AJR 2005; 185:717-726
© American Roentgen Ray Society
Inferior Vena Cava Filling Defects on CT and MRI
Lauren B. Kaufman,
Benjamin M. Yeh,
Richard S. Breiman,
Bonnie N. Joe,
Aliya Qayyum and
Fergus V. Coakley
Department of Radiology, University of California San Francisco, Box
0628, C-324C, 505 Parnassus Ave., San Francisco, CA 94143-0628.
Received November 21, 2004;
accepted after revision January 28, 2005.
Address correspondence to B. M. Yeh
(benyeh{at}itsa.ucsf.edu).
Abstract
OBJECTIVE. The purpose of this article is to describe the appearance
and causes of inferior vena cava (IVC) filling defects, how such findings may
be accurately characterized, and the clinical significance of IVC filling
defects. Filling defects in the IVC observed at MDCT and MRI may be a result
of flow artifacts, anatomic variants, or bland or malignant thrombus.
CONCLUSION. Familiarity with anatomy and flow effects is critical
for distinguishing true from false filling defects in the IVC. Delayed imaging
after administration of IV contrast material and dedicated MRI sequences may
be helpful for further characterization of such findings. Once a true filling
defect of the IVC is established, identification of the cause, whether benign
or malignant, and extent will guide clinical treatment.
Introduction
Filling defects in the inferior vena cava (IVC) are a frequent
finding on CT and MRI. Many of these defects are artifactual and require
distinction from real defects that are of critical importance to clinical
management. The objective of this pictorial essay is to review the spectrum of
IVC filling defects, with an emphasis on the distinction of apparent from true
filling defects and the identification of underlying disease. The clinical
features and therapeutic implications of IVC filling defects are also
discussed. This topic is timely because of the introduction of MDCT, which
allows rapid and high resolution multiplanar vascular reformation, and the
recognition of several new causes of IVC filling defects over the last decade,
such as pseudolipoma and previously un-described coagulopathies. MRI is useful
to evaluate ambiguous CT findings. For purposes of description, we have
classified IVC filling defects as artifactual, benign, or malignant.
Artifactual Filling Defects
The most common IVC filling defect seen on CT is pseudothrombosis caused by
laminar flow of enhanced blood from the renal veins streaming parallel to the
column of unopacified blood returning from the lower body
[1] (Figs.
1A, and
1B). The appearance is usually
characteristic. Artifactual filling defects may also result from poorly
enhanced blood, such as from an accessory hepatic vein, flowing into an
opacified IVC (Figs. 2A, and
2B) or from laminar reflux of
opacified blood from the heart into the IVC, usually in the setting of right
heart disease or a high injection rate
(Fig. 3). Delayed images to
show resolution of the filling defect are usually sufficient to confirm the
artifactual nature of such pseudolesions, but occasionally, problematic cases
may require further evaluation with flow-sensitive
[1] (Figs.
4A,
4B, and
4C) or delayed
contrast-enhanced MRI sequences. The so-called pseudolipoma is a rarer and
more recently described pseudolesion of the IVC and represents a partial
volume artifact of pericaval fat above the caudate lobe rather than a true
intraluminal lesion [2] (Figs.
5A, and
5B). This artifact is common
in patients with chronic liver disease in whom prominent pericaval fat
collections commonly develop
[2]. Coronal MRI or reformatted
CT images help to confirm the true nature of this finding.
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Fig. 1A —64-year-old man with incidental CT finding of pseudothrombus
caused by opacified blood from renal veins streaming into unopacified inferior
vena cava (IVC). Axial enhanced CT image shows filling defect (arrow)
caused by inflow of opacified blood from renal veins mixing with poorly
opacified blood in IVC.
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Fig. 1B —64-year-old man with incidental CT finding of pseudothrombus
caused by opacified blood from renal veins streaming into unopacified inferior
vena cava (IVC). Curved multiplanar image reveals opacified blood from renal
veins streaming into IVC (arrows). This case illustrates how axial
image can show IVC filling defect.
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Fig. 2A —54-year-old man with pseudothrombus in intrahepatic inferior
vena cava (IVC) resulting from flow artifact. Axial enhanced CT image obtained
in portal venous phase shows filling defect (arrow) in intrahepatic
IVC.
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Fig. 2B —54-year-old man with pseudothrombus in intrahepatic inferior
vena cava (IVC) resulting from flow artifact. Axial enhanced CT image, delayed
venous phase, reveals accessory right hepatic vein inflow (arrow)
that accounts for filling defect seen on earlier phase images.
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Fig. 3 —78-year-old man with pseudothrombus in inferior vena cava
(IVC) caused by high contrast-injection rate. Axial enhanced CT image, early
arterial phase, shows IVC filling defect (arrowhead) due to laminar
flow of refluxed contrast from hepatic veins. Bright enhancement in hepatic
veins (arrows) is seen because of reflux of contrast from heart.
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Fig. 4A —50-year-old woman with renal cell carcinoma and acquired
cystic kidney disease. Axial enhanced CT image shows heterogenous enhancement
of inferior vena cava (IVC) (arrow), suggesting tumor invasion.
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Fig. 4B —50-year-old woman with renal cell carcinoma and acquired
cystic kidney disease. Axial gadolinium-enhanced T1-weighted MR image shows
filling defect (arrow) of intrahepatic IVC, also suggesting tumor
invasion.
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Fig. 4C —50-year-old woman with renal cell carcinoma and acquired
cystic kidney disease. Axial steady-state gradient-echo flow-sensitive MR
image shows patency of IVC (arrow) and absence of true filling
defect. Low venous return from failed kidneys may have contributed to apparent
intracaval defect.
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Fig. 5B —73-year-old man with incidental CT finding of pseudolipoma.
Coronal T2-weighted MR image shows shelf of pericaval fat (arrow)
above caudate lobe. Fat collection may appear intraluminal on axial
images.
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Benign Filling Defects
The most common true filling defect of the IVC is bland thrombus, which may
be idiopathic or reflect a hypercoagulable state, venous stasis, or the
presence of a foreign body. Hypercoagulable states include oral contraceptive
use, antiphospholipid syndrome
[3], paroxysmal nocturnal
hemoglobinuria, vascular injury, paraneoplastic syndromes, and various
coagulopathies, such as factor V Leiden deficiency and protein C resistance.
Antiangiogenesis agents are also known to cause vascular thrombosis. Venous
stasis, which can occur from immobility, heart failure, and external
compression, can also facilitate the formation of thrombus. External
compression is most commonly due to retroperitoneal adenopathy, but other
sources include hepatic masses and hepatomegaly; renal, adrenal, and
pancreatic masses; abdominal aortic aneurysms; and retroperitoneal hematomas,
neoplasms, and fibrosis [4].
Foreign bodies, such as IVC filters or venous catheters (Figs.
6A, and
6B), may promote thrombus
formation. Intracaval thrombosis has been reported to develop in 2.7% of
patients after placement of an IVC filter
[5] due to new local thrombus
formation, trapped embolus of a thrombus from a more distant site, or cephalad
extension of a more distally located deep venous thrombus from the pelvis or
lower extremities. Bland thrombus can extend superiorly past the level of an
IVC filter. Thrombus occurring at the site of a venous catheter can persist in
the form of a fibrin sheath even after removal of the catheter
(Fig. 7). Benign tumor
thrombus in the IVC may be a result of vascular invasion by renal
angiomyolipoma [6], IV
leiomyomatosis (Figs. 8A,
8B, and
8C), or adrenal
pheochromocytoma [7].
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Fig. 6A —50-year-old man with bland thrombus in inferior vena cava
(IVC) and left renal vein that extends proximally after filter placement.
Axial enhanced CT image before IVC filter placement shows bland thrombus
(arrow) in IVC.
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Fig. 6B —50-year-old man with bland thrombus in inferior vena cava
(IVC) and left renal vein that extends proximally after filter placement.
Coronal multiplanar image reconstructed from CT data after IVC filter
placement shows extension of bland thrombus into both renal veins
(arrowheads) and intrahepatic IVC. Note IVC filter (arrow)
and decreased enhancement of right kidney due to hypoperfusion.
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Fig. 7 —36-year-old man with previously removed IV catheter. Axial
enhanced CT image shows circular filling defect (arrows) within
infrahepatic inferior vena cava consistent with fibrin sheath.
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Fig. 8A —45-year-old woman with uterine leiomyomatosis. Axial enhanced
CT image obtained at level of pelvis shows heterogenous hyper-enhancing lesion
(arrowheads) in uterus consistent with uterine leiomyoma.
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Fig. 8B —45-year-old woman with uterine leiomyomatosis. Axial enhanced
CT image obtained below inferior vena cava (IVC) bifurcation shows IV
leiomyomatosis (arrow) within right common iliac vein.
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Fig. 8C —45-year-old woman with uterine leiomyomatosis. Axial enhanced
CT image obtained at level of gallbladder reveals filling defect
(arrow) of IVC due to cephalad extension of IV leiomyomatosis.
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Malignant Filling Defects
A malignant cause should be considered for all true IVC filling defects,
particularly because pathognomonic symptomatology is rare in malignant
involvement of the IVC and the existence of tumor thrombus is often first
recognized at imaging. Cancers can extend directly into the IVC from adjacent
organs or occasionally arise as primary malignancies of the IVC. Malignancies
that commonly extend directly into the IVC include renal cell, hepatocellular,
and adrenocortical carcinoma (Fig.
9), but invasion from other adjacent cancers such as metastases to
the lung (Figs. 10A, and
10B) and kidney
[8] can occur. Pancreatic
carcinoma, Wilms' tumor, and metastases in retroperitoneal lymph nodes can
occasionally extend into the IVC
[4]. Features that distinguish
malignant from bland thrombus include presence of a contiguous adjacent mass
and enhancement of the filling defect (Figs.
11A,
11B,
12A,
12B, and
12C). However, it should be
remembered that malignancy predisposes to thrombosis due to hypercoagulability
and that bland downstream thrombus may coexist with malignant thrombus more
superiorly in the IVC (Figs.
12A,
12B, and
12C). If an adjacent tumor is
not identified, an enhancing IVC mass may be the result of primary
intraluminal sarcoma (Figs.
13A, and
13B).
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Fig. 9 —66-year-old woman with adrenocortical carcinoma. Coronal
T2-weighted MR image shows large adrenal mass (arrowheads) with tumor
thrombus extending into infrahepatic inferior vena cava (arrow).
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Fig. 10A —46-year-old woman with metastatic colon carcinoma to lung.
Axial steady-state gradient-echo flow-sensitive MR image shows direct
extension of lung mass (arrowheads) into inferior vena cava (IVC)
(arrow).
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Fig. 10B —46-year-old woman with metastatic colon carcinoma to lung.
Coronal T1-weighted MR image shows lung metastasis (white arrow)
invading supradiaphragmatic IVC (black arrow) and another metastasis
(arrowheads) invading right pulmonary artery.
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Fig. 12A —46-year-old man with renal cell carcinoma. Axial unenhanced
T1-weighted MR image shows tumor thrombus (arrowheads) extending into
right renal vein, abutting bland thrombus (arrow) of higher signal
intensity in inferior vena cava (IVC). Note large lesion (asterisk)
in upper pole of right kidney consistent with renal cell carcinoma.
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Fig. 12B —46-year-old man with renal cell carcinoma. Axial
gadolinium-enhanced T1-weighted MR image shows enhancing renal mass with tumor
thrombus (arrowheads) extending into right renal vein adjacent to
non-enhancing bland thrombus in IVC (arrow).
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Fig. 12C —46-year-old man with renal cell carcinoma. Coronal unenhanced
T1-weighted MR image reveals bland thrombus (arrowheads) that formed
inferior in relation to tumor thrombus (arrows) seen in infrahepatic
IVC. Lesion of low signal intensity is present in right kidney
(asterisk), representing renal cell carcinoma.
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Clinical Features and Therapeutic Implications
Obstruction of the IVC can be clinically silent or result in bilateral
lower extremity edema, Budd-Chiari syndrome
(Fig. 14), or venous
collateral formation. Embolization of bland and tumor thrombus to the
pulmonary circulation is another potential complication and can be assessed by
CT pulmonary angiography (Figs.
15A,
15B, and
15C), although it is often
impossible to distinguish bland and tumor emboli. In cases of IVC extension of
renal cell carcinoma and other tumors, curative treatment may still be
possible with aggressive resection. The superior extent of the tumor thrombus
has surgical implications; thrombus extension into the supradiaphragmatic IVC
or right atrium requires resection accompanied by cardiopulmonary bypass and
is associated with increased morbidity and mortality.
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Fig. 14 —47-year-old man with Budd-Chiari syndrome 1 year after
nephrectomy was performed for right-sided renal cell carcinoma. Axial enhanced
CT image shows tumor thrombus in inferior vena cava lumen (large
arrow) and adjacent surgical clips (small arrow) from previous
nephrectomy. Heterogenous enhancement of liver and ascites
(arrowheads) is seen, consistent with hepatic outflow
obstruction.
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Fig. 15A —54-year-old woman with renal cell carcinoma invading inferior
vena cava (IVC) and pulmonary emboli. Axial T2-weighted MR image with fat
saturation shows right-sided renal mass (arrowheads) with
heterogeneous high signal consistent with renal cell carcinoma. Tumor thrombus
is present in adjacent IVC (arrow).
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Fig. 15C —54-year-old woman with renal cell carcinoma invading inferior
vena cava (IVC) and pulmonary emboli. Axial enhanced CT image shows large
thrombus in right main pulmonary artery (arrowheads) and left lower
lobe pulmonary artery (arrow).
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Familiarity with anatomy and flow effects is critical for distinguishing
true from false filling defects in the IVC. Delayed imaging after
administration of IV contrast material and dedicated MRI sequences may be
helpful for further characterization of such findings. Once a true filling
defect of the IVC is established, identification of the cause, whether benign
or malignant, and extent will guide clinical treatment.
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Top
Abstract
Introduction
