninvasive evaluation of the
biliary tree. With MR cholangiography, computer manipulation and reconstruction of stacked cross-sectional images can yield three-dimensional maximum intensity projection (MIP) reconstructions, which can be rotated in
different directions to provide views of the bile ducts from
different angles. Various MR techniques are available for
391
392 J. J. Trambert
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FIGURE 32-1. Ultrasound of the liver demonstrating dilated
intrahepatic ducts (
curved arrow
(
peripancreatic lymph nodes (
open white arrows
(
solid white arrows
) resulting from metastatic gastric carcinoma to
white arrowheads
) lies posterior to the common hepatic duct.
) and extrahepatic duct
). Portal vein
A
suppressing surrounding tissues and enhancing the cholangiographic quality of the acquired image.
1
Contrast cholangiography can be performed either by
direct retrograde catheterization of the bile ducts through
an endoscope (endoscopic retrograde cholangiography
or ERC) (Fig. 32-3) or by percutaneous transhepatic cholangiogram (PTC)using a skinny needle (21or 22 gauge).
The endoscopic approach has the advantage of studying
the biliary tract without some of the risks associated with
the percutaneous transhepatic needle route. It also affords the possibility of studying the pancreatic duct as well
as the common bile duct (endoscopic retrograde cholangiopancreatography, or ERCP). In addition, if desired,
definitive therapy for a biliary stricture may be instituted
in the form of transendoscopic papillotomy or placement
of an internal stent.
ERCP does have potential complications, including a
1% incidence of pancreatitis and 0.8% incidence of septic cholangitis in experienced hands. The rate of complications is approximately four times higher in less experienced hands.
2
ERCP is technically infeasible in certain situations, such
as previous Roux-en-Y hepaticojejunostomies and high
proximal biliary strictures refractory to contrast opacification of the peripheral intrahepatic bile ducts. In such
situations as well as in centers that do not have skilled
endoscopists, contrast cholangiography can be obtained
FIGURE 32-2. Computed tomography (CT) with intravenous
contrast in a patient with gallbladder carcinoma and biliary
obstruction. A: Dilated intrahepatic ducts are seen as circular
and tubular hypodense structures. B: Thickened irregular gallbladder wall
(arrows)
is seen in a more caudal image.
only through the percutaneous transhepatic route. In
percutaneous transhepatic cholangiography, a 21- or 22gauge needle is passed through an anesthetized area on
the overlying skin, through the liver parenchyma, to a
biliary radicle, allowing direct contrast opacification of
the bile duct.
Specific cholangiographic findings
Contrast cholangiography yields definitive information
about the morphology and location of the stricture or
obstruction. The morphology of the stricture can often
give an indication as to its etiology (Fig. 32-4). The location of the stricture provides additional clues to its etiology (Table 32-1).
3
Stricture etiology
Nonmalignant etiologies
Nonmalignant etiologies of bile duct strictures, or “benign” bile duct strictures, include postoperative strictures,
B
FIGURE 32-3. Endoscopic retrograde cholangiopancreato-
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graphy (ERCP) showing proximal common hepatic duct stricture
(arrowhead)
ing cholecystectomy (see also Fig. 32-14).
that resulted from inadvertent duct injury dur-
calculi, inflammatory strictures related to chronic cholecystitis (Mirizzi syndrome), chronic pancreatitis, and sclerosing cholangitis. Postoperative strictures can occur at
the site of previous duct injury or repair (see Fig. 32-3) or
at a site unassociated with the previous duct anastomosis.
Strictures that occur after duct transsection and reanastomosis are often due to scar formation at the anastomosis
site. Stricturesthat occur somewhat remote to the original
site of ductal manipulation are presumed to be ischemic
in etiology, perhaps related to pressure injury or thermal
injury.
Purely inflammatory strictures of the common hepatic
duct (CHD) or common bile duct (CBD) are usually the
result of chronic cholecystitis or chronic pancreatitis. In
chronic cholecystitis, inflammation of the gallbladder
and cystic duct can cause them to thicken to the extent
that they extrinsically compress and obstruct the adjacent
CHD or CBD (Mirizzi syndrome) (Fig. 32-5). Chronic
pancreatitis also can result in more distal extrinsic narrowing or stricturing of the CBD (Fig. 32-6).
Sclerosing cholangitis is a disease of unknown etiology
The Biliary Tree and Pancreas 393
characterized by diffuse periductal fibrosis. Intrahepatic
or extrahepatic ducts or both can be involved. The incidence of ulcerative colitis and Crohn’s disease is increased in patients with sclerosing cholangitis, although
the exact relationship between inflammatory bowel disease and sclerosing cholangitis is unknown. The typical
cholangiographic finding in sclerosing cholangitis is diffuse multifocal strictures of the intrahepatic or extrahepatic bile ducts, which gives them a “beaded” appearance. Diffuse intrahepatic and extrahepatic bile duct
disease, identical cholangiographically to sclerosing cholangitis, can be seen after liver transplantation as a result
of transplant ischemia and in patients with the acquired
immunodeficiency syndrome (AIDS). Diffuse cholangiocarcinoma and diffuse liver metastases encasing the bile
ducts are sometimes cholangiographically indistinguishable from sclerosing cholangitis (Fig. 32-7) (see the discussion of malignant biliary strictures following).
Malignant etiologies
Malignant bile duct strictures comprise both primary
hepatobiliary tract neoplasms and extrinsic bile duct involvement by metastatic lesions (Table 32-1). Primary
hepatobiliary tumors include bile duct epithelial adenocarcinomas (referred to as cholangiocarcinoma when they
involve the intrahepatic or most proximal extrahepatic
ducts) and hepatocellular carcinoma (hepatoma). Cholangiocarcinoma frequently involves the confluence of
the right and left hepatic ducts and proximal common
hepatic duct (Fig. 32-8). Pancreatic carcinoma displays
the prototypical appearance of extrinsic malignant duct
encasement, often with a “rat tail”-like luminal termination (Fig. 32-9). Metastatic disease to extrahepatic periductal lymph nodes can produce abrupt obstruction or
irregular encasement of the CHD or CBD (Figs. 32-10
and 32-11).
Unfortunately, much overlap may exist between the
cholangiographic appearance of benign and malignant
strictures. Sclerosing cholangitis can be mimicked by
diffuse liver metastases and cholangiocarcinoma. Postoperative or inflammatory strictures or obstructions occasionally are indistinguishable from those of malignant
etiology. The clinical and surgical history might be helpful in differentiating malignant from nonmalignant
causes. A brush biopsy by endoscope or percutaneous
transhepatic tract can be used to help make a diagnosis,
as can percutaneous needle biopsy of periductal tissue
using a previously placed biliary stent for fluoroscopic
guidance to the lesion. Occasionally, the definitive diagnosis is not known until surgery.
Biliary tract intervention
The best possible therapeutic option for a patient with
obstructive jaundice is a surgical resection of the offen-
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