DOI:10.2214/AJR.05.0310
AJR 2006; 187:682-687
© American Roentgen Ray Society
Incidental Nonneoplastic Hypervascular Lesions in the Noncirrhotic Liver: Diagnosis with 16-MDCT and 3D CT Angiography
Ihab R. Kamel1,
Eleni Liapi1 and
Elliot K. Fishman1
1 All authors: Russell H. Morgan Department of Radiology, Johns Hopkins School
of Medicine, 601 N Caroline St., Ste. 3235A, Baltimore, MD 21287.
Received February 25, 2005;
accepted after revision June 21, 2005.
Address correspondence to I. R. Kamel
(ikamel{at}jhmi.edu).
CME
This article is available for 1 CME credit. See CME data for this article
at
www.arrs.org.
Abstract
OBJECTIVE. The purpose of this pictorial essay is to review the MDCT
features of uncommon hypervascular lesions seen with advanced image
processing.
CONCLUSION. MDCT with advanced image processing is useful in
delineating uncommon hypervascular liver lesions that simulate tumors.
Familiarity with the appearance of these lesions may reduce the need for
additional imaging, follow-up, and histologic correlation.
Keywords: CT angiography • liver disease • MDCT
Introduction
The rate of detection of incidental hypervascular liver lesions has
increased over the past decade, probably because of increased use of arterial
phase imaging and fast scanning techniques. Benign hypervascular tumors
include hemangioma, focal nodular hyperplasia, and hepatic adenoma. Malignant
hypervascular tumors include hepatocellular carcinoma and metastatic lesions
from islet cell tumors, melanoma, sarcoma, renal cell carcinoma, and some
subtypes of breast and lung carcinoma
[1]. In addition to these
common lesions, hypervascular nonneoplastic lesions must be considered. These
lesions, which must be distinguished from benign and malignant neoplasms,
include hepatic artery aneurysm and pseudoaneurysm, arterioportal venous shunt
or fistula, portosystemic shunt, and anomalous paraumbilical venous drainage
to the left hepatic lobe.
MDCT combined with multiplanar reconstruction and volume rendering
facilitates detailed assessment of uncommon hypervascular lesions. This
pictorial essay reviews the spectrum of these lesions seen on MDCT scans
obtained with advanced image processing. Familiarity with the appearance of
these lesions will reduce the incidence of false-positive diagnosis of
neoplasms and will increase the overall diagnostic accuracy of MDCT.
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Fig. 1A —79-year-old woman with hepatic artery aneurysm. Conventional
axial CT scan in arterial phase reveals small hypervascular lesions
(arrow) abutting left hepatic artery (arrowheads) in left
lobe of liver.
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Fig. 2 —50-year-old woman with transient perfusion change after
biopsy. Coronal maximum-intensity-projection image in arterial phase shows
wedge-shaped transient subsegmental enhancement (arrow) at site of
needle biopsy.
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Fig. 3A —41-year-old woman with arterioportal fistula. See also Figure
S3C, cine loop, in supplemental data online. Conventional axial CT scan in
arterial phase shows early enhancement and distention of left portal vein
(arrow).
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Fig. 3B —41-year-old woman with arterioportal fistula. See also Figure
S3C, cine loop, in supplemental data online. Coronal
maximum-intensity-projection image in arterial phase shows arterioportal
fistula between left hepatic artery (arrowhead) and left portal vein
(arrow).
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Fig. 4A —25-year-old man with arterioportal fistula after biopsy.
Conventional axial CT scan in arterial phase shows early enhancement of left
portal vein (arrow) and increased perfusion of left hepatic lobe.
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Fig. 4B —25-year-old man with arterioportal fistula after biopsy.
Coronal maximum-intensity-projection image in arterial phase shows
arterioportal fistula between left hepatic artery (arrowhead) and
left portal vein (arrow).
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Imaging and Postprocessing Technique
Scanning was performed with a Sensation 16 scanner (Siemens Medical
Solutions). Gantry time rotation was 500 milliseconds with detector
collimation and slice thickness of 0.75 mm for arterial and portal venous
phase image acquisition. Patients received 750 mL of water as a negative
contrast agent 15 minutes before the study and another 250 mL at the time of
the study. All patients received 120 mL of iohexol nonionic contrast medium
(Omnipaque 350 mg/mL, GE Healthcare) injected IV at a rate of 3-4 mL/s with a
power injector. Scan delay was 20-25 seconds for the arterial phase and 55-60
seconds for the portal venous phase. All CT data, in the original resolution
of 512 x 512, were sent from the scanner to a freestanding workstation
for postprocessing with InSpace Software (Leonardo, Siemens Medical
Solutions). Real-time axial and multiplanar (coronal and sagittal) scrolling,
interactive maximum intensity projection, and volume-rendering techniques were
used to scrutinize the hepatic parenchyma. Sliding maximum intensity
projections allowed fast visualization of the lesion of interest, and rotation
in various planes facilitated tracing the full course of a feeding vessel or
draining vein.
Hepatic Artery Aneurysm and Pseudoaneurysm
The hepatic artery is the fourth most common abdominal artery for
development of aneurysms, after the infrarenal aorta, iliac arteries, and
splenic artery. The most common cause of aneurysm formation is
atherosclerosis, followed by medial degeneration, vasculitis, and mycotic
infection [2]. Pseudoaneurysm
of the hepatic artery also has been reported after trauma and after liver
transplantation [3]. On axial
arterial phase CT, aneurysms and pseudoaneurysms appear as well-defined focal
enhancing lesions that may simulate hypervascular tumors
[4]. These lesions become
enhanced with attenuation similar to that of the hepatic arteries in the
arterial and portal venous phases. Although aneurysms and pseudoaneurysms
usually are detected on axial images, image processing easily delineates the
size and extent of the aneurysm and establishes the presence of communication
with the hepatic artery (Figs.
1A and
1B). Confident diagnosis can be
made in most of these cases. Endovascular treatment entails transcatheter coil
embolization. Surgical management includes bypass, ligation, and
aneurysmorrhaphy.
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Fig. 5A —72-year-old woman with arterioportal fistula after biopsy.
Conventional axial CT scan in arterial phase shows small hypervascular lesions
(arrow) abutting left hepatic artery (arrowhead) in left
lobe of liver.
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Fig. 5B —72-year-old woman with arterioportal fistula after biopsy.
Coronal maximum-intensity-projection image in arterial phase shows
arterioportal fistula between left hepatic artery (arrowhead) and
left portal vein, which contains varix (arrow).
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Fig. 6A —60-year-old woman with spontaneous arteriovenous
malformation. See also Figure S6D, cine loop, in supplemental data online.
Coronal (A) and axial (B) maximum-intensity-projection images in
arterial phase show grapelike hypervascular lesions (arrows) in dome
of liver supplied by branches of hepatic artery. Surrounding increased
perfusion is evident.
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Fig. 6B —60-year-old woman with spontaneous arteriovenous
malformation. See also Figure S6D, cine loop, in supplemental data online.
Coronal (A) and axial (B) maximum-intensity-projection images in
arterial phase show grapelike hypervascular lesions (arrows) in dome
of liver supplied by branches of hepatic artery. Surrounding increased
perfusion is evident.
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Fig. 6C —60-year-old woman with spontaneous arteriovenous
malformation. See also Figure S6D, cine loop, in supplemental data online.
Coronal maximum-intensity-projection image in portal venous phase shows
persistent enhancement of lesions that drain into right hepatic vein
(arrow).
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Arterioportal Shunt
Communications exist between a hepatic arterial branch and the portal veins
at the level of the main vessels, sinusoids, and peribiliary venules
[4]. These connections can
result in differences in transient hepatic attenuation, which are commonly
seen in cirrhotic livers in response to the compromise of portal venous flow
[5]. Hepatic arterioportal
shunts occur in a wide spectrum of liver disorders, including hepatocellular
carcinoma and metastatic liver disease, and may precede the appearance of
obvious hepatic neoplasms [6].
In these cases, the hepatic parenchyma should be scrutinized for possible
neoplasm.
After trauma or interventional procedures such as hepatic biopsy
(Fig. 2) and percutaneous
biliary or abscess drainage, CT may show wedge-shaped transient subsegmental
enhancement at the site of needle entry
[7]. Arterioportal fistula
occasionally occurs and can result in rapid development of portal hypertension
and high-output cardiac failure. Passage of contrast material from a
high-pressure arterial branch into a low-pressure portal branch leads to early
enhancement of a focal area of the liver before the adjacent parenchyma. These
areas are easily detected with MDCT. Early enhancement of the peripheral
portal vein can occur during the hepatic arterial phase and before enhancement
of the main portal vein (Figs.
3A,
3B,
4A,
4B,
5A, and
5B). (See
www.ajronline.org
for Fig. S3C.) The abnormally enhancing vein is often distended because of
high systemic pressure transmitted by the hepatic artery. An enlarged feeding
hepatic artery proximal to the shunt also may be seen. Arterioportal shunting
also may be seen in cases of arteriovenous malformation of the liver (Figs.
6A,
6B, and
6C). (See online for Fig.
S6D.) At MDCT these lesions may have a beaded or grapelike appearance with
surrounding heterogeneous mottled capillary blush.
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Fig. 7C —85-year-old woman with spontaneous venous malformation. Axial
oblique maximum-intensity-projection image in arterial phase shows tubular
venous malformation arising from left portal vein (arrow).
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Fig. 8A —65-year-old man with spontaneous hepatic artery aneurysms and
portosystemic venous shunt. See also Figure S8C, cine loop, in supplemental
data online. Coronal maximum-intensity-projection image in arterial phase
shows small aneurysms of hepatic artery (arrows).
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Fig. 8B —65-year-old man with spontaneous hepatic artery aneurysms and
portosystemic venous shunt. See also Figure S8C, cine loop, in supplemental
data online. Axial maximum-intensity-projection image in portal venous phase
shows branch of posterior right portal vein (arrow) draining into
large right hepatic vein (arrowhead).
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Intrahepatic Portosystemic Venous Shunt
Intrahepatic portosystemic venous shunt is a high-flow shunt between the
portal vein and the hepatic vesupplementalins that results in compromise of
the portal venous supply to the liver parenchyma. Congenital shunt can be
caused by persistent communication between the omphalomesenteric venous system
and the inferior vena cava. This shunt is considered a portosystemic
collateral vessel because it usually occurs in association with portal
hypertension and hepatic encephalopathy
[8]. Acquired shunts can occur
in patients with cirrhosis or after biopsy. A concomitant increase in hepatic
arterial flow to the affected segment of the liver usually compensates for the
decrease in hepatic perfusion. On MDCT with image processing, communication
between a portal vein branch and a hepatic vein branch can be established with
early and asymmetric enhancement of the involved hepatic vein (Figs.
7A,
7B,
7C,
8A,
8B,
9A,
9B,
9C, and
10). (See online for Fig.
S8C.) Treatment is transcatheter coil embolization or surgical ligation.
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Fig. 9A —81-year-old man with spontaneous portosystemic venous shunt.
Coronal maximum-intensity-projection image in portal venous phase shows direct
communication between left portal vein (arrow) and left hepatic vein
(arrowhead).
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Fig. 9B —81-year-old man with spontaneous portosystemic venous shunt.
Axial (B) and coronal (C) volume-rendered images in portal
venous phase show large tubular vascular channel (arrow,
B; arrowhead, C) draining into left hepatic vein and
inferior vena cava.
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Fig. 9C —81-year-old man with spontaneous portosystemic venous shunt.
Axial (B) and coronal (C) volume-rendered images in portal
venous phase show large tubular vascular channel (arrow,
B; arrowhead, C) draining into left hepatic vein and
inferior vena cava.
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Fig. 10 —73-year-old man with spontaneous portosystemic venous shunt.
Axial maximum-intensity-projection image in portal venous phase shows direct
communication between right portal vein (arrow) and right hepatic
vein (arrowhead).
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Anomalous Paraumbilical Venous Drainage
The falciform ligament is the remnant of the ventral mesentery and contains
the round ligament, which is the obliterated umbilical vein, and persistent
paraumbilical vein draining the ventral surface of the diaphragm and the
epigastric abdominal wall. These vessels act as portosystemic collateral
vessels in case of portal hypertension resulting in recanalization of the
umbilical vein. The vessels may communicate inferiorly with the inferior
epigastric vein, a configuration that results in caput medusae. Communication
of these vessels with the inferior vein of Sappey can result in hypoperfusion
adjacent to the falciform ligament, seen in the portal venous phase of
imaging. In addition, these vessels communicate with the superior vein of
Sappey, which receives systemic blood flow from the diaphragm and chest wall.
In cases of superior vena caval obstruction, increased flow through these
collaterals can cause early hepatic enhancement adjacent to the falciform
ligament in segment IVa (Figs.
11,
12A, and
12B). MDCT with advanced image
processing can easily delineate the vascular communication between the region
of hepatic hyperenhancement and the systemic venous channels along the chest
wall.
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Fig. 11 —62-year-old man with superior vena caval obstruction. Axial
image in arterial phase shows early hepatic enhancement (arrow)
adjacent to falciform ligament and collaterals along anterior abdominal
wall.
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Fig. 12B —45-year-old man with superior vena caval obstruction. Axial
maximum-intensity-projection image in arterial phase shows early hepatic
enhancement (arrow) adjacent to falciform ligament.
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Conclusion
MDCT with advanced image processing is useful in delineating uncommon
hypervascular hepatic lesions that can simulate tumors on arterial phase
imaging. Many of these lesions can be recognized by their characteristic
appearance on MDCT. Familiarity with the appearance of the lesions can reduce
the need for additional imaging, follow-up, and histologic correlation.
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Abstract
Introduction
