DOI:10.2214/AJR.07.2133
AJR 2007; 189:1243-1251
© American Roentgen Ray Society
Imaging of the Inferior Vena Cava with MDCT
Sheila Sheth1 and
Elliot K. Fishman
1 Both authors: The Russell H. Morgan Department of Radiology and Radiological
Science, Johns Hopkins University, 600 N Wolfe St., Nelson B176D, Baltimore,
MD 21287.
Received February 9, 2007;
accepted after revision May 22, 2007.
Address correspondence to S. Sheth
(ssheth{at}jhmi.edu).
Abstract
OBJECTIVE. The purpose of this pictorial essay is to illustrate the
role of MDCT in the diagnosis of disease processes affecting the inferior vena
cava (IVC).
CONCLUSION. High-speed MDCT has the potential to replace traditional
imaging techniques in the evaluation of pathologic processes involving the
IVC. The ability to acquire near-isotropic data allows high-quality
reconstructions in the sagittal and coronal planes and thus overcomes one of
the major limitations of CT in evaluating the IVC.
Keywords: bland thrombus • Budd-Chiari syndrome • heart • inferior vena cava • leiomyosarcoma • MDCT • tumor thrombus • vascular imaging
Introduction
Conventional venography, the historical gold standard for diagnosing
abnormalities of the inferior vena cava (IVC), has been replaced by
noninvasive imaging techniques for the diagnosis of venous disorders and is
now reserved for therapeutic intervention. Until recently, MRI and, to a
lesser extent, color Doppler sonography were the preferred methods with which
to evaluate the IVC because of their multiplanar capability. With the
availability of high-speed MDCT scanners allowing collection of near-isotropic
data, superior spatial resolution is combined with high-quality sagittal and
coronal reconstructions and 3D volumetric rendering to obtain exquisite
depictions of the normal and abnormal IVC. Several recent studies have shown
that MRI and MDCT results are comparable in staging malignancies affecting the
IVC [1,
2].
The purpose of this pictorial essay is to illustrate the role of MDCT in
the diagnosis of disease processes affecting the IVC.
Technique and Protocol
Currently at our institution, CT scans are obtained on a 64-MDCT scanner
(Sensation 64, Siemens Medical Solutions) using 0.6-mm detectors, 120 kVp, and
150–180 mAs. Data are reconstructed with a 0.75-mm slice thickness at a
0.5-mm interval. One hundred twenty milliliters of iohexol (Omnipaque 300,
Nycomed Amersham) is injected via an antecubital vein at a rate of 3.0
mL/s.
There are some technical challenges that need to be considered. In many
cases, primary or secondary involvement of the IVC by a disease process is not
anticipated: CT is typically requested either to stage tumors that may spread
to the IVC, such as renal cell, adrenocortical, or hepatocellular carcinoma,
or to evaluate patients with nonspecific abdominal symptoms. Abnormalities of
the IVC can also be found incidentally. Typical CT sequences include venous
phase, obtained after a scanning delay of 60–70 seconds after injection,
and arterial phase in cases of hypervascular primary tumors or in preparation
for surgery.
Although the venous phase allows good opacification of the suprarenal IVC,
evaluation of the infrarenal IVC and its tributary is more challenging because
of the admixture of less opacified blood from the lower extremities. The ideal
timing of an imaging sequence for visualization of the entire IVC is a
scanning delay of 70–90 seconds and can be used if imaging of the IVC is
specifically requested or is anticipated. However, this additional imaging
sequence involves additional radiation to the patient and thus cannot be
justified routinely.
All data are then sent to a freestanding workstation (Leonardo running
Inspace, Siemens Medical Solutions) where multiplanar and 3D images are
generated in real time using interactive techniques.
Normal Anatomy
The IVC is formed by the confluence of the right and left common iliac
veins draining blood from the lower extremities and pelvis. As it ascends in
the retroperitoneum to the right of the abdominal aorta, the IVC receives
major tributaries including the lumbar veins, the left and right renal veins,
the right gonadal vein, and the hepatic veins. The azygos venous system
connects to the IVC either directly or through the renal veins. The IVC and
its branches are best seen in the coronal plane
(Fig. 1).
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Fig. 1 —36-year-old asymptomatic female renal donor. Coronal
reconstruction image from contrast-enhanced CT shows normal anatomy of
inferior vena cava and its tributaries. LRV = left renal vein, HV = hepatic
veins.
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Anatomic Variants
The IVC is formed between the sixth and eighth gestational weeks by the
sequential formation, anastomoses, and regression of three paired veins: the
posterior cardinal vein, the subcardinal veins, and the supracardinal veins.
It is composed of four segments: infrarenal, renal, suprarenal, and hepatic
segments [3].
Aberrations in the complex embryogenesis of the IVC result in several
potential anatomic variants, present in approximately 4% of the population.
The three most common developmental abnormalities and their genesis are
described later in this article. Anatomic variation in the number or position
of the left renal vein is even more common. In the embryo, the kidneys are
drained by paired dorsal and ventral veins that form a collar around the
abdominal aorta. This is normally followed by regression of both dorsal veins,
thus the left renal vein crosses anterior to the aorta to join the IVC.
Most IVC anomalies are found incidentally, although patients with anatomic
variations are considered at higher risk for developing deep venous thrombosis
of the common femoral or iliac veins at a younger age than those without IVC
anomalies [4]. IVC anomalies
may pose a special challenge at surgery and should be carefully described in
individuals being considered for laparoscopic donor nephrectomy. The most
common anatomic variants include a retroaortic left renal vein, double IVC,
left-sided IVC, and a circumaortic left renal vein. Multiple anomalies may
occur in combination. Some anomalies, particularly the azygos continuation,
have been associated with significant congenital heart disease.
Circumaortic Left Renal Vein
A circumaortic left renal vein is the most common anomaly and is found
incidentally in as many as 8% of the population: Two left renal veins are
present with the superior vein crossing over the aorta anteriorly. The
posterior vein often lies lower than the anterior renal vein, which may make
harvesting a donor kidney problematic (Fig.
2). Therefore, the presence of this anatomic variant should be
clearly communicated to the surgeon. Compression of the retroaortic renal vein
between the aorta and the lumbar vertebral body may lead to decreased flow in
the vein; formation of collateral circulation through the left gonadal vein or
adrenal and ureteric veins; and symptoms of hematuria, flank pain, and
proteinuria in some patients, the so-called "posterior nutcracker
syndrome." These dilated venous tributaries can be nicely depicted on
MDCT [5].
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Fig. 2 —41-year-old asymptomatic male renal donor. Coronal
reconstruction image from contrast-enhanced CT shows incidentally noted
circumaortic left renal vein with posterior retroaortic branch coursing
inferiorly (arrow).
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Left-Sided IVC
Persistence of a left supracardinal vein with regression of its right
counterpart results in a left-sided IVC (Fig.
3A,
3B,
3C). The infrarenal IVC is
found to the left of the aorta up to the left renal vein, which crosses
anterior to the aorta to join the right renal vein and forms a normal right
IVC above that level.
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Fig. 3A —46-year-old woman with epigastric pain. Coronal
reconstruction image from contrast-enhanced CT shows infrarenal left-sided
inferior vena cava (IVC) with interrupted suprarenal IVC and azygos
continuation. Note right renal vein drains into azygos vein.
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Double IVC
A double IVC results from persistence of both supracardinal veins (Fig.
4A,
4B). The left IVC typically
ends at the level of the left renal vein. However, variations in the
development of the suprarenal IVC are possible.
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Fig. 4A —61-year-old man with history of resection of carcinoid tumor.
Coronal reconstruction image from contrast-enhanced CT shows there is
duplication of inferior vena cava (IVC) with azygos continuation. Note that
each renal vein drains into ipsilateral IVC.
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Azygos Continuation of the IVC
In this anomaly, the right subcardinal–hepatic anastomosis does not
form, the hepatic IVC is absent, and blood from the renal IVC drains into the
azygos system to empty in the superior vena cava (Figs.
3A,
3B,
3C and
4A,
4B).
IVC Thrombosis
Bland Thrombus
Bland thrombus in the IVC can be isolated, but it more often spreads from
the veins of the lower extremities. Risk factors include hypercoagulable
states, malignancies, and venous stasis. Local compression of the IVC by
adenopathy, large retroperitoneal masses, or fibrosis; venous stasis; and
foreign bodies, such as IVC filters or catheters, are known to promote local
clot formation.
The presence of a persistent filling defect within the column of contrast
material leads to the diagnosis of bland thrombus. If the IVC thrombosis
becomes extensive and long-standing, pericaval and periaortic collateral veins
form to bypass the obstruction (Fig.
5).
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Fig. 5 —50-year-old man with history of inferior vena cava (IVC)
occlusion. Coronal reconstruction image from contrast-enhanced CT shows there
is lack of opacification of midportion of IVC (arrows), which is
consistent with occlusion by thrombus. Extensive retroperitoneal collaterals
are seen bypassing occluded segment (arrowheads). There is stent in
suprarenal portion of IVC.
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Pseudolesions
Artifactual filling defects are common in the IVC and result most commonly
from the mixing of unopacified blood from the lower extremity with enhanced
blood from the renal veins. Pseudolesions can occasionally be mistaken for a
clot by an inexperienced reviewer. Other causes of pseudothrombus include
streaming of opacified blood refluxing into the hepatic veins from the heart,
usually in patients with right heart failure or in the setting of a rapid
contrast injection rate. In equivocal cases, delayed imaging that shows
complete opacification of the IVC clarifies the finding
[6].
In patients with parenchymal liver disease, prominent pericaval fat may
appear to project into the lumen of the IVC, a rare cause of a pseudolesion
(Fig. 6A,
6B,
6C). On axial images,
prominent fat adjacent to the IVC may project into the suprahepatic IVC and
may be mistakenly diagnosed as an IVC lipoma (Fig.
6A,
6B,
6C). Spread of an
angiomyolipoma into the IVC is another rare cause of intraluminal fat
[7].
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Fig. 6B —Axial contrast-enhanced CT images of 57-year-old man with
abnormal liver function test results. This fat projects into inferior vena
cava (IVC) creating apparent low-attenuation filling defect
(arrow).
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Fig. 6C —Axial contrast-enhanced CT images of 57-year-old man with
abnormal liver function test results. IVC is normal, which confirms this case
is pseudolesion due to partial volume averaging.
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Malignant Thrombus
Renal cell carcinoma is the most common malignancy extending into the IVC
and producing malignant thrombus, which has been reported in 4–10% of
patients with renal cell carcinoma. For proper planning of the surgical
approach, it is of paramount importance to define the superior extension of
the thrombus. According to the TNM classification of renal cell carcinoma,
tumor spread into the infradiaphragmatic portion of the IVC is categorized as
a T3c stage tumor, whereas extension into the supradiaphragmatic IVC is
classified as T4b. Further subclassification into infrahepatic, hepatic, and
suprahepatic extension of the tumor thrombus is critical to predict the
complexity of the resection, select the surgical team, and plan the surgical
approach. Although tumor thrombus is confined to the infrahepatic IVC in
approximately 50% of cases with IVC extension (Fig.
7A,
7B), 40% of clots involve the
hepatic IVC and 2–16% of patients have a clot in the right atrium
[1,
8,
9] (Fig.
8A,
8B).
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Fig. 7A —65-year-old man with large left renal mass. Coronal
reconstruction image from contrast-enhanced CT in venous phase shows there is
large hypervascular mass (arrows) in mid upper pole of left kidney.
Thrombus (arrowheads) extends into renal vein and infrahepatic
inferior vena cava (IVC).
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Fig. 7B —65-year-old man with large left renal mass. Axial
contrast-enhanced CT image in late arterial phase shows hypervascularity in
left renal vein thrombus (arrowheads), which is consistent with tumor
thrombus. Patient underwent left nephrectomy for Fuhrman grade IV clear cell
renal carcinoma and thrombectomy of 2-cm mobile clot (arrows) in
IVC.
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Fig. 8A —51-year-old man with shortness of breath. Coronal
reconstruction image from contrast-enhanced CT in venous phase shows there is
hypervascular infiltrating mass (black arrows) in right kidney that
is extending into and occluding right renal vein. Thrombus extends into
inferior vena cava (IVC), obstructing and expanding it. Note neovascularity
within thrombus and extension into right atrium (white arrow).
Inferior to level of right renal vein, clot in IVC (arrowhead) is
lower in attenuation, suggesting small portion is bland thrombus.
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Fig. 8B —51-year-old man with shortness of breath. Image obtained in
arterial phase shows there is neovascularity in main thrombus
(arrowheads), which confirms finding is tumor thrombus. Embolus in
branch of right pulmonary artery (arrow) is seen. Patient underwent
right nephrectomy and removal of tumor thrombus from IVC and right atrium,
confirming stage T4b tumor.
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Recent studies comparing MDCT and surgical findings have reported MDCT as
having an accuracy of 78–93% in predicting the uppermost extension of
IVC thrombus in patients with renal cell carcinoma
[1,
9]. Sagittal and coronal
reconstructions can reliably delineate the extent of tumor thrombus and allow
differentiation between bland and tumor thrombus by depicting direct
continuity between the primary tumor and the thrombus. In contrast to external
compression by a tumor, the vein is generally expanded and dilated.
Neovascularity within the thrombus in the arterial phase confirms the
malignant nature of an IVC clot
[6] (Figs.
7A,
7B and
8A,
8B).
Invasion of the wall of the IVC is difficult to diagnose on imaging and is
best assessed by careful examination of axial images
[10]. Detection of arterial
recruitment from adjacent organs may also indicate vessel wall invasion.
In addition to renal cell carcinoma, other cancers that may spread to the
IVC include hepatocellular carcinoma and adrenocortical cancer and Wilms'
tumor in children [10]
(Fig. 9).
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Fig. 9 —56-year-old woman with right-sided back pain and abdominal
distention. Coronal reconstruction image from contrast-enhanced CT in venous
phase shows large heterogeneously enhancing mass (arrows) displacing
right kidney inferiorly and filling defect (arrowhead) in hepatic
portion of inferior vena cava (IVC). Appearance is most suggestive of
adrenocortical carcinoma with IVC extension. This diagnosis was confirmed at
surgery and pathology. Large right adrenal mass was excised, and IVC thrombus
was removed.
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Primary Tumor of the IVC
Primary tumors of the IVC are exceedingly rare. Leiomyosarcoma of the IVC
is a tumor of mesenchymal origin arising from the smooth-muscle cells found in
the vessel wall and is associated with a poor prognosis, with a reported
10-year survival of 14%. Most leiomyosarcomas are large at presentation and
manifest with nonspecific complaints of abdominal pain, a palpable right upper
quadrant mass, or progressive lower extremity edema. Patients occasionally
present with ascites or Budd-Chiari syndrome if the tumor extends into the
hepatic veins. Wide surgical excision combined with adjuvant radiotherapy and
chemotherapy offers the only potential for cure or prolonged survival.
Leiomyosarcomas of the IVC are classified according to their location
[11–13].
Data gathered from a compiled review of 218 cases from the world literature
reveal that approximately 37% of tumors occur in segment I, below the level of
the renal veins and above the iliac vein bifurcation; 43% involve segment II,
between the renal veins and the level of the hepatic veins; and 20% form in
segment III at or above the hepatic veins level and may extend into the right
atrium [11]. Tumors affecting
segment II may be associated with a slightly better prognosis
[11]. More than two thirds of
tumors exhibit a predominantly extraluminal growth (Fig.
10A,
10B,
10C,
10D), whereas the remaining
grow within the IVC [11] (Fig.
11A,
11B).
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Fig. 10A —75-year-old man with history of bilateral lower extremity
edema and shortness of breath. Axial contrast-enhanced CT image shows large
homogeneous soft-tissue mass (arrows) anterior to infrarenal inferior
vena cava (IVC).
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Fig. 10B —75-year-old man with history of bilateral lower extremity
edema and shortness of breath. Axial contrast-enhanced CT image shows mass
(arrows) is arising from and expanding anterior IVC below level of
renal veins and is partially exophytic, compressing adjacent duodenum
(arrowhead).
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Fig. 10C —75-year-old man with history of bilateral lower extremity
edema and shortness of breath. Coronal reconstruction image from
contrast-enhanced CT shows large, partially exophytic soft-tissue mass
(arrows) is occluding IVC and extends from below renal veins to
hepatic IVC. Note superior border of mass in hepatic IVC does not extend into
right atrium. These findings were confirmed on axial CT (not shown).
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Fig. 10D —75-year-old man with history of bilateral lower extremity
edema and shortness of breath. There is abundant neovascularity within IVC
mass (arrowheads). Note early enhancement of distal IVC and extension
into left renal vein (arrow). Diagnosis of leiomyosarcoma was
established by percutaneous biopsy.
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At imaging, exophytic leiomyosarcomas appear as large retroperitoneal
masses with heterogeneous contrast enhancement. Cystic necrotic areas are not
rare. Because the origin of these large tumors may be difficult to ascertain
on imaging, percutaneous biopsy is valuable to achieve a definitive diagnosis
[12,
14] (Fig.
12A,
12B). The predominantly
intraluminal leiomyosarcoma focally dilates and usually obstructs the IVC and
may display homogeneous contrast enhancement
[14] (Fig.
11A,
11B).
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Fig. 12A —50-year-old woman with right flank mass. Coronal
reconstruction image from contrast-enhanced CT shows there is large
heterogeneously enhancing mass (arrows) displacing right kidney
inferiorly. Note calcifications within mass. Inferior vena cava (IVC) is not
visualized. Mass was displacing aorta (not shown). Because of large size of
tumor, its origin could not be definitely ascertained. Differential diagnosis
included adrenocortical cancer, gastrointestinal stromal tumor, or
retroperitoneal sarcoma. Diagnosis of leiomyosarcoma was obtained by
sonographically guided percutaneous biopsy.
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Budd-Chiari Syndrome
Budd-Chiari syndrome results from obstruction of the hepatic vein outflow
tracts, usually at the level of the hepatic veins, and is most commonly
associated with a hypercoagulable state. Obstruction of the hepatic portion of
the IVC by a congenital web, stenosis, clot, or tumor is a relatively rare
cause of Budd-Chiari syndrome. More frequently, the IVC is narrowed and
compressed by a massively enlarged caudate lobe.
The CT appearance of Budd-Chiari syndrome is well recognized. In the acute
phase of the syndrome, there is preferential enhancement of the hypertrophied
caudate lobe during the arterial phase. Portal venous phase imaging shows
heterogeneous enhancement of the liver with peripheral linear low-attenuation
bands and areas of infarction. In patients with chronic Budd-Chiari syndrome,
patchy hepatic enhancement is best depicted in the portal venous phase.
Regenerating nodules may present as hypervascular lesions in the arterial
phase. Low-attenuation thrombus may be visible in the hepatic veins and IVC.
In addition, enlarged and tortuous collateral veins from the azygos,
hemiazygos, and lumbar venous system can be seen bypassing the occluded IVC
[15] (Fig.
13A,
13B).
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Fig. 13A —21-year-old woman with coagulopathy. Axial contrast-enhanced
CT image obtained in venous phase shows liver is enlarged and exhibits
heterogeneous enhancement with enlarged caudate lobe and peripheral fatty
infiltration. Regenerating nodules are seen in right lobe. Hepatic veins are
not visualized.
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Fig. 13B —21-year-old woman with coagulopathy. Neither hepatic nor
infrahepatic inferior vena cava is visualized on this coronal reconstruction
image from contrast-enhanced CT. Note prominent periaortic venous collaterals
(arrow). Diagnosis of Budd-Chiari syndrome was confirmed by
histologic analysis of liver at liver transplantation.
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IVC Stents and Filters
IVC stents are placed routinely to bypass areas of occlusion or stenosis.
Placement of long-standing indwelling venous catheters or creation of surgical
anastomoses in patients undergoing liver transplantation increases the risk of
IVC stenosis. MDCT with volume rendering can exquisitely display the stent and
confirm its patency.
Similarly, MDCT can accurately display the location of IVC filters; their
relationship with the renal veins; and potential complications such as
thrombosis (Fig. 14),
migration, and embedding in the wall of the IVC (Fig.
15A,
15B).
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Fig. 14 —50-year-old man with history of recurrent deep vein
thrombosis and ulcerative colitis. Coronal reconstruction image from
contrast-enhanced CT shows inferior vena cava (IVC) filter is in place with
its tip at level of renal veins, which are patent. Small thrombus
(arrowhead) is present just above tip of filter. There is thrombus in
IVC (arrow) distal to filter.
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Fig. 15A —56-year-old woman with history of inferior vena cava (IVC)
filter migration. Coronal reconstruction image from contrast-enhanced CT shows
birdcage IVC filter is in suprarenal IVC, with its tip extending into hepatic
IVC. Inferior portion of filter is very close to junction of IVC and renal
veins (arrows).
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Fig. 15B —56-year-old woman with history of inferior vena cava (IVC)
filter migration. Coronal reconstruction image from contrast-enhanced CT shows
one of filter's prongs (arrow) may be embedded in medial wall of
IVC.
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Miscellaneous Conditions
Retrograde Opacification of the IVC
Retrograde opacification of the IVC and hepatic veins during
contrast-enhanced CT has been associated with right-sided heart disease
causing reflux of brightly enhanced blood from the right atrium into the IVC.
This CT finding has been shown to be a specific (98%) but relatively
insensitive (31%) sign of right heart dysfunction. However, the frequency of
this finding varies with the rate of contrast injection: Retrograde
opacification of the IVC is observed more commonly at injection rates of more
than 3 mL/s [16].
IVC Fistulas
Early enhancement of the IVC in the arterial phase suggests the presence of
an arteriovenous fistula or a significant arteriovenous malformation (Fig.
16A,
16B,
16C). Fistulas between the IVC
and adjacent organs are potentially life threatening and fortunately are quite
uncommon. They are most often posttraumatic or can occur as a rare
complication of an abdominal aortic aneurysm
[17].
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Fig. 16A —45-year-old woman with history of congestive heart failure
and abnormal findings on CT performed at outside institution. Coronal
reconstruction image from contrast-enhanced CT in arterial phase shows there
is early filling of dilated left iliac vein and inferior vena cava. Note
tangle of vessels (arrows) in pelvis.
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Fig. 16B —45-year-old woman with history of congestive heart failure
and abnormal findings on CT performed at outside institution. Axial
reconstruction image from contrast-enhanced CT in arterial phase shows there
is tangle of vessels (arrow) in left adnexa.
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Fig. 16C —45-year-old woman with history of congestive heart failure
and abnormal findings on CT performed at outside institution. Single image
from selective left iliac arteriography confirms early filling of left iliac
vein (arrow) and tangle of tortuous arteries and prominent veins
(arrowheads). This large arteriovenous malformation may have been
responsible for patient's congestive heart failure.
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Flattened IVC
A flattened IVC—defined as a transverse-to-anteroposterior diameter
ratio of 3:1 or more—seen at multiple levels has been associated with
significant hypotension, impending shock, or both in trauma patients. A
surrounding hypodense halo and small caliber of the abdominal aorta are useful
adjunct signs. Investigators who performed a retrospective study of this sign
in a nontrauma setting reported that, although this sign was associated with
hypotension in one third of the cases, the majority (66%) of patients were
normotensive and normovolemic. The authors concluded that a flat IVC can be a
normal variant, particularly in elderly women
[18].
Conclusions
MDCT can exquisitely depict pathologic conditions affecting the IVC and
offers an excellent alternative to MRI. Advantages of MDCT include superior
spatial resolution; very fast image acquisition; and evaluation of adjacent
and distant organs with one single imaging technique, which is critical in
patients with tumor involving the IVC. Isotropic data acquisition allows
excellent resolution in any plane, which is essential for diagnosis and
surgical planning. The principal challenge for the radiologist is to tailor
the examination and choose optimal imaging sequences to minimize radiation
exposure.
However, MRI remains an excellent imaging technique for evaluating the IVC
and is the only option in patients who cannot receive iodinated contrast
material. With its greater tissue contrast resolution compared with CT, MRI
can show intracaval thrombus even without IV contrast administration and can
depict the IVC even when it is severely compressed by a large retroperitoneal
tumor [10]. A lack of ionizing
radiation is another important advantage of MRI, particularly in children and
young adults. Because both techniques are equally effective, the choice
between MDCT and MRI as the primary imaging technique for evaluation of the
IVC relies primarily on availability, the individual radiologist's expertise
and preference, the patient's underlying condition, and the patient's age.
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Abstract
Introduction
