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578
Imaging Evaluation of the
Inferior Vena Cava1
Richard P. Smillie, MD
Monisha Shetty, MD
Andrew C. Boyer, MD
Beatrice Madrazo, MD, RVT
Syed Zafar Jafri, MD
Abbreviation: IVC = inferior vena cava
RadioGraphics 2015; 35:578–592
Published online 10.1148/rg.352140136
Content Codes:
From the Department of Diagnostic Radiology,
Beaumont Health System, Beaumont Hospital
Royal Oak, 3601 W 13 Mile Rd, Royal Oak,
MI 48073 (R.P.S., M.S., A.C.B., S.Z.J.); and
Department of Medicine, University of Miami
Health System, University of Miami Hospital,
Miami, Fla (B.M.). Recipient of a Certificate of
Merit award for an education exhibit at the 2013
RSNA Annual Meeting. Received April 3, 2014;
revision requested July 10 and received August
4; accepted August 13. For this journal-based
SA-CME activity, the authors, editor, and reviewers have disclosed no relevant relationships.
Address correspondence to R.P.S. (e-mail:
[email protected]).
1
SA-CME LEARNING OBJECTIVES
After completing this journal-based SA-CME
activity, participants will be able to:
■■Classify congenital IVC variants and
understand their implications for patient
treatment.
IVC involvement in malignancy and its potential impact on surgical planning.
The inferior vena cava (IVC) is an essential but often overlooked
structure at abdominal imaging. It is associated with a wide variety
of congenital and pathologic processes and can be a source of vital
information for referring clinicians. Initial evaluation of the IVC is
most likely to occur at computed tomography performed for another indication. Many routine abdominal imaging protocols may
result in suboptimal evaluation of the IVC; however, techniques to
assist in specific evaluation of the IVC can be used. In this article,
the authors review the spectrum of IVC variants and pathologic
processes and the relevant findings from magnetic resonance imaging, angiography, sonography, and positron emission tomography.
Embryologic development of the IVC and examples of congenital
IVC variants, such as absence, duplication, left-sided location,
azygous or hemiazygous continuation, and web formation, are described. The authors detail IVC involvement in Wilms tumor, leiomyosarcoma, adrenal cortical carcinoma, testicular carcinoma, hepatocellular carcinoma, renal cell carcinoma, and other neoplasms,
as well as postsurgical, traumatic, and infectious entities (including
filter malposition, mesocaval shunt, and septic thrombophlebitis).
The implications of these entities for patient treatment and instances in which specific details should be included in the dictated
radiology report are highlighted. Furthermore, the common pitfalls
of IVC imaging are discussed. The information provided in this
review will allow radiologists to detect and accurately characterize
IVC abnormalities to guide clinical decision making and improve
patient care.
©
RSNA, 2015 • radiographics.rsna.org
■■Identify
■■Describe
the appearance of the IVC
after intervention and in the context of
trauma or infection.
See www.rsna.org/education/search/RG.
Introduction
The inferior vena cava (IVC) is the main conduit of venous return to
the right atrium from the lower extremities and abdominal viscera.
It can be a source of critical information for referring clinicians, and
recognition of IVC variants and pathologic characteristics can help
guide patient treatment. The purpose of this article is to increase
knowledge of both congenital IVC variants and other processes affecting the IVC and to emphasize their effect on patient care. After a
brief overview of IVC imaging techniques and embryologic features,
cases in which computed tomography (CT) was performed with
relevant correlates from magnetic resonance (MR) imaging, angiography, ultrasonography (US), and positron emission tomography
(PET) will highlight the spectrum of congenital variants, neoplasms,
and other entities related to surgery, intervention, trauma, and infection. Furthermore, potential imaging pitfalls will be discussed.
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TEACHING POINTS
• Increasing the delay after contrast material injection to 70–90
seconds allows more uniform enhancement of the entire IVC
at CT.
• Because of anomalous persistence, regression, and anastomoses of the vitelline, posterior cardinal, subcardinal, and supracardinal veins, several classic congenital variations, including
IVC absence or duplication, a left-sided IVC, anomalous continuation of the IVC to the thorax, and a retrocaval ureter, can
occur alone or in combination.
• Identification of duplication of the IVC is important in patient
treatment because if the entity is not recognized before routine placement of an infrarenal IVC filter, recurrent pulmonary
embolism can develop.
• Malignant IVC involvement is most often attributable to direct
endovascular extension and/or intraluminal thromboembolization. Tumor thrombus, the most common manifestation of
IVC involvement, can be differentiated from bland thrombus
on the basis of expansion of the vessel lumen and enhancement of the filling defect.
• Pseudolipoma is a volume-averaging artifact due to prominent pericaval fat above the caudate lobe and is often seen
in patients with cirrhosis. Admixture artifact may also occur
at the level of the renal veins when contrast-enhanced blood
from the kidneys mixes with nonenhanced blood from the
lower extremities.
Smillie et al 579
tection while still not requiring the use of ionizing
radiation. However, anesthesia may be required in
the pediatric population at MR imaging.
Embryologic Development
and Normal Anatomic Structure
The IVC is the main conduit of venous return
from the lower extremities and abdominal viscera.
The mature IVC has four segments: the hepatic,
suprarenal, renal, and infrarenal IVC (4). Formation of the IVC involves complex anastomoses and
regression of multiple embryonic veins, including
the vitelline vein and the paired posterior cardinal,
subcardinal, and supracardinal veins (Fig 1). The
vitelline vein contributes to the hepatic segment
of the IVC. The suprarenal IVC is composed of a
segment of the right subcardinal vein that does not
regress. The renal segment of the IVC is formed by
the anastomosis between the right subcardinal and
right supracardinal veins. A segment of the right
supracardinal vein persists as the infrarenal segment. The embryonic veins also lead to the azygos,
hemiazygos, and common iliac veins (4,5).
Congenital IVC Variants
IVC Imaging Techniques
Because CT is used to evaluate a wide variety of
abdominal symptoms, it is likely to be the most
common imaging modality for initial detection
of IVC variants and pathologic findings. Routine
abdominal imaging at 60–70 seconds after intravenous administration of contrast material (portal
venous phase) shows enhancement in the renal
and suprarenal IVC but may also show admixture
artifact in the infrarenal IVC (1,2). Increasing the
delay after contrast material injection to 70–90
seconds allows more uniform enhancement of the
entire IVC at CT (2). Another advanced imaging
technique available for IVC evaluation is MR imaging. MR imaging, specifically with breath-hold
contrast material–enhanced three-dimensional
T1-weighted imaging and balanced steady-state
free-precession techniques, is more reliable than
CT for evaluation of IVC tumor thrombus (1). US
is also useful for initial evaluation when an IVC
pathologic condition is suspected, although US
is subject to operator dependence and evaluation
of the infrahepatic IVC may be limited because
of artifact resulting from overlying bowel gas and
body habitus (1). Doppler US may show absent or
abnormal flow in the IVC at the site of occlusion
or narrowing caused by an intraluminal mass (3).
In pediatric patients, US is generally the first-line
modality for cross-sectional imaging. If US is not
sufficient because of operator or patient factors,
MR imaging is sensitive for IVC abnormality de-
Congenital variations of the IVC are the result
of abnormal embryologic development involving the vitelline, posterior cardinal, subcardinal,
and supracardinal veins (5). They are present in
approximately 4% of the population, and these
individuals are often asymptomatic (1,2). Because of anomalous persistence, regression, and
anastomoses of the vitelline, posterior cardinal,
subcardinal, and supracardinal veins, several classic congenital variations, including IVC absence
or duplication, left-sided IVC, anomalous continuation of the IVC to the thorax, and retrocaval
ureter, can occur alone or in combination.
Absence of the IVC
Congenital absence of the entire IVC or of only
the infrarenal IVC (6–10) has been previously described but has an unknown incidence and unclear
cause. IVC absence may result from complete
failure of embryonic vein development; however,
perinatal venous thrombosis and atrophy have also
been suggested (8–10). In addition to inability to
identify the IVC at imaging, prominent venous
collateralization may be a finding (Fig 2). Patients
may experience lower extremity venous insufficiency or idiopathic deep vein thrombosis or have
prominent lumbar collateral vessels, which can be
mistaken for paraspinal masses (6–11).
Duplication of the IVC
IVC duplication is the result of persistence of
both supracardinal veins forming duplicated
infrarenal IVC segments (5). The left infrarenal
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Figure 1. Schematic shows embryologic features of the IVC. The
IVC (dark blue) is composed of
multiple segments derived from
anastomosis (light blue) of embryonic veins. The vitelline vein
contributes to the hepatic IVC. The
suprarenal IVC is composed of a
segment of persistent right subcardinal vein. The subsupracardinal
anastomosis persists as the renal
segment. A segment of the right
supracardinal vein persists as the
infrarenal IVC. The caudal aspects
of the posterior cardinal veins persist as the iliac veins. The superior
supracardinal veins also persist as
the azygos venous system (green).
Figure 2. Coronal abdominal CT images of congenital IVC variants. (a) Absence of the intrahepatic IVC (arrow).
The superior mesenteric vein and portal venous confluence appear to be normal (arrowhead), but the IVC is absent. (b) Duplication of the IVC (arrows), with a left-sided IVC draining into the left renal vein (black arrowhead)
and normal continuation of the suprarenal IVC (white arrowhead). (c) Left-sided IVC (arrow) below the level of
the renal veins joins the left renal vein (arrowhead) and continues as the intrahepatic IVC. (d) Azygos continuation of the IVC is indicated by a prominent azygos vein (arrow) running parallel to the aorta and absence of the
intrahepatic IVC (arrowhead).
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Figure 3. Retrocaval ureter. Axial CT
urogram shows the right ureter coursing
posterior to the IVC (arrow). The right
ureter descends into the pelvis between
the IVC and the aorta and anterior to the
right iliac vessels. A duplicated IVC is also
present (arrowhead), highlighting that
multiple congenital IVC anomalies may
be present in various combinations.
IVC joins the left renal vein and drains into a
normal suprarenal IVC (Fig 2). The prevalence
of this anomaly is 0.2%–0.3% (5). Identification
of duplication of the IVC is important in patient
treatment because if the entity is not recognized
before routine placement of an infrarenal IVC
filter, recurrent pulmonary embolism can develop
(5). Therefore, for each patient, a review of prior
cross-sectional images is an essential step before
filter placement. If no images are available, cavography should be performed through the left iliac
vein. A filter can then be placed into each cava. In
addition, the IVC lying to the left of the abdominal aorta can be mistaken for a lymph node if not
followed along its course (1).
Left-sided IVC
A left-sided IVC, as it is classically described,
results from regression of the right supracardinal
vein, with abnormal persistence of the left supracardinal vein, and has a prevalence of 0.2%–0.5%
(5). Similar to a duplicated IVC, a left-sided IVC
courses cranially to the left of the abdominal aorta,
joins with the left renal vein, and drains into a normal suprarenal IVC (Fig 2). Although the clinical
effect is minimal, a left-sided IVC can cause difficult central venous access during interventional
procedures if the endovascular operator is unaware
of the anatomic structure. Specifically, a left-sided
IVC may cause confusion between venous and
arterial access, limit access options for IVC filter
placement, or complicate pulmonary thrombolysis.
Anomalous Continuation of the IVC
Continuation of the suprarenal IVC as the azygos
or hemiazygos vein is attributable to embryonic
failure to form the right subcardinal–hepatic anastomosis and, in the case of azygos continuation,
has a prevalence of 0.6% (4,12). The suprarenal
IVC drains either into the azygos vein and returns
to the heart through the superior vena cava or into
the hemiazygos vein and subsequently into the
azygos vein (Fig 2). The hemiazygos vein may also
drain directly into the coronary sinus through a
persistent left-sided superior vena cava or into
the left brachiocephalic vein through the accessory
hemiazygos vein (13). Because of the absence of the
intrahepatic segment of the IVC, the hepatic veins
drain directly into the right atrium. The azygos vein,
enlarged to accommodate increased flow, could be
mistaken for retrocrural lymphadenopathy and a
prominent azygos and superior vena cava confluence for a right paratracheal mass (12). Drainage
through the hemiazygos vein may simulate a leftsided mediastinal mass or, in the event of accessory
hemiazygos drainage, an aortic dissection (13,14).
There is also potential for inadvertent ligation of the
hemiazygos vein during thoracic surgery (15).
Retrocaval Ureter
Although the genitourinary system develops
separately, the spatial relationship between the
ureter and the IVC depends on IVC embryologic
features. If the infrarenal IVC develops from the
right posterior cardinal vein instead of the right
supracardinal vein, the result will be a retrocaval
ureter, also known as a circumcaval ureter (4). The
ureter, usually situated on the right side, courses
posterior to the IVC and descends to the right
of the aorta (Fig 3). There is potential for partial
urinary outflow obstruction and recurrent urinary
tract infections (4). Diagnosis of a retrocaval ureter can easily be facilitated with CT urography. If
the patient is symptomatic, treatment necessitates
surgical relocation of the ureter (1,5).
IVC Webs
IVC web formation is an uncommon IVC anomaly
that has been described as resulting from a congenital vascular anomaly or the sequela of thrombus formation (16). IVC webs are rare in North
American and northern European populations
and more common in Asian and South African
populations (16). Imaging shows a complete or
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Figure 4. IVC webs. (a) Coronal CT image shows stenosis of the intrahepatic IVC with a soft-tissue membrane at the
level of stenosis (arrow). (b) Cavogram shows complete obstruction (arrowhead).
Figure 5. Abernethy malformation. (a) Color Doppler US image shows an abnormal aneurysmal connection between
the portal vein (arrow) and IVC (white arrowhead) near the superior mesenteric vein (black arrowhead). Intrahepatic
portal flow is absent. (b) Axial T2-weighted MR image shows an end-to-side congenital anastomosis between the portal
vein (arrow) and IVC (arrowhead), a finding compatible with type 2 Abernethy malformation.
fenestrated membrane in the intrahepatic IVC
or a segment of fibrotic occlusion that may be of
variable length (1,16). Prominent intrahepatic and
extrahepatic collateral vessels also develop (Fig 4).
Clinically, a web causes hepatic outflow obstruction and can lead to congenital Budd-Chiari syndrome, which may then lead to hepatocellular carcinoma. Inferior venacavography can be performed
to help confirm the diagnosis (16). Depending on
the severity of the associated liver disease, treatment may include angioplasty, placement of a
stent, or creation of a transjugular intrahepatic
portosystemic shunt, interventions that would relieve the resultant portal hypertension (17).
Extrahepatic Portocaval
Shunt (Abernethy Malformation)
The Abernethy malformation is classified into
two categories (18). Type 1 is characterized by
complete shunting of portal blood into the IVC
and congenital absence of the portal vein. It is
more common in females and is associated with
polysplenia and biliary atresia. A type 2 shunt is a
partial end-to-side anastomosis between an intact
portal vein and the IVC and is most commonly
seen as an isolated finding in males (19) (Fig 5).
These extrahepatic portocaval shunts are thought
to be attributable to either excessive involution
of the vitelline vein or failure of the vitelline vein
to establish an anastomosis with the hepatic sinusoids or hepatic veins (20,21). The presence or
absence of the portal vein is an important imaging finding because it helps distinguish between
the two types. The Abernethy malformation is
associated with focal nodular hyperplasia and
hepatocellular carcinoma; MR imaging with a
hepatobiliary contrast agent may be beneficial
for distinguishing between the two liver lesions
because focal nodular hyperplasia will retain such
contrast material (19).
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Figure 6. Leiomyosarcoma. (a) Axial CT image shows expansion of the IVC lumen by a heterogeneously contrastenhancing partially necrotic mass (arrow). (b) Coronal CT image from a different patient shows extraluminal extension
of a heterogeneous mass (arrow) and intraluminal tumor (arrowhead).
IVC Involvement by Neoplasms
Both primary and secondary malignant neoplasms can involve the IVC and often have similar imaging features. Primary IVC malignancy
is extremely rare; although leiomyosarcoma
represents less than 1% of all malignancies, it accounts for more than 75% of tumors arising from
large veins (22,23). Primary IVC leiomyoma is
also possible, and this benign tumor accounts
for 15% of tumors arising from large veins (23).
Secondary involvement of the IVC in abdominal
malignancy is more common than primary IVC
neoplasms. Malignant IVC involvement is most
often attributable to direct endovascular extension and/or intraluminal thromboembolization.
Tumor thrombus, the most common manifestation of IVC involvement, can be differentiated
from bland thrombus on the basis of expansion
of the vessel lumen and enhancement of the filling defect (24,25). Correct identification of the
extent of IVC involvement is essential to staging
and determining surgical intervention.
Primary IVC Leiomyosarcoma
Leiomyosarcoma is the most common primary
malignancy involving the IVC (26). It arises
from the smooth muscle cells in the vessel wall.
Seventy-four percent of cases of IVC leiomyosarcoma occur in women, and women aged 40–60
years are the most frequently affected (22,27).
The initial growth of an IVC leiomyosarcoma
is intramural (3,28). Two-thirds of tumors will
demonstrate predominantly extraluminal growth,
and one-third will demonstrate predominantly
intraluminal growth (3,22,28). The intraluminal
tumors may cause venous obstruction. At imaging, the mass may appear as a heterogeneously
contrast material–enhancing filling defect of the
IVC that may show cystic necrosis (Fig 6). Ex-
traluminal tumors can invade adjacent structures
and should be differentiated from neoplasms
arising from the surrounding organs or directly
from the retroperitoneum (26). The level of IVC
involvement is important because tumors involving the renal and suprarenal IVC (42%–50%)
are associated with the most favorable prognosis.
Involvement of the intrahepatic IVC is associated
with the worst prognosis and is seen in 6%–20%
of cases. The remaining 37%–44% of tumors
involve the infrarenal IVC (3,27–29). Complete
surgical resection is required for cure, and en
bloc resection of the IVC with a subsequent IVC
graft may be necessary, depending on location
and characteristics (30). Overall, 10-year survival
is 14% and more than 50% of patients develop
recurrent disease (3,28).
Renal Cell Carcinoma
Renal cell carcinoma is the most common ma­
lignancy that extends into the IVC, with 4%–
10% of cases involving venous invasion (31,32).
Frequently, patients with malignant tumor
thrombus are asymptomatic and the thrombus
is first identified at imaging. The appearance at
imag­ing is similar to that of other tumor thrombi,
with expansion of the IVC lumen and enhancement of the thrombus, findings suggestive of a
malignant process (Fig 7). CT shows IVC extension of renal cell carcinoma with 96% accuracy
and is the first choice for imaging renal cell carcinoma because it also allows simultaneous metastatic survey (33). Although the superior extension of tumor thrombus may be underestimated,
accurate description of the tumor thrombus is
essential because it affects surgical intervention
(31). IVC involvement changes TNM system
staging to T3b for infradiaphragmatic involvement and T3c for supradiaphragmatic extension.
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Figure 7. Renal cell carcinoma. Axial
CT image shows a heterogeneously
enhancing mass (*) involving the right
kidney and extending through the renal vein and into the IVC (arrow).
Figure 8. Adrenal cortical carcinoma. Coronal (a) and axial (b) contrast-enhanced CT images show a large left-sided
adrenal cortical carcinoma (*), with extension of the tumor thrombus through the left renal vein (arrowhead in b) and
into the IVC (arrows in a).
Supradiaphragmatic extension requires cardiopulmonary bypass during the surgical procedure,
increasing morbidity and mortality during the
procedure (25). Invasion of the IVC wall is rare
in the context of renal cell carcinoma tumor
thrombus and may necessitate segmental resection of the IVC (1). Renal cell carcinoma with
IVC extension and without distant metastasis is
associated with a 5-year survival rate of 32%–
64% after complete surgical resection (32,34,35).
Adrenal Cortical Carcinoma
Adrenal cortical carcinoma is a rare malignancy,
with a reported prevalence of 0.5–2 cases per
million persons. Adrenal cortical carcinoma may
develop at any age, but there is a bimodal age distribution during the 1st and the 4th–5th decades
of life. Sixty-two percent of adrenal cortical carcinoma cases involve functional tumors and may
lead to Cushing syndrome, virilization, or feminization (36). The imaging feature of adrenal cortical carcinoma is a heterogeneous mass replacing
the entire adrenal gland and often displacing the
adjacent kidney, liver, or spleen (Fig 8). Calcifications are common (31). Intravascular extension
into the IVC may be seen in up to 30% of cases
and is more common in right-sided tumors and
tumors that are larger than 9 cm (33). The differential diagnosis should include renal cell carcinoma, pheochromocytoma, and metastatic disease (31). Adrenal cortical carcinoma is more aggressive and has more rapid disease progression
in adults than in children. Approximately 50%
of adults will have a relatively advanced disease
stage at presentation. Local recurrence is common, and the most common sites of metastasis
are the liver, lungs, lymph nodes, and bone (36).
Hepatocellular Carcinoma
Invasion into and thrombosis of the portal
venous system is typical in patients with hepatocellular carcinoma, but invasion into hepatic
veins and the IVC occurs in 4.0%–5.9% of patients (23,24) (Fig 9). Right atrial involvement
is also possible because of the right atrium’s
proximity to the hepatic venous confluence (37).
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Figure 9. Hepatocellular carcinoma.
Contrast-enhanced T1-weighted MR image shows direct invasion of hepatocellular carcinoma (arrowhead) into the intrahepatic IVC (arrow).
Figure 10. Transitional cell carcinoma. Axial contrast-enhanced CT (a) and T1-weighted MR (b) images
show high-grade urothelial carcinoma in the renal pelvis (* in a) and extending into the IVC (arrow) through
the right renal vein. (Case courtesy of Isaac R. Francis, MD, University of Michigan, Ann Arbor, Mich.)
Expansion of the hepatic veins and an enhancing thrombus are the typical imaging findings.
Occlusion of the IVC and hepatic veins may
lead to Budd-Chiari syndrome, and patients
may have the classic triad of ascites, abdominal
pain, and hepatomegaly at presentation (38).
Systemic venous invasion by hepatocellular
carcinoma is associated with an extremely poor
prognosis, and patients with symptomatic intraatrial extension of tumor thrombus have a median survival of 1–4 months (37). Invasion of
the systemic venous system also predisposes the
patient to distant metastasis (23).
Transitional Cell Carcinoma
Although microscopic vascular invasion commonly occurs in transitional cell carcinoma, extension into the IVC is rare (fewer than 20 cases
have been reported in the literature) (39,40)
(Fig 10). Imaging characteristics include a filling defect of the renal collecting system at CT
urography, lack of renal contour distortion, and
a filling defect in the IVC and/or renal vein. Aggressive surgical intervention is required, including nephroureterectomy (39,41). Invasion of the
IVC wall is more common in transitional cell
carcinoma than in renal cell carcinoma and may
precipitate a need for segmental IVC resection.
The prognosis associated with this type of carcinoma is poor; in one study, eight of 14 patients
died within 6 months after surgery (39).
Wilms Tumor
Wilms tumor is the most common renal tumor
in children and involves IVC invasion in 4%–8%
of cases (33,42). Wilms tumor manifests as a
large heterogeneous mixed solid and cystic mass
arising from the kidney and is often first identified at US (Fig 11). Although US can show vascular extension, CT and MR imaging are better
for evaluation of metastatic disease (42). Recognition of IVC involvement is important because
it advances the tumor staging from I to II, and
a stage II tumor may necessitate neoadjuvant
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Figure 11. Wilms tumor. (a) Coronal CT image shows heterogeneously contrast-enhancing tumor in the right
kidney (*), with tumor thrombus extending into the right atrium (arrow). (b) Transverse US image shows thrombus in the IVC (arrowhead). * = tumor.
Figure 12. Metastatic mixed germ cell testicular
carcinoma. (a) Coronal contrast-enhanced CT image
shows para-aortic lymphadenopathy (*) and tumor
thrombus invading the IVC (arrow) and extending
cranially in the IVC lumen (arrowhead). (b) Coronal PET/CT image confirms fluorodeoxyglucose-avid
adenopathy (arrowhead) and tumor thrombus (arrow). (c) Gray-scale US image of the right testicle
confirms testicular origin of the tumor thrombus.
chemotherapy or radiation therapy. IVC extension is also associated with increased morbidity
during nephrectomy (33,42).
Nonseminomatous
Testicular Carcinoma
Bulky retroperitoneal lymphadenopathy is a common finding in metastatic testicular cell carcinoma in which an aggressive neoplasm may be in
proximity to the IVC (Fig 12) (43). Some studies
have shown that 3%–11% of nonseminomatous
testicular tumors involve the IVC (44,45). The
tumor thrombus may result from intravascular
spread through gonadal veins, or bulky retroperitoneal lymphadenopathy may invade directly
through the IVC wall (43). Testicular cancer is
the most common cancer in males aged 15–34
years. Because the testes are not routinely included at CT imaging, scrotal US should be recommended in young men with bulky retroperitoneal lymphadenopathy and IVC tumor thrombus.
Other Sources of Tumor Thrombus
Metastatic disease in the liver, kidneys, and adrenal glands may involve the IVC through
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Figure 13. Mesocaval interposition shunt in a patient with portal hypertension. Axial CT images show a patent mesocaval shunt
(arrowhead) extending from the superior mesenteric vein (arrow in a) to the IVC (arrow in b).
intravascular spread. As previously described,
retroperitoneal lymphadenopathy may also invade directly through the IVC wall. It is important to differentiate tumor thrombus from bland
thrombus by using contrast enhancement and
luminal expansion, because a neoplasm predisposes patients to coagulopathy and development
of bland deep vein thrombosis that can propagate to the IVC (24,25).
Surgery, Intervention, Trauma,
Infection, and Imaging Pitfalls
Noncongenital and nonneoplastic processes can
also affect the IVC. Knowledge of postsurgical and postprocedural changes is necessary
for correct interpretation. In the context of an
emergency, the appearance of the IVC can alert
the clinician to impending hypovolemic shock.
Recognition of infection can allow timely and appropriate treatment, and recognition of imaging
pitfalls can prevent inappropriate treatment.
Postsurgical Changes
Creation of a mesocaval shunt is a surgical interposition between the superior mesenteric vein
and the IVC. This was a popular treatment in
the 1970s and 1980s for uncontrollable variceal
bleeding associated with cirrhosis and portal hypertension; however, the treatment has decreased
in popularity since the advent of the transjugular
intrahepatic portosystemic shunt procedure. Despite this decrease in popularity, surgical creation
of shunts is still relevant for decompression of variceal bleeding, because portal vein occlusion can
make creation of transjugular intrahepatic portosystemic shunts technically difficult or impossible.
Although shunt creation was traditionally an open
vascular procedure, recent advances in intravascular US guidance allow endovascular shunt creation
(46). A mesocaval shunt may be detected incidentally, or imaging may be performed intentionally to
assess for patency (Fig 13).
IVC filter placement is a common procedure
performed by interventional radiologists, vascular
surgeons, and even interventional cardiologists.
Careful evaluation of cross-sectional imaging is
very important before IVC filter placement to
ensure appropriate protection from deep vein
thrombosis. However, many of the complications
after placement of IVC filters can also be assessed at cross-sectional imaging (47) (Fig 14).
Continued advancements in liver transplantation result in more frequent postoperative imaging
and treatment of complications. Stenosis of the IVC
after liver transplantation is a complication caused
by compression due to postoperative swelling (48).
IVC anastomoses differ between cadaveric donor
and living donor transplantations. In recipients
of cadaveric transplants, the donor IVC is anastomosed end to end with the recipient IVC or is
“piggybacked” onto the recipient’s hepatic vein.
Conversely, in recipients of living transplants, the
donor hepatic veins are anastomosed to the recipient IVC. Doppler US plays an important role in
detecting IVC complications. For example, there is
a three- to four-fold increase in IVC velocity at the
site of stenosis at spectral Doppler imaging. There
is also loss of phasicity of the hepatic veins that
is normally the result of atrial modulation (Fig 15).
Vascular complications are the second leading cause
of graft failure after acute rejection, and treatment
includes angioplasty and stent placement (48).
En bloc surgical resection of the vena cava may
be a treatment option for patients with retroperitoneal sarcoma arising from or invading the IVC.
The optimal treatment of the IVC after resection is controversial and options include ligation
or reconstruction. Choices for resection include
primary repair if luminal narrowing of less than
50% will result. A bowel or venous graft can also
be used if the resection site is localized. If a large
segment of the IVC is resected, circumferential
replacement with a ringed polytetrafluoroethylene
graft may be performed (49,50) (Fig 16).
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Figure 14. IVC filters. (a) Coronal CT image shows an IVC
filter with a metallic prong extending beyond the IVC wall
(arrow). (b) Axial CT image shows a misplaced filter (arrow)
causing right-sided ureteral obstruction and hydronephrosis (*). (c) Axial CT image shows a single IVC filter in the
“normal” right-sided IVC (arrow). This patient had a duplicated IVC, however, and remained vulnerable to pulmonary embolism due to a clot in the unprotected left-sided
IVC (arrowhead). To avoid this pitfall, venography of the
left iliac vein should be performed before IVC filter placement if no cross-sectional images are available for review.
Figure 15. IVC stenosis in a hepatic transplant recipient. (a) Three-dimensional MR image shows focal narrowing of
the IVC (arrow) in a patient with a “piggyback” anastomosis after orthotopic transplantation. (b) Spectral Doppler US
image shows a peak systolic velocity (PS) of 357 cm/sec at the narrowed anastomosis. ED = end-diastolic velocity, RI =
resistive index.
Other Abnormalities
The IVC can be particularly important in emergency imaging, with two entities requiring
immediate recognition and treatment: slitlike
IVC and aortocaval fistula (Fig 17). A slitlike
IVC is defined as an IVC with a transverseto-anteroposterior diameter ratio greater than
3:1 that is seen at multiple levels. In patients
with trauma, a slitlike IVC is associated with
significant hypotension and impending shock.
However, it is a nonspecific finding in patients
without a history of trauma, and up to twothirds of patients with this imaging finding can
be euvolemic and normotensive (1,2).
An aortocaval fistula is a rare but often
catastrophic complication of abdominal trauma
or abdominal aortic aneurysm. Patients often present with acute symptoms related to
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Smillie et al 589
Figure 16. IVC graft after en bloc resection to treat leiomyosarcoma. Coronal CT
image shows the immediate postoperative
appearance of an IVC reconstruction with
a ringed polytetrafluoroethylene graft (arrow). Air (arrowheads) and fluid surrounding the graft are related to the patient’s
recent postoperative state.
Figure 17. Emergency imaging of a hypotensive patient. (a) Axial CT image shows a slitlike IVC (arrow)
and bowel wall thickening (arrowhead), findings consistent with shock bowel. (b) Aortogram shows early
filling of a dilated IVC during the arterial phase, a finding consistent with an aortocaval fistula.
high-throughput congestive heart failure, and
80%–90% of aortocaval fistula formation is the
result of rupture or erosion of an abdominal aortic aneurysm into the IVC. The remaining cases
are attributable to posttraumatic fistulization,
although neoplastic and inflammatory causes are
also possible (51). The imaging findings of an
aortocaval fistula include early contrast opacification in the IVC during arterial phase imaging,
loss of a normal fat plane between the aorta and
IVC, and enlarged IVC (due to the high flow
state). Prompt recognition and early surgical or
endovascular repair are important for improved
patient outcomes (51).
Bland thrombus is the leading cause of IVC
obstruction, which places the patient at high risk
for pulmonary embolism. Risk factors for thrombus formation include a hypercoagulable state,
malignancy, venous stasis, focal compression, and
IVC filters. Bland thrombus in the IVC may be
isolated but most often extends from pelvic and
lower extremity deep vein thrombosis. Unlike
tumor thrombus, bland thrombus lacks luminal
expansion and enhancement (1). Anticoagulation
drugs are the mainstay of therapy. However, IVC
filters can be placed if anticoagulation therapy is
contraindicated (1,2).
Gonadal vein thrombophlebitis commonly
involves the ovarian vein in postpartum patients;
approximately 80% of cases are right sided, but
the entity can extend into the IVC (52). The
ovarian vein is expanded by bland thrombus; this
expansion results in enhancement of the venous
wall and perivascular inflammation (Fig 18).
Treatment includes anticoagulation drugs and
antibiotics (52).
Calcified IVC thrombus was first reported in
1961 and is thought to occur primarily in pediatric populations. Potential causes are abdominal
malignancy, adrenal hemorrhage, coagulopathy,
and infection. IVC calcification in adults is exceptionally rare (53).
IVC Imaging Pitfalls
The pitfalls of IVC imaging involve mistaking
artifacts for IVC thrombus. Pseudolipoma is
a volume-averaging artifact due to prominent
pericaval fat above the caudate lobe and is often
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Figure 18. Right gonadal vein thrombophlebitis in a postpartum patient. Axial (a) and coronal (b) CT images show
an enlarged well-defined right-sided tubular structure with peripheral enhancement and a low-attenuation filling defect
(arrowhead), findings consistent with thrombus and inflammation of the right ovarian vein. The vein drains directly into
the IVC, and caval extension of the thrombus (arrow in b) is visible.
seen in patients with cirrhosis. Admixture artifact
may occur at the level of the renal veins when
contrast-enhanced blood from the kidneys mixes
with nonenhanced blood from the lower extremities (Fig 19). Admixture artifact can also result
from retrograde flow of contrast material into the
IVC because of right heart failure or a contrast
material injection rate faster than 3 mL/sec (1,2).
Conclusion
Recognition of IVC processes is essential to patient treatment. The spectrum of abnormalities
involving the IVC include congenital anomalies,
which may be mistaken for adenopathy or may
cause difficulty in vascular access and IVC filter
placement; neoplasms, which may cause venous
occlusion and alter staging and surgical management; and other postsurgical, traumatic, and
infectious causes. Knowledge of these processes
can markedly affect patient care, and evaluation
of the IVC should be a fundamental part of the
search pattern for abdominal radiologists. This
will allow detection of a congenital or postsurgical abnormality. An accurate and informative description of the IVC is particularly important in
the context of abdominal neoplasm, recent liver
transplantation, and trauma. Radiologists should
be aware that routine abdominal CT with a delay
of 60–70 seconds after injection of contrast material may lead to admixture artifact in the infrarenal IVC, potentially resulting in the misdiagnosis
of a filling defect. A delay of 70–90 seconds will
yield more uniform contrast enhancement. In
pediatric patients, US may be a valuable firstline modality if a caval pathologic condition is
suspected, because Doppler US can be used to
evaluate IVC thrombus without the risk of radiation exposure.
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TM
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