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J.SilberzweigLiver and Spleen
https://t.me/med1917
31
■■■
Liver and Spleen
JAMES E. SILBERZWEIG
The use of angiography and venography for the diagnosis
and staging of liver and splenic lesions has been nearly
eliminated in recent years as a result of the advent of
sonography, computed tomography (CT), and magnetic
resonance imaging (MRI); however, interventional radiology procedures are being used more frequently for the
treatment of these disorders. Advances in catheter, guidewire, stent, and embolization technology resulted in the
development of innovative percutaneous procedures for
the management of tumors, trauma, and portal hypertension.
■ Liver
Liver tumors
The two most frequent types of primary malignant liver
tumors are hepatocellular carcinoma and cholangiocarcinoma. Metastases are the most common malignant neoplasms affecting the liver. Most patients with multiple
liver metastases are not candidates for surgical resection
and have a poor prognosis. Patients with metastases from
neuroendocrine tumors have a better prognosis but may
experience severe symptoms related to excessive hormone production.
Hepatocellular carcinoma
Hepatocellular carcinoma (HCC, or hepatoma) is the
most common primary liver malignancy, with most cases
occurring in Asia and southern Africa.
million patients die of HCC per year worldwide. The
prognosis of HCC without treatment is poor, with a me-
1
More than one
dian survival of 1.6 months reported in the Asian popula-
2
tion.
The development of HCC is associated with a history of hepatitis B or hepatitis C infection and cirrhosis.
Seventy-five percent of hepatomas occur in cirrhotic livers. Ninety percent of patients with hepatomas are hepatitis B or C virus antigen carriers.
Frequently, HCC is discovered as an incidental finding
in patients with cirrhosis and portal hypertension. Symptoms include hepatomegaly, abdominal pain, fever, weight
loss, ascites, and jaundice. HCC produces alpha-fetoprotein, which is elevated in the serum of about 70% of pa-
3
tients.
as well as a measure of response to therapy.
modalities for the screening, diagnosis, and staging of
HCC.
giographic features that may be found in HCC include
enlarged feeding arteries, neovascularity, irregular tumor
stain, arteriovenous (AV) shunting, and portal vein invasion (Fig. 31-1). Hepatic vein invasion may be identified
during the parenchymal phase of a hepatic arteriogram
or an inferior venacavogram. The arteriographic findings
of hypervascular metastases or hemangiomas may appear
similar on arteriography. Therefore, arteriography frequently lacks specificity for the diagnosis of HCC.
ing may be the first clinical sign of HCC. HCC may invade
the portal venous system and lead to portal hypertension.
During angiography, invasion of the portal vein by HCC
may be identified as a filling defect within the portal vein
or thrombosis of the portal vein (Fig. 31-2). The tumor
thrombus may contain vascular “threads and streaks.”
The portal vein normally is not opacified on hepatic artery
Alpha-fetoprotein level can be used for diagnosis
Sonography, CT, and MRI are commonly used imaging
4
HCC may be solitary, multicentric, or diffuse. An-
Portal hypertension that is newly diagnosed or worsen-
1
5
375
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A
FIGURE 31-1. A: Solitary. B: Multicentric hepatocellular carcinomas.
injection; however, arteriovenous shunting is often present in cases of HCC. This high-output communication
between the hepatic artery and the portal vein may cause
reversal of portal venous flow and portal hypertension.
Surgical resection and liver transplantation are the
treatment methods most likely to result in cure; however,
they are not options in patients with diffuse disease. At
initial diagnosis, many patients already have satellite nodules, extrahepatic metastases, or vascular invasion that
FIGURE 31-2. Hepatocellular carcinoma. Hepatic artery injection demonstrates arteriovenous shunting and invasion of the
portal vein (
arrow
). H, hepatic artery; P, portal vein.
may preclude surgical therapy. The median survival is 4
to 6 months for patients with unresectable tumors. Systemic chemotherapy has not been shown to be effective.
Several percutaneous techniques have been described
for the treatment of HCC and unresectable metastatic
liver disease. These include percutaneous injection of
ethanol, acetic acid, or hot saline into the tumor and thermal ablation with radiofrequency, laser, microwaves, or
freezing (cryoablation). Therapy can be delivered through
a catheter into the hepatic artery, including chemotherapy infusion, hepatic artery embolization, or hepatic ar-
7–13
tery chemoembolization.
The rationale for therapy via
the hepatic artery is that the blood supply to hepatic tumors is typically from the hepatic artery, not from the
portal vein.
Chemoembolization is a combination of intraarterial
infusion of a chemotherapeutic agent and the introduction of an embolizing agent for occlusion of the tumor
vascular supply. Chemoembolization decreases bloodflow
to the tumor,resulting inischemia and extending the time
of contact of thechemotherapeutic drug with the tumor.
Embolization materials such as polyvinyl alcohol (PVA),
gelfoam, and iodized oil (Ethiodol) have been used in
15
combination with chemotherapeutic agents.
One study
described the use of hepatic artery embolization with PVA
1
particles without any chemotherapeutic agent.
No treat-
ment method has proven to be superior.
Chemoembolization can be technically challenging,
with a great potential for complications. Preembolization
arteriography of the celiac, superior mesenteric, and hepatic arteries is performed to define the blood supply of
the tumors, to identify variant arterial anatomy, and to
assess the patency of portal vein and the direction of
portal venous flow. The presence of portal vein occlusion
is a poor prognostic factor that increases the risk of liver
B
6
14
necrosis following chemoembolization. Other contrain-
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dications to chemoembolization are severe liver failure,
tumor involvement of greater than 70% of the liver, and
biliary obstruction.
6
Complications of chemoembolization include liver failure, liver abscess, liver infarction, biloma, cholecystitis,
and unintentional embolization to extrahepatic organs.
Prophylactic intravenous antibiotics are routinely used.
Coil embolization of the gastroduodenal artery may be
required to prevent inadvertent chemoembolization of
the pancreas and duodenum. A postembolization syndrome may occur that may include fever, nausea, and
pain for several days following the procedure.
Cholangiocarcinoma
Cholangiocarcinoma is the only primary liver tumor that
commonly causes vascular encasement and arterial occlu-
17
sion.
Encasement of the hepatic artery and splenic artery is seen frequently in cases of pancreatic carcinoma
(Fig. 31-3).
Liver and Spleen 377
16
Metastases
Hepatic metastases arise from hypervascular or hypovascular primary tumors and usually reflect the vascularity of
the primary lesion. Unlike HCC, metastases typically are
not associated with arteriovenous shunting or portal venous occlusion. The most frequent tumors that metastasize to the liver arise from the gastrointestinal tract (Fig.
31-4). Currently, hepatic resection is the only potentially
curative therapy for patients with colorectal cancer metas-
18
tases.
The use of hepatic arterial chemotherapy infu-
FIGURE 31-4. Metastasis to liver from colon carcinoma.
sion and chemoembolization for colorectal metastases is
being investigated.
19–21
Resection of hepatic metastases has been associated
with prolonged survival, particularly for metastases from
colorectal primaries.
22
Patients with more than four hepatic metastases, involvement of both hepatic lobes, or an
estimated remaining liver that is less than 30% of the
initial liver volume are not considered good candidates
for resection.
23
Computed tomography arterial portography and MRI
are the imaging studies used to determine the extent of
hepatic metastases. CT arterial portography is based on
portal enhancement of the liver by infusion of contrast
material through the superior mesenteric arter y or
splenic artery. Because all the injected contrast medium
is delivered to the liver from the portal vein, the enhancement of the disease-free liver is high. Hepatic tumors
generally do not have a portal venous blood supply, and
they are detected as areas of low attenuation compared
with the normal enhanced liver.
FIGURE 31-3. Hepatic artery and splenic artery encasement
by pancreatic carcinoma. Irregular “sawtooth” narrowing of the
hepatic and splenic arteries (
croachment on the arterial walls.
arrows
) is caused by tumor en-
Neuroendocrine tumors
The two most common neuroendocrine tumors that metastasize to the liver are carcinoid and islet cell tumors.
These are slow-growing neoplasms that frequently produce hormonal substances. The appendix is the most
common site or origin of carcinoid tumors. Islet cell tumors typically arise from the pancreas. Patients with hepatic metastases from neuroendocrine tumors may remain relatively free of symptoms until the tumor replaces
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a significant volume of liver parenchyma. Symptoms are
caused by production of hormones or mass effect. Surgical resection of neuroendocrine tumors is not a therapeutic option because these tumors are often metastatic at
presentation. Hepatic artery embolization or chemoembolization is a recognized method of controlling hor-
24–26
monal symptoms and tumor bulk.
Patients with carcinoid tumor refractory to other therapy can experience
considerable relief of symptoms by such treatment. In
addition, somatostatin is used during and after chemoembolization to prevent a carcinoid crises in hormonally active tumors. Somatostatin also can be used intravenously
in the event of a carcinoid crisis.
Cavernous hemangioma
Cavernous hemangiomas are benign hepatic tumors that
consist of thin-walled, endothelium-lined, septated vascular spaces. Cavernous hemangiomas frequently are identified incidentally during imaging. Hemangiomas are the
most common benign tumors in the liver with an incidence of up to 7%. It is estimated that 70 to 95% of
hemangiomas occur in women. Multiple hemangiomas
27
have been identified in 10% of cases.
Rarely, a large
hemangioma (⬎4 cm) may cause symptoms from mass
effect or bleeding.
28
Hemangiomas may be seen on ultrasound as hyperechoic masses. On dynamic contrast-enhanced CT, hemangiomas initially appear hypodense and then show
peripheral areas of focal enhancement, followed by diffuse hyperdensity at 2 minutes, and finally isodense on
delayed scans. Red cell radionuclide scanning also can be
used to make a reliable diagnosis. Hemangiomas produce intense signal on T2-weighted MR images.
29
Rare
cavernous hemangiomas may not exhibit conventional
features and require needle biopsy for diagnosis.
Angiographic features of cavernous hemangiomas include a well-marginated tumor arising in the late arterial
or capillary phase and persisting into the venous phase
with early peripheral opacification. Cavernous hemangiomas have a normal-sized feeding artery with no neovascularity or arteriovenous shunting (Fig. 31-5).
Focal nodular hyperplasia
Focal nodular hyperplasia (FNH) is a benign tumor that
contains liver elements, including hepatocytes, Kupffer
cells, and bile ducts. FNH occurs in young women, is
asymptomatic, and is not associated with oral contraceptive use; nor is it associated with malignant degeneration
or spontaneous hemorrhage. An enhancing central scar
is sometimes seen on CT or MR, but findings in FNH are
typically nonspecific.
30
The angiographic features include a well-marginated hypervascular tumor with feeding vessels entering from the periphery and a dense parenchymal stain (Fig. 31-6). There is no neovascularity or
arteriovenous shunting present. There may be a central
scar resulting in a “spoke-wheel” appearance.
Hepatic adenoma
Hepatic adenoma is a neoplasm that is associated with
hemorrhage caused by spontaneous necrosis. There ex-
A
FIGURE 31-5. Giant cavernous hemangioma. A: Arterial Phase. B: Venous phase of a celiac trunk injection shows progressive
opacification of the tumor periphery (
hypervascularity or arteriovenous shunting.
arrows
). P, portal vein. The feeding hepatic artery branches are of normal size with no
B
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A B
FIGURE 31-6. Focal nodular hyperplasia. (A). Large feeding artery (
mal stain.
arrow
) at the periphery of the lesion. (B). Dense parenchy-
ists a small potential for malignant degeneration. Most
hepatic adenomas arise in young women, and there is a
strong association with the use of oral contraceptives.
Because of hemorrhage and necrosis, most adenomas are
symptomatic when discovered. The CT and angiographic
appearances of hepatic adenomas are nonspecific.
Portal hypertension
Cirrhosis is characterized by hepatic necrosis, regeneration, and fibrosis. In early cirrhosis, fibrosis develops
around the sinusoidal spaces and obstructs central veins
while preser ving portal venules. Portal venous hypertension results from an increase in the vascular resistance
within the liver. The portal venous system is decompressed
through enlarged portosystemic collateral channels.
Several hemodynamic changes in the portal venous
system occur as cirrhosis progresses. The most important
is the enlargement of portosystemic collateral vessels.
The direction of flow in the portal vein also changes as
portal hypertension worsens. With mild cirrhosis, portal
vein flow is hepatopetal. As resistance increases, bidirectional flow in the portal vein may develop, and the portal
vein may not fill at all. With severe portal hypertension,
the portal vein becomes an outflow conduit for the liver,
and flow is hepatofugal. In patients with advanced cirrhosis, the hepatic arteries may have a corkscrew appearance
because of increased arterial flow and liver shrinkage. As
hepatic fibrosis worsens and portal flow decreases, cirrhotic patients become increasingly dependent on arterial perfusion of the liver.
The most common complication of portal hyperten-
sion is bleeding from gastroesophageal varices (Fig. 31-
31
7). Normally, the portosystemic gradient is less than 5
mm Hg. Portal hypertension is defined as a portosystemic
gradient of 6 mm Hg or greater. The risk of bleeding
from gastroesophageal varices becomes significant when
FIGURE 31-7. Gastroesophageal varices. Portal venogram
during a TIPS procedure. P, portal vein; S, splenic vein; E,
esophageal varices; G, gastric varices.
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the gradient is 12 mm Hg or greater.
32,33
Between 40 and
70% of patients die of the first episode of variceal bleeding. Other complications of cirrhosis and portal hypertension include ascites, hepatic encephalopathy, hepatorenal syndrome, bacterial peritonitis, splenomegaly,
pancytopenia, hepatocellular carcinoma, and fulminant
hepatic failure.
Management of acute variceal hemorrhage from portal
hypertension traditionally included the use of pharmacologic agents, mechanical compression with tamponading balloons, and endoscopic techniques that include
sclerotherapy and variceal banding. Intravenous infusions of medications—including vasopressin, nitroglycerin, propranolol, and octreotide—have been used for
temporary control of variceal bleeding. Systemic infusion
is as effective as intraarterial administration. Endoscopic
banding and sclerotherapy are effective techniques for
the initial management of variceal hemorrhage in most
patients; however, sclerotherapy and banding do not correct portal hypertension.
Surgical treatments for portal hypertension include ligation and portosystemic shunt creation. Surgical shunt
procedures provide long-term prevention of variceal
hemorrhage byreducing portalvenous pressure; however,
surgical mortality ofoperative shunts has been reported to
be as high as 20%.
34
Liver transplantation is the definitive
treatment for relieving portal hypertension from chronic
liver disease.
Transjugular intrahepatic portosystemic shunts
The transjugular intrahepatic portosystemic shunt (TIPS)
procedure was developed to relieve portal hypertension
without the mortality and morbidity of an open surgical
procedure. In this percutaneous procedure, an expandable metallic stent is placed in the liver to create a channel
between the portal vein and hepatic vein (Fig. 31-8).
The most common indications for the TIPS procedure
include acute or recurrent variceal bleeding unresponsive to medical therapy, including endoscopic banding
and sclerotherapy. Preliminar y endoscopic examination
is mandatory because bleeding actually may arise from
nonvariceal causes such as peptic ulcer disease, alcoholic
gastritis, esophageal ulcer, and Mallory–Weiss tear. TIPS
has been performed to treat intractable ascites and to
treat portal hypertension from Budd–Chiari syndrome.
Contraindications for the TIPS procedure include severe hepatic failure, severe right-sided heart failures, severe hepatic encephalopathy, primary or metastatic liver
tumor, polycystic liver disease, portal vein thrombosis,
and severe active infection.
TIPS procedure
Duplex sonography is performed before the procedure
to establish portal and splenic vein patency and flow
direction, to determine the status of the hepatic veins, to
FIGURE 31-8. Transjugular intrahepatic portosystemic shunt.
Wallstent extends from the portal vein to the hepatic vein
(
arrows
).
assess liver size, and to exclude the presence of a liver
tumor or polycystic liver disease.
Access for the TIPS procedure usually is gained
through the right internal jugular vein. A vascular sheath
is passed into the right hepatic vein. The portal vein
catheter–needle access system then is inserted through
the sheath and passed from the hepatic vein through liver
parenchyma into a branch of the intrahepatic portal vein.
Several methods are used to select a site for puncture
from the hepatic vein toward the portal vein. The most
commonly used techniques are the use of bony landmarks and wedged injection of iodinated contrast material or carbon dioxide, which usually fills the central
portal venous system.
35–37
The needle access system then is exchanged over a
guidewire for a diagnostic catheter. Portal venography
and pressure measurements then are obtained. The parenchymal tract from the hepatic vein to the portal vein
then is dilated with an 8-mm angioplasty balloon. A 10- or
12-mm diameter self-expandable Wallstent is deployed
across the parenchymal tract. The stent then is dilated
with a 10- or 12-mm balloon. Additional stents may be
required to cover the entire tract from the hepatic vein
to the portal vein.
The procedural complication rate for TIPS is less than
10%. Major complications of TIPS procedure include
bleeding, liver dysfunction, sepsis, and stent malposition
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or migration. Between 5 and 35% of patients experience
new or worsened hepatic encephalopathy.
38,39
Rarely,needle passes may result in gallbladder perforation, hepatic
artery pseudoaneurysms, and arteriovenous fistula forma-
40
tion.
Massive hemorrhage from extracapsular, inferior
vena cava, or portal vein perforation is rare.
The immediate procedure-related mortality rate is less
than 2%. Early death is usually the result of bleeding
related to extracapsular liver perforation or hepatic artery injury, hepatic artery thrombosis with fulminant hepatic failure, extrahepatic portal vein puncture, or acute
right heart failure.
38,39
The TIPS procedure is technically successfully in more
than 95% of cases.
38
In patients treated for variceal hemorrhage, rebleeding within 6 months occurs in up to 15%
of patients; however, late rebleeding may occur in up to
30% of cases. Most patients treated for intractable ascites
have partial or complete resolution within 1 month of
placement.
41
Despite the excellent short-term results of the TIPS
procedure, most shunts require secondary inter ventions
such as angioplasty of the shunt or additional stent insertion to maintain patency. Late post-TIPS stenoses may
develop within the stent, portal vein, or most commonly
the draining hepatic vein. TIPS stenosis or occlusions
occur in 25 to 37% of patients within 6 months.
42–44
FIGURE 31-9. Budd–Chiari syndrome. Right hepatic venogram shows occlusion (arrow) with spider web–like collaterals.
Budd–Chiari syndrome
Budd-Chiari syndrome (BCS) is caused by occlusion of
hepatic venous outflow resulting in hepatic congestion,
hepatic necrosis, and ultimately cirrhosis and portal hypertension. The onset of BCS may be acute, with rapidly
progressive liver failure or chronic. BCS has been associated with congenital webs of the inferior vena cava, neoplasms, myeloproliferative disorders, hypercoagulable
states, paroxysmal nocturnal hemoglobinuria, and oral
contraceptive use.
most cases.
pain, hepatomegaly, and ascites.
Budd–Chiari syndrome is diagnosed by liver biopsy and
imaging studies. BCS can be definitively diagnosed by
inferior cavography and hepatic venography. An inferior
vena cavogram may show narrowing of the inferior vena
cava as a result of compression from an enlarged caudate
lobe or occlusion from thrombosis or venous webs. Catheterization of the hepatic veins may not be possible if the
veins are occluded at their origins. Injection of contrast
in a wedged position may show a spider web–like system
of collaterals from the hepatic veins to other venous
channels (Fig. 31-9). Contrast-enhanced CT demonstrates hepatomegaly with a diffuse mottled pattern of
enhancement throughout the liver.
Surgical treatment of BCS consists of portosystemic
shunt placement and liver transplantation.
45
46
No definite cause can be identified in
Typical initial symptoms include abdominal
47
Several per-
cutaneous interventions have emerged as treatment options to recanalize the hepatic vein, including thrombolysis, percutaneous transluminal angioplasty, and stent
48
implantation.
Transjugular intrahepatic portosystemic
shunt insertion has been used to treat portal hypertension caused by BCS.
46,49
Hepatic artery aneurysms
About 15% of visceral artery aneurysms occur in the hepatic artery. Hepatic artery aneurysms are the second
most common visceralaneurysm aftersplenic artery aneurysms. Hepatic artery aneurysms are usually extrahepatic,
solitary, and atherosclerotic (Fig. 31-10). Multiple aneurysms of small hepatic artery branches are seen in polyarteritis nodosa. Intrahepatic artery pseudoaneurysms are
usually posttraumatic. The most common iatrogenic
causes of traumatic hepatic arter y pseudoaneurysms include percutaneous liver biopsy and percutaneous biliary
drainage (Fig. 31-11).
Bleeding into the bile ducts (hemobilia) may occur
when the aneur ysm is intrahepatic and intraperitoneal
bleeding may occur when the aneurysm is extrahepatic.
The treatment of choice for hemobilia caused by a hepatic artery pseudoaneur ysm is superselective embolization of the hepatic artery branch supplying the lesion. All
hepatic arter y aneurysms should be treated because of
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FIGURE 31-10. Hepatic artery aneurysm.
the high risk of rupture. Most extrahepatic aneurysms
are treated with surgical resection and bypass grafting.
Liver transplantation
Indications
Orthotopic liver transplantation (OLT) in adults is indicated for irreversible liver diseases, including acute fulminant hepatic necrosis, congenital or acquired end-stage
cirrhosis, sclerosing cholangitis, metabolic disorders resulting in liver failure, BCS, and primary hepatocellular
malignancy.
Liver-transplant techniques
The orthotopic liver-transplant surgical procedure typically consists of four end-to-end vascular anastomoses and
a biliary anastomosis. The donor hepatic artery anastomotic site is at the branch point of the common hepatic
and splenic arteries or at the celiac axis with an aortic
Carrel patch (aortic patch containing the origin of the
celiac axis). The recipient hepatic artery anastomotic site
is at the bifurcation of the right and left hepatic arteries
or at the branch point of the gastroduodenal and proper
hepatic arteries. Sometimes a donor iliac artery interposition graft is anastomosed directly to the supraceliac or
infrarenal aorta if adequate inflow from the native celiac
artery cannot be ensured, as in extremely small vessels or
in severe celiac artery stenosis.
During removal of the diseased liver, the inferior vena
cava is transected superior and inferior to the intrahepatic segment. End-to-end suprahepatic and infrahepatic
inferior vena cava anastomoses then are made with the
donor intrahepatic inferior vena cava.
An end-to-end anastomosis is made between the donor
and recipient portal veins. A venous jump graft from the
donor portal vein to the recipient superior mesenteric
vein may be used in cases of portal vein thrombosis.
The biliary anastomosis is usually made between the
donor and recipient common ducts. A T-tube may be left
in place to stent the anastomosis and facilitate cholangiography. If the recipient common hepatic duct is
diseased, too short, or too narrow, a choledochojejeunostomy is performed. A cholecystectomy is routinely performed.
FIGURE 31-11. Hepatic artery pseudoaneurysm. Pseudoaneurysm (
arrow
) following percutaneous liver biopsy.
Complications
The most common transplant complications include vascular thrombosis or stenosis, biliary obstruction or leakage, hepatic infarction, hemorrhage, posttransplantation
neoplasms, and rejection. Factors that affect OLT outcome include the extent of pretransplantation liver dis-
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ease, complexity of the transplantation surgical procedure, and the use of immunosuppressive drugs.
50
Sonography is frequently the initial diagnostic modality used to
evaluate for complications. Arteriography and venography are used as confirmatory examinations or during
percutaneous interventions.
Vascular complications
After transplantation, the donor bile duct is entirely dependent on the hepatic arterial blood supply. Occlusion
of the hepatic artery leads to bile duct ischemia and
necrosis. Clinical presentations of hepatic artery thrombosis (HAT) include massive hepatic necrosis, delayed
biliary leak/biloma, and intermittent episodes of sepsis
without an obvious source (Fig. 31-12). Causes of HAT
include faulty surgical technique, clamp injury, intimal
trauma caused by perfusion catheters, disrupted vasa vasorum leading to ischemia of the arterial ends, and rejection. HAT has been reported to occur in 4 to 25% of
liver transplants.
51–53
Sonographic evaluation demonstrates the absence of proper hepatic and intrahepatic
arterial flow. Abrupt hepatic artery cutoff is identified
during arteriography. In adult patients with HAT, collateral vessels to the transplanted liver do not form. The
treatment for acute HAT consists of surgical thrombectomy or retransplantation.
Hepatic artery stenosis occurs in up to 11% of cases,
with most stenoses occurring at the anastomosis (Fig.
31-13). Nonanastomotic stenoses are usually the result of
rejection. Sonographic features of hepatic artery stenosis
include focal accelerated velocity of greater than 200 to
300 cm per second, with turbulence present at or distal
to the stenosis.
54
Treatment for hepatic artery stenosis is
surgical anastomotic revision, retransplantation, or balloon angioplasty.
55,56
Frequently, chronic irreversible
changes are present within the liver parenchyma by the
time a hepatic artery stenosis is diagnosed.
Hepatic artery pseudoaneurysm is an uncommon but
potentially fatal complication. Pseudoaneurysms typically
FIGURE 31-12. Hepatic artery thrombosis following liver transplantation. Celiac trunk injection demonstrating abrupt cutoff of
the hepatic artery (
arrow
).
FIGURE 31-13. Hepatic artery stenosis following liver transplantation. Tortuous hepatic artery with stenosis (
surgical anastomosis.
arrow
)atthe
occur at vascular anastomoses; however, intrahepatic
pseudoaneurysms mayoccur following percutaneous needle biopsy, biliary procedure, or focal infection.
Inferior vena cava stenosis or thrombosis is a rare complication of livertransplantation. Sonography shows echogenic thrombus or obvious narrowing, with a substantially
increased flow velocity through the stenosis or reversal of
flow in the hepatic veins.
57,58
Venography demonstrates
the stenosis at the surgical anastomosis (Fig. 31-14). Successful balloon angioplasty and stent placement in the
treatment of inferior vena cava stenosis have been reported.
59
Care must be taken that a potential size discrepancy between donor and recipient inferior vena cavae not
be mistaken for a stenosis.
Portal vein thrombosis or anastomotic stenosis occurs
in fewer than 3% of liver-transplant recipients. The clinical presentation includes symptoms of portal hypertension, hepatic failure, massive ascites, or edema.
60
Biliary complications
Biliary complications occur in 13 to 25% ofcases afterliver
transplantation. Most biliary complications present within
the first 3 months after transplantation. Biliary stricture is
the most common cause of biliary obstruction after transplantation. Nonanastomotic bile leaks and strictures usually are caused by bile duct ischemia resulting in bile duct
necrosis. Causes of bile duct ischemia include hepatic artery thrombosis, prolonged cold ischemia time of the donor liver, ABO blood-type incompatibility, and chronic
rejection.
61,62
Biliary stricture may occur anywhere in the liver. Ischemic strictures often start at the liver hilus and progress
to involve the intrahepatic bile ducts. Anastomotic strictures are usually secondary to scar formation or ischemia.
Anastomotic strictures are treated with balloon dilatation
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