DOI: 10.1148/rg.283075101
RadioGraphics 2008;28:669-689
© RSNA, 2008
Imaging the Inferior Vena Cava: A Road Less Traveled1
Harsh Kandpal, MD,
Raju Sharma, MD,
Shiva Gamangatti, MD,
Deep N. Srivastava, MD, and
Sushma Vashisht, MD
1 From the Department of Radiodiagnosis, All India Institute of Medical Sciences, Ansari Nagar, New Delhi 110029, India. Recipient of an Excellence in Design award for an education exhibit at the 2006 RSNA Annual Meeting. Received May 7, 2007; revision requested July 3 and received August 23; accepted August 27. All authors have no financial relationships to disclose.
Address correspondence to R.S. (e-mail: raju152{at}yahoo.com).
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Abstract
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A broad spectrum of congenital anomalies and pathologic conditions can affect the inferior vena cava (IVC). Most congenital anomalies are asymptomatic; consequently, an awareness of their existence and imaging appearances is necessary to avoid misinterpretation. Imaging also plays a central role in the diagnosis of Budd-Chiari syndrome secondary to membranous obstruction of the intrahepatic IVC. Primary malignancy of the IVC is far less common than intracaval extension of malignant tumors arising in adjacent organs, and imaging can accurately help determine the presence and extent of tumor thrombus, information that is crucial for surgical planning. However, the radiologist should be aware that artifactual filling defects at computed tomography and magnetic resonance imaging can mimic true thrombus in the IVC and must be able to differentiate true from pseudo filling defects. Other imaging findings such as flat IVC and early enhancement of the IVC are useful in limiting the differential diagnosis. Familiarity with the imaging features of the various congenital and pathologic entities that can affect the IVC is paramount for early diagnosis and management.
© RSNA, 2008
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LEARNING OBJECTIVES
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After reading this article and taking the test, the reader will be able to:
- Discuss the imaging features and therapeutic implications of various pathologic conditions of the IVC.
- Describe the collateral pathways that open up in obstructive lesions of the IVC.
- Identify pseudolesions of the IVC and differentiate them from pathologic conditions of this vascular structure.
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Introduction
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Imaging plays a crucial role in the diagnosis and management of diverse conditions that affect the inferior vena cava (IVC). Ultrasonography (US), including color Doppler flow imaging, is a useful modality for initial evaluation. It complements computed tomography (CT) and magnetic resonance (MR) imaging in the diagnosis of Budd-Chiari syndrome (BCS) and in the depiction of tumor thrombus and its cranial extent, and helps differentiate artifactual filling defects from true thrombus. However, US is operator dependent, and visualization of the IVC (especially the infrahepatic portion) may be hampered due to bowel gas or obesity. CT and MR imaging are essential for staging and treatment planning. There is no standard CT protocol for imaging of the IVC. The IVC is typically evaluated in the portal venous phase (60–70 seconds after the injection of 100–150 mL of nonionic contrast material at a rate of 3–5 mL/sec), and dynamic multiphasic imaging is performed only if otherwise indicated (eg, in renal cell carcinoma). In the portal venous phase, there is denser contrast material in the renal and suprarenal IVC than in the infrarenal portion due to venous return from the kidneys. This fact should be borne in mind to avoid pitfalls (discussed later), and, in cases of a possible filling defect, delayed imaging should be performed. The isotropic volume data sets that are possible with the latest-generation multidetector CT scanners allow superior-quality multiplanar reformation, which is useful in delineating IVC disease. MR imaging is the most reliable technique for depicting the presence and extent of tumor thrombus, although limited availability and cost considerations prohibit its routine use. Three-dimensional breath-hold T1-weighted MR imaging performed after the intravenous administration of contrast material and balanced steady-state free precession are the most robust MR imaging sequences for imaging of the IVC.
In this article, we review the imaging features of various congenital anomalies of the IVC, including left IVC, double IVC, retrocaval ureter, absence of the infrarenal IVC, retroaortic and circumaortic left renal vein, interruption of the IVC with azygous or hemiazygous continuation, and portocaval shunt. In addition, we discuss and illustrate membranous obstruction of the intrahepatic IVC, bland thrombus and intracaval tumors, the appearance of the IVC in trauma patients, and conditions resulting in early IVC enhancement. We also discuss pitfalls in imaging of the IVC.
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Congenital Anomalies
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A basic knowledge of IVC embryogenesis is essential for understanding the anomalies of the IVC. A detailed review of IVC formation is beyond the scope of this article, but the interested reader can refer to an excellent review by Phillips (1). Briefly, during the 4th week of fetal life, paired posterior cardinal veins drain the caudal portion of the embryo. These veins are progressively replaced, first by the subcardinal veins and later by the supracardinal veins, which together form the subhepatic IVC (2).
As their names imply, the subcardinal veins are ventromedial and the supracardinal veins dorso-medial to the posterior cardinal veins. The right subcardinal vein forms the suprarenal segment of the IVC, and the right supracardinal vein forms the infrarenal segment. Anastomotic channels between the supracardinal and subcardinal veins form the intervening renal segment of the IVC. Cranially, the subcardinal vein (suprarenal IVC) forms an anastomosis with the hepatic segment, which is derived from the right vitelline vein. Caudally, the infrarenal IVC (right supracardinal vein) forms an anastomosis with the iliac veins, which are derived from the persistent posterior cardinal veins (Fig 1) (2).
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Figure 1. Drawing illustrates the embryologic development of the IVC. Three pairs of veins—the posterior cardinal (blue), subcardinal (vertical red), and supracardinal (purple) veins—develop in succession on either side of the aorta (gray). Portions of these venous channels regress (dashed colored lines), whereas others persist (solid colored lines) to form the infrahepatic IVC. The right subcardinal vein forms the suprarenal segment of the IVC, and the right supracardinal vein forms the infrarenal segment. The hepatic segment is derived from the vitelline vein (green). Anastomotic channels (black) connect the various segments of the IVC. An intersubcardinal anastomosis that passes anterior to the aorta forms the left renal vein (horizontal red line), whereas intersupracardinal and interposterior cardinal anastomoses normally regress. The supracardinal veins continue as the azygous and hemiazygous veins; the iliac veins are derived from the persistent posterior cardinal veins. AN = anastomosis, V = vein.
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IVC anomalies reflect an abnormal regression or persistence of the various embryonic veins (3). 
Although most anomalies are asymptomatic (4) and are encountered incidentally, their correct identification is useful in the planning of vascular interventions and prevents their being mistaken for disease.
Left IVC
Left IVC has a prevalence of 0.2%–0.5% (1) and represents a persistent left supracardinal vein. The right supracardinal vein regresses in these cases, resulting in a mirror image variant. A left-sided IVC typically joins the left renal vein, and together they course anterior to the aorta to join the normal (right-sided) IVC (Fig 2). A left-sided IVC per se is of no clinical importance. However, it may be mistaken for left paraaortic adenopathy (5), complicate surgical repair of an aortic aneurysm (6), and cause difficulty in placing an infrarenal IVC filter with a transjugular approach (3).
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Figure 2. Left IVC. Coronal curved reformatted CT image shows a left-sided IVC (large arrow) joining the left renal vein (small arrow), which unites with the right renal vein to form a normal right-sided suprarenal IVC.
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Double IVC
Double (right and left) IVC has a prevalence of 1%–3% and results from persistence of both the right and left supracardinal veins (1). Typically, the left IVC drains into the left renal vein, which then joins the right IVC (Fig 3). There may be significant discrepancy in the size of the two veins. Double IVC has clinical implications that are similar to those of left IVC and may be mistaken for adenopathy, especially if contrast enhancement of the vein is poor due to technical reasons or thrombosis (7). Double IVC should be suspected in cases of recurrent episodes of pulmonary embolism despite placement of an IVC filter (1). There are only a few reports describing the technique of filter placement in patients with venous thrombosis and double IVC. The options vary from placing a single filter in the common suprarenal IVC (8), to infrarenal filter placement in the IVC on each side (9), to steel coil embolization of the smaller IVC coupled with filter placement in the contralateral IVC (10).
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Figure 3a. Double IVC. (a) Contrast material–enhanced caudocranial CT scan shows right and left infrarenal IVCs (arrows). (b) Contrast-enhanced caudocranial CT scan shows the left IVC opening into the left renal vein (arrow), which crosses anterior to the aorta to form a single right-sided suprarenal IVC.
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Figure 3b. Double IVC. (a) Contrast material–enhanced caudocranial CT scan shows right and left infrarenal IVCs (arrows). (b) Contrast-enhanced caudocranial CT scan shows the left IVC opening into the left renal vein (arrow), which crosses anterior to the aorta to form a single right-sided suprarenal IVC.
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Retrocaval Ureter
Retrocaval ureter is one of the few congenital anomalies of the IVC that can be symptomatic (4). Unlike other congenital ureteral obstructions, this embryologic defect lies in the developing vena cava rather than the ureter. In this condition, the infrarenal IVC develops from the right posterior cardinal vein, which lies anterior and lateral to the ureter—unlike the normal situation, in which the IVC is formed by the right supracardinal vein, located posterior and medial to the ureter. As a result, part of the right ureter becomes trapped posterior and medial to the IVC. En route, the ureter can undergo significant compression, resulting in hydronephrosis or recurrent urinary tract infections (3). The diagnosis can be made at intravenous urography, which reveals the abnormal course of the proximal ureter as it projects over or medial to the lumbar pedicles on frontal images with proximal hydronephrosis, resulting in the characteristic "fish hook" or "reverse J" appearance (11). CT elegantly depicts the abnormal course of the ureter. Treatment consists of surgical relocation of the ureter anterior to the IVC (1).
Absence of the Infrarenal IVC
Complete absence of the infrarenal IVC with preservation of the suprarenal segment is an extremely rare anomaly (Fig 4) (12). This condition may be a sequela of intrauterine or perinatal thrombosis of the IVC and not truly embryologic in origin (13,14). Affected patients are prone to develop deep venous thrombosis (15) and chronic venous insufficiency (14,16). Lower-extremity venous return in these patients occurs via the ascending lumbar veins, which drain into the azygous-hemiazygous system. Enlarged collateral vessels may simulate a paraspinal mass (13).
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Figure 4a. IVC agenesis. Axial contrast-enhanced CT scan (a) and sagittal curved reformatted CT image (b) show absence of the infrarenal IVC. Note the prominent ascending lumbar veins (arrows in a) and the patent suprarenal IVC (arrow in b).
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Figure 4b. IVC agenesis. Axial contrast-enhanced CT scan (a) and sagittal curved reformatted CT image (b) show absence of the infrarenal IVC. Note the prominent ascending lumbar veins (arrows in a) and the patent suprarenal IVC (arrow in b).
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Retroaortic and Circumaortic Left Renal Vein
Anomalies of the renal segment of the IVC include variants of the left renal vein. Normally, the left renal vein is derived from the intersubcardinal anastomoses, which course anterior to the aorta (2). The left renal vein is retroaortic in 1.7%–3.4% of individuals (Fig 5) and occurs when the vein derives from the intersupracardinal veins, which lie posterior to the aorta. Persistence of both the intersupracardinal and intersubcardinal veins results in a circumaortic venous ring, with one vein coursing anterior and the other posterior to the aorta (prevalence, 2.4%–8.7%) (Fig 6) (4). The posteriorly located renal vein is caudad with respect to the preaortic vein (4). These renal vein anomalies assume significance in the preoperative planning of nephrectomy and can be misdiagnosed as adenopathy (3). On rare occasions, compression of the renal vein as it courses posterior to the aorta (nutcracker phenomenon) can result in periureteric varices, hypertension, and hematuria (Fig 5) (17).
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Figure 5a. Retroaortic left renal vein causing hypertension and hematuria in a 45-year-old woman. (a) Contrast-enhanced CT scan shows compression of the left renal vein as it courses posterior to the aorta (arrow) ("nutcracker phenomenon"), along with prominent periureteric collateral vessels (*). (b) Volume-rendered image (anterolateral view) shows the left renal vein (arrows) coursing posterior to the aorta (A), with a prominent periureteric collateral vessel (arrowhead) draining into the portosplenic confluence. P = portal vein, S = splenic vein.
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Figure 5b. Retroaortic left renal vein causing hypertension and hematuria in a 45-year-old woman. (a) Contrast-enhanced CT scan shows compression of the left renal vein as it courses posterior to the aorta (arrow) ("nutcracker phenomenon"), along with prominent periureteric collateral vessels (*). (b) Volume-rendered image (anterolateral view) shows the left renal vein (arrows) coursing posterior to the aorta (A), with a prominent periureteric collateral vessel (arrowhead) draining into the portosplenic confluence. P = portal vein, S = splenic vein.
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Figure 6a. Circumaortic left renal vein in a 47-year-old patient with right renal cell carcinoma. Contrast-enhanced craniocaudal CT scans show the left renal vein coursing anterior (arrow in a) and posterior (arrow in b) to the aorta.
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Figure 6b. Circumaortic left renal vein in a 47-year-old patient with right renal cell carcinoma. Contrast-enhanced craniocaudal CT scans show the left renal vein coursing anterior (arrow in a) and posterior (arrow in b) to the aorta.
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Interruption of the IVC with Azygous or Hemiazygous Continuation
Interruption of the IVC with azygous or hemiazygous continuation results from failed formation of the right subcardinal-hepatic anastomosis, with consequent atrophy of the subcardinal vein (suprarenal IVC) (3). The infrarenal IVC continues as the azygous vein and, in cases of left IVC, as the hemiazygous vein (Fig 7) (4). Associated situs anomalies are present in many of these cases. It is important not to misinterpret the enlarged azygous or hemiazygous veins as adenopathy (18). Preoperative knowledge of this anomaly is important in planning cardiopulmonary bypass surgery and can help avoid difficulties in cardiac catheterization (19).
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Figure 7. IVC interruption with hemiazygous continuation. Contrast-enhanced CT scan shows hemiazygous continuation (arrow) of a left-sided IVC (not shown). Associated findings of a midline liver and a portion of the stomach (S) in the right upper quadrant are suggestive of situs ambiguous.
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Portocaval Shunt
Congenital extrahepatic portocaval shunt is a rare anomaly (20). Two types have been described (21): Type I shunt is a complete end-to-side shunt between the portal vein and the IVC, with the main portal vein distal to the shunt being absent (Fig 8); type II shunt is a partial side-to-side shunt between the portal vein and the IVC. Both types result in metabolic derangements and often have associated cardiac, renal, skeletal, or other anomalies (20). Regenerative benign liver nodules are commonly seen in these patients and have been attributed to hepatic ischemia with a compensatory increase in hepatic arterial flow (22). Liver transplantation is the only definitive treatment for type I shunt, whereas treatment of patients with type II shunt is simpler (ligation or coil embolization of the shunt vessel) (20). Congenital intrahepatic shunts between the portal vein branches and the IVC have also been described and can cause hepatic encephalopathy (23).
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Figure 8. Portocaval shunt in a 6-year-old girl with elevated serum ammonia levels. Axial balanced steady-state (true fast imaging with steady-state precession [FISP]) MR image shows complete end-to-side fistulous communication (arrow) between the portal vein and the IVC.
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Membranous Obstruction of the Intrahepatic IVC
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Membranous obstruction of the intrahepatic IVC accounts for most cases of primary BCS in India, Nepal, South Africa, Japan, China, and Korea (24). It is typically a disease of adulthood with an insidious onset and a chronic course that eventually leads to congestive cirrhosis (24,25). In contrast, in most Western nations, BCS results from hepatic venous thrombosis due to an underlying prothrombotic state, has an acute onset, and is often fatal. The cause of membranous obstruction of the intrahepatic IVC remains unclear in the majority of cases; however, evidence is mounting that it is a sequela of IVC thrombosis (26,27). Color Doppler flow US, CT, MR imaging, hepatic venography, and cavography are used in the imaging of IVC obstruction. The imaging appearance of membranous obstruction of the intrahepatic IVC ranges from a short weblike narrowing to a longer segmental occlusion with or without narrowing of the hepatic veins. Intrahepatic venovenous, portocaval, and spider web collateral vessels develop to decompress the liver parenchyma (Fig 9) (28). The inferior (accessory) right hepatic vein (when present) serves as an important draining channel for the intrahepatic collateral vessels (Fig 10). Extrahepatic collateral vessels commonly seen in membranous obstruction of the intrahepatic IVC include the ascending lumbar veins, which drain into the azygous vein on the right side and the hemiazygous vein on the left (Fig 10). Flow may also be directed via the left renal-hemiazygous collateral pathway (Fig 11), inferior phrenicpericardiophrenic collateral vessels, extrahepatic portosystemic collateral vessels, and superficial collateral vessels of the abdominal wall (29). Occasionally, these venous collateral vessels may form a large varix (Fig 11), which can simulate a mass on poorly enhanced images. Because the caudate lobe drains directly into the IVC, it is least affected in BCS and most commonly undergoes hypertrophy (80% of cases) (Fig 9) (30). An enlarged caudate vein measuring over 2 mm is seen in 50% of cases and was recently reported to be a specific sign of BCS (Fig 9) (31). Caudate lobe hypertrophy is not specific for BCS; it can also be seen in patients with cirrhosis and extrahepatic portal venous obstruction (32). An enlarged caudate lobe from any cause may also result in a long-segment smooth extrinsic impression on the IVC, which is distinct from the intrinsic narrowing of the cavoatrial junction seen in membranous obstruction of the intrahepatic IVC.
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Figure 9a. Membranous obstruction of the intrahepatic IVC in a 30-year-old woman who presented with abdominal pain and distention of 3 years duration. (a) Sagittal oblique US image shows tapered occlusion of the IVC at the cavoatrial junction (arrowhead). (b) Color Doppler US image shows cardiofugal flow in the IVC with loss of transmitted cardiac pulsations. (c) Color Doppler US image shows associated ostial narrowing of the hepatic veins (arrows), along with multiple intrahepatic collateral vessels. (d) Color Doppler US image shows a hypertrophic caudate lobe, with a prominent caudate vein (arrow) draining into the IVC.
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Figure 9b. Membranous obstruction of the intrahepatic IVC in a 30-year-old woman who presented with abdominal pain and distention of 3 years duration. (a) Sagittal oblique US image shows tapered occlusion of the IVC at the cavoatrial junction (arrowhead). (b) Color Doppler US image shows cardiofugal flow in the IVC with loss of transmitted cardiac pulsations. (c) Color Doppler US image shows associated ostial narrowing of the hepatic veins (arrows), along with multiple intrahepatic collateral vessels. (d) Color Doppler US image shows a hypertrophic caudate lobe, with a prominent caudate vein (arrow) draining into the IVC.
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Figure 9c. Membranous obstruction of the intrahepatic IVC in a 30-year-old woman who presented with abdominal pain and distention of 3 years duration. (a) Sagittal oblique US image shows tapered occlusion of the IVC at the cavoatrial junction (arrowhead). (b) Color Doppler US image shows cardiofugal flow in the IVC with loss of transmitted cardiac pulsations. (c) Color Doppler US image shows associated ostial narrowing of the hepatic veins (arrows), along with multiple intrahepatic collateral vessels. (d) Color Doppler US image shows a hypertrophic caudate lobe, with a prominent caudate vein (arrow) draining into the IVC.
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Figure 9d. Membranous obstruction of the intrahepatic IVC in a 30-year-old woman who presented with abdominal pain and distention of 3 years duration. (a) Sagittal oblique US image shows tapered occlusion of the IVC at the cavoatrial junction (arrowhead). (b) Color Doppler US image shows cardiofugal flow in the IVC with loss of transmitted cardiac pulsations. (c) Color Doppler US image shows associated ostial narrowing of the hepatic veins (arrows), along with multiple intrahepatic collateral vessels. (d) Color Doppler US image shows a hypertrophic caudate lobe, with a prominent caudate vein (arrow) draining into the IVC.
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Figure 10a. Membranous obstruction of the intrahepatic IVC in a 25-year-old patient who had experienced repeated episodes of hematemesis. Sagittal (a) and coronal (b) balanced steady-state (true FISP) MR images show segmental occlusion of the IVC at the cavoatrial junction (large arrow in a) with enlarged pericardiophrenic veins (small arrow in a), anterior abdominal wall collateral vessels (arrowhead in a), a dilated inferior (accessory) hepatic vein (small arrow in b), and an enlarged azygous vein draining into the superior vena cava (large arrow in b). The dilated portal vein (p), ascites, and gross splenomegaly are suggestive of portal hypertension.
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Figure 10b. Membranous obstruction of the intrahepatic IVC in a 25-year-old patient who had experienced repeated episodes of hematemesis. Sagittal (a) and coronal (b) balanced steady-state (true FISP) MR images show segmental occlusion of the IVC at the cavoatrial junction (large arrow in a) with enlarged pericardiophrenic veins (small arrow in a), anterior abdominal wall collateral vessels (arrowhead in a), a dilated inferior (accessory) hepatic vein (small arrow in b), and an enlarged azygous vein draining into the superior vena cava (large arrow in b). The dilated portal vein (p), ascites, and gross splenomegaly are suggestive of portal hypertension.
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Figure 11a. Membranous obstruction of the intrahepatic IVC in a 34-year-old patient with abdominal distention. (a) Cavogram shows occlusion of the intrahepatic IVC with retrograde enhancement of the left renal vein (arrow), as well as a large venous pouch (*) with faint enhancement of the hemiazygous vein (arrowhead). (b) Coronal balanced steady-state (true FISP) MR image shows the large venous pouch (large arrow) and a prominent, tortuous azygous vein (small arrow).
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Figure 11b. Membranous obstruction of the intrahepatic IVC in a 34-year-old patient with abdominal distention. (a) Cavogram shows occlusion of the intrahepatic IVC with retrograde enhancement of the left renal vein (arrow), as well as a large venous pouch (*) with faint enhancement of the hemiazygous vein (arrowhead). (b) Coronal balanced steady-state (true FISP) MR image shows the large venous pouch (large arrow) and a prominent, tortuous azygous vein (small arrow).
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As a result of outflow tract obstruction, portal venous flow becomes sluggish or even reversed, resulting in thrombosis in 10%–20% of patients (30). In acute BCS, the central regions of the liver, including the caudate lobe and part of the left lobe, enhance normally and appear hyper-enhancing relative to the peripheral liver, which shows decreased enhancement. Later, as the contrast medium washes out of the central portion of the liver and accumulates peripherally, the central region appears relatively hypoenhancing (flip-flop pattern of enhancement). In chronic BCS, liver parenchymal enhancement is more variable, being heterogeneous in the early phase and becoming more uniform over time (33).
The association between membranous obstruction of the intrahepatic IVC and hepatocellular carcinoma (HCC) is well established as varying greatly between geographic regions: 40%–48% in South Africa (in the black population) (34,35), 41% in Japan (36), 11% in India, and 4.7% in Nepal (24,37). It is postulated that hepatic congestion causing centrilobular necrosis and perpetual regenerative activity, in conjunction with an as yet unidentified hepatocarcinogen prevalent in these geographic regions, underlies the development of HCC in these patients (24,25).
The diagnosis of HCC in patients with BCS is not straightforward, since these patients are also known to develop regenerative nodules with overlapping imaging features (38,39). Regenerative nodules are observed at pathologic examination in 60%–80% of patients with BCS (40,41) and are thought to result from a decrease in portal venous flow (42). Because most lesions are small, only a few are identified at imaging (39). They are typically multiple, hyperattenuating at unenhanced CT, hyperintense at T1-weighted MR imaging, iso- or hypointense at T2-weighted MR imaging, and uniformly enhancing in the arterial phase (Fig 12).
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Figure 12a. Membranous obstruction of the intrahepatic IVC with regenerative nodules. (a) Sagittal true FISP MR image reveals occlusion of the IVC (arrow). (b–d) T1-weighted (b), T2-weighted (c), and gadolinium benzyloxypropionic tetraacetate (Gd-BOPTA)–enhanced (d) MR images show multiple focal liver lesions, which are hyperintense in b, are hypointense in c, and show prominent arterial enhancement in d. Arrow in b indicates a central scar, which is a characteristic feature of benign hepatic nodules. (e) MR image shows the uptake and retention of Gd-BOPTA that had been administered 1 hour earlier, a finding that indicates the presence of hepatocytes and delayed clearance of bile. Arrow indicates the central scar.
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Figure 12b. Membranous obstruction of the intrahepatic IVC with regenerative nodules. (a) Sagittal true FISP MR image reveals occlusion of the IVC (arrow). (b–d) T1-weighted (b), T2-weighted (c), and gadolinium benzyloxypropionic tetraacetate (Gd-BOPTA)–enhanced (d) MR images show multiple focal liver lesions, which are hyperintense in b, are hypointense in c, and show prominent arterial enhancement in d. Arrow in b indicates a central scar, which is a characteristic feature of benign hepatic nodules. (e) MR image shows the uptake and retention of Gd-BOPTA that had been administered 1 hour earlier, a finding that indicates the presence of hepatocytes and delayed clearance of bile. Arrow indicates the central scar.
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Figure 12c. Membranous obstruction of the intrahepatic IVC with regenerative nodules. (a) Sagittal true FISP MR image reveals occlusion of the IVC (arrow). (b–d) T1-weighted (b), T2-weighted (c), and gadolinium benzyloxypropionic tetraacetate (Gd-BOPTA)–enhanced (d) MR images show multiple focal liver lesions, which are hyperintense in b, are hypointense in c, and show prominent arterial enhancement in d. Arrow in b indicates a central scar, which is a characteristic feature of benign hepatic nodules. (e) MR image shows the uptake and retention of Gd-BOPTA that had been administered 1 hour earlier, a finding that indicates the presence of hepatocytes and delayed clearance of bile. Arrow indicates the central scar.
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Figure 12d. Membranous obstruction of the intrahepatic IVC with regenerative nodules. (a) Sagittal true FISP MR image reveals occlusion of the IVC (arrow). (b–d) T1-weighted (b), T2-weighted (c), and gadolinium benzyloxypropionic tetraacetate (Gd-BOPTA)–enhanced (d) MR images show multiple focal liver lesions, which are hyperintense in b, are hypointense in c, and show prominent arterial enhancement in d. Arrow in b indicates a central scar, which is a characteristic feature of benign hepatic nodules. (e) MR image shows the uptake and retention of Gd-BOPTA that had been administered 1 hour earlier, a finding that indicates the presence of hepatocytes and delayed clearance of bile. Arrow indicates the central scar.
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Figure 12e. Membranous obstruction of the intrahepatic IVC with regenerative nodules. (a) Sagittal true FISP MR image reveals occlusion of the IVC (arrow). (b–d) T1-weighted (b), T2-weighted (c), and gadolinium benzyloxypropionic tetraacetate (Gd-BOPTA)–enhanced (d) MR images show multiple focal liver lesions, which are hyperintense in b, are hypointense in c, and show prominent arterial enhancement in d. Arrow in b indicates a central scar, which is a characteristic feature of benign hepatic nodules. (e) MR image shows the uptake and retention of Gd-BOPTA that had been administered 1 hour earlier, a finding that indicates the presence of hepatocytes and delayed clearance of bile. Arrow indicates the central scar.
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It is crucial to differentiate benign nodules from HCC in these patients. HCC is more likely to manifest as lesions of different sizes with internal heterogeneity, encapsulation, and portal or hepatic venous invasion (Fig 13) (38). On the other hand, T1 hyperintensity, T2 hypointensity, and a central scar are more suggestive of benign lesions (Fig 12) (38,39). The use of gadobenate dimeglumine increases diagnostic confidence because, unlike most HCCs, benign nodules appear hyperintense relative to normal liver in the delayed hepatocyte-specific phase (Figs 12, 13) (38).
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Figure 13a. Membranous obstruction of the intrahepatic IVC with HCC in a 55-year-old noncirrhotic woman who presented with abdominal pain and markedly elevated  -fetoprotein levels. (a) Sagittal true FISP MR image shows a short weblike narrowing of the IVC (large arrow) with pericardiophrenic collateral vessels (small arrow). The mass was heterogeneously enhancing in the arterial phase. (b–d) The mass is hypointense on a T1-weighted MR image (b), is hyperintense on a T2-weighted MR image (c), and does not show Gd-BOPTA uptake on a delayed hepatocyte-specific phase MR image (d). The portal vein flow void is replaced by tumor thrombus (arrow in b and c).
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Figure 13b. Membranous obstruction of the intrahepatic IVC with HCC in a 55-year-old noncirrhotic woman who presented with abdominal pain and markedly elevated -fetoprotein levels. (a) Sagittal true FISP MR image shows a short weblike narrowing of the IVC (large arrow) with pericardiophrenic collateral vessels (small arrow). The mass was heterogeneously enhancing in the arterial phase. (b–d) The mass is hypointense on a T1-weighted MR image (b), is hyperintense on a T2-weighted MR image (c), and does not show Gd-BOPTA uptake on a delayed hepatocyte-specific phase MR image (d). The portal vein flow void is replaced by tumor thrombus (arrow in b and c).
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Figure 13c. Membranous obstruction of the intrahepatic IVC with HCC in a 55-year-old noncirrhotic woman who presented with abdominal pain and markedly elevated -fetoprotein levels. (a) Sagittal true FISP MR image shows a short weblike narrowing of the IVC (large arrow) with pericardiophrenic collateral vessels (small arrow). The mass was heterogeneously enhancing in the arterial phase. (b–d) The mass is hypointense on a T1-weighted MR image (b), is hyperintense on a T2-weighted MR image (c), and does not show Gd-BOPTA uptake on a delayed hepatocyte-specific phase MR image (d). The portal vein flow void is replaced by tumor thrombus (arrow in b and c).
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Figure 13d. Membranous obstruction of the intrahepatic IVC with HCC in a 55-year-old noncirrhotic woman who presented with abdominal pain and markedly elevated -fetoprotein levels. (a) Sagittal true FISP MR image shows a short weblike narrowing of the IVC (large arrow) with pericardiophrenic collateral vessels (small arrow). The mass was heterogeneously enhancing in the arterial phase. (b–d) The mass is hypointense on a T1-weighted MR image (b), is hyperintense on a T2-weighted MR image (c), and does not show Gd-BOPTA uptake on a delayed hepatocyte-specific phase MR image (d). The portal vein flow void is replaced by tumor thrombus (arrow in b and c).
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Bland Thrombus and Intracaval Tumors
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Bland thrombus, which is the leading cause of IVC obstruction, typically originates in the lower extremities or the pelvis (29). Affected patients often have an underlying predisposing condition such as dehydration, sepsis, localized inflammation, pelvic inflammatory disease, coagulopathy, congestive heart failure, immobility, or trauma (29). Intracaval extension of benign tumors is an extremely rare occurrence that has been reported in renal angiomyolipoma and adrenal pheochromocytoma (43,44). Very rarely, malignant or even benign pheochromocytoma can extend into the IVC. Benign tumor extends via the adrenal veins, whereas malignant pheochromocytoma directly invades the caval wall (44,45).
Intravenous leiomyomatosis is a smooth muscle tumor that either arises in the uterine veins or represents intravenous invasion by a uterine fibroma (46–48). Although this tumor is usually confined to the pelvic veins, it can have intracaval or even intracardiac extension. Despite being histologically benign, its potential to result in distant metastases betrays its malignant nature (48). Intravenous leiomyomatosis is strictly confined to females of reproductive age, the majority of whom either harbor uterine leiomyoma or have undergone hysterectomy for this disease entity in the past (46). Tumor thrombus seen at imaging is nonspecific and indistinguishable from primary caval leiomyosarcoma. However, imaging depicts the extent of the tumor, information that is crucial for surgical planning.
Leiomyosarcoma is the most common primary malignant tumor of the IVC, most frequently affecting women in the 5th and 6th decades of life (49). Symptomatology and surgical resectability are both dependent on the location of the tumor.The majority arise in the middle (50.8% of cases) or lower (44.2%) third of the IVC (49). Leiomyosarcoma of the upper third of the IVC is rare (4.2% of cases) and is least amenable to surgical resection. The tumor can be completely intraluminal or can have both extra- and intraluminal components (Fig 14) and has a poor prognosis (49). Apart from a primary IVC tumor, leiomyosarcoma arising in the retroperitoneum can secondarily invade the IVC, a peculiar growth pattern not seen in other retroperitoneal sarcomas (50).
Contiguous tumor extension directly into the IVC is common in renal cell carcinoma (Fig 15), HCC, adrenocortical carcinoma (Fig 16), and Wilms tumor (Fig 17) (51). Expansion of the vessel lumen and enhancement of the filling defect help differentiate malignant from bland thrombus (29,51). Malignant thrombi in the IVC are often clinically asymptomatic, although occasionally they can result in BCS (51,52) and can embolize into the pulmonary circulation (51). Especially in renal cell carcinoma, tumor thrombi show little tendency to invade the venous wall, allowing complete surgical removal in most cases. Imaging findings dictate the surgical technique: Thrombus extension into the supradiaphragmatic IVC requires cardiopulmonary bypass surgery and is associated with increased morbidity and mortality rates (51) In the unlikely event of tumor thrombus infiltrating the venous wall, segmental resection of the IVC becomes essential (53). Unfortunately, involvement of the venous wall is difficult to assess at imaging and is usually diagnosed only at surgical exploration (53).
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Figure 15. Renal cell carcinoma with tumor thrombus in the left renal vein and IVC. Coronal true FISP MR image shows a large, mildly hyperintense left renal mass with tumor thrombus distending the left renal vein (*) and suprarenal IVC (arrow). The cranial extent of the thrombus is well seen. Thrombus is also seen in the infrarenal IVC (arrowhead) but is not distending the lumen, findings that suggest bland thrombus.
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Figure 16. Adrenocortical carcinoma with IVC invasion. Axial T2-weighted MR image reveals a large, heterogeneous right adrenal mass with tumor thrombus and anteromedial displacement of the IVC (arrow).
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Figure 17a. Wilms tumor with pulmonary embolism in a 3-year-old child. (a) Contrast-enhanced CT scan shows a large, heterogeneous left renal mass with tumor thrombus distending the renal vein (black arrow) and extending into the IVC (white arrow). (b) Contrast-enhanced CT scan shows cranial extension of the tumor into the right atrium and across the tricuspid valve (arrow). The patient died 2 days later, possibly due to massive embolism or tumor occlusion of the tricuspid valve orifice.
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Figure 17b. Wilms tumor with pulmonary embolism in a 3-year-old child. (a) Contrast-enhanced CT scan shows a large, heterogeneous left renal mass with tumor thrombus distending the renal vein (black arrow) and extending into the IVC (white arrow). (b) Contrast-enhanced CT scan shows cranial extension of the tumor into the right atrium and across the tricuspid valve (arrow). The patient died 2 days later, possibly due to massive embolism or tumor occlusion of the tricuspid valve orifice.
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Trauma
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In blunt trauma patients, a flattened IVC at multiple levels is a strong indicator of hypovolemia or hypotension and may signify impending cardiovascular collapse (Fig 18) (54). A flat IVC together with (a) a decreased caliber of the aorta, (b) marked diffuse bowel distention, (c) moderate to extensive hemoperitoneum, and (d) hyperenhancement of the bowel wall, kidneys, and pancreas constitutes the "hypoperfusion complex" seen at abdominal CT in blunt trauma patients (55). On the other hand, a CT finding of a flat IVC in patients without trauma usually does not signify hypotension, and only a few of these patients have evidence of hypovolemia (56). Traumatic laceration of the IVC with herniation of intraabdominal fat or the presence of intravascular gas is a rare but striking finding in trauma victims (Fig 19) (57,58).
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Figure 18. Flat IVC in a 47-year-old man who had been involved in a traffic accident. Contrast-enhanced CT scan reveals a collapsed IVC (black arrow). A collapsed aorta and gross hemoperitoneum (white arrow) are other indicators of hypoperfusion.
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Figure 19. Posttraumatic air in the IVC in a 29-year-old man who had sustained blunt trauma to the abdomen. CT scan shows hemoperitoneum (arrow) with air forming a level in the IVC (*). The patient succumbed to his injuries.
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Early Enhancement of the IVC
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Early enhancement of the IVC with dense undiluted contrast material can be due to reflux from the right atrium, aortocaval fistula, superior vena cava obstruction, or arteriovenous shunting in hypervascular liver tumors.
Retrograde contrast enhancement of the IVC at a low injection rate (<3 mL/sec) is a highly specific although insensitive CT sign of right-sided heart diseases such as tricuspid regurgitation, pulmonary hypertension, and right ventricular systolic dysfunction (Fig 20) (59). The predictive value of this sign diminishes at a higher injection rate (>3 mL/sec), since contrast material can then reflux from the right atrium into the IVC even in the absence of heart disease (Fig 21) (59).
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Figure 20. Retrograde contrast enhancement of the IVC in a 34-year-old woman with primary pulmonary hypertension and right-sided heart failure. Coronal maximum-intensity-projection image reveals dense undiluted contrast material in the IVC and hepatic veins. Note the dilatation of the central pulmonary arteries, right atrium, and IVC, all of which are manifestations of the patient’s conditions. The filling defect in the IVC simulating thrombus (arrow) is artifactual and was not seen in the venous phase.
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Figure 21. Retrograde contrast enhancement of the IVC in a 62-year-old man with normal cardiac function. Coronal maximum-intensity-projection reformatted image from CT angiographic data obtained at a high injection rate (4.5 mL/sec) shows the reflux of dense contrast material from the right atrium into the IVC and hepatic veins (arrows). Poor mixing between the unenhanced stream of blood in the IVC and the refluxed contrast material results in a filling defect (*) that may simulate thrombus, especially on axial images and in the absence of venous phase images, on which such artifactual lesions usually resolve.
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On rare occasions, abdominal aortic aneurysm can erode into and form a fistulous communication with the IVC (prevalence, 0.2%–0.9%) (60). The rarity of this complication makes clinical diagnosis difficult unless the classic symptoms of abdominal pain, palpable aneurysm, and continuous bruit are present. Noninvasive imaging modalities including contrast-enhanced MR imaging and CT angiography are preferred over catheter angiography for the diagnosis of aortocaval fistula. Key imaging findings include the presence of an aortic aneurysm with early detection of dense contrast material in the dilated IVC (Fig 22). The actual site of fistulous communication, represented by the loss of normal anatomic space between the aorta and the IVC, is often unclear at imaging (61). MR imaging has an advantage over CT in that many patients with aortocaval fistula have renal insufficiency, which discourages the use of iodinated contrast material (61). Time-of-flight MR angiography also helps in making the diagnosis by revealing persistent flow in the IVC despite the use of inferior saturation bands to eliminate venous inflow signal (61). Untreated aortocaval fistula is invariably fatal, but prompt diagnosis and surgical intervention can be life saving in many of these patients (62).
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Figure 22a. Aortocaval fistula in a 67-year-old man with rapid onset of dyspnea and pedal edema. (a) Coronal reformatted CT image shows a large, infrarenal saccular aortic aneurysm (*) with aortocaval fistulous communication (arrow), resulting in simultaneous enhancement of the aorta (A) and IVC (V). The infrarenal IVC is compressed and displaced by the aneurysm. (b) CT scan shows the reflux of dense contrast material into the hepatic veins (small white arrows), abdominal wall collateral vessels (large white arrows), and azygous-hemiazygous veins (black arrows). The intrahepatic IVC is dilated, and bilateral pleural effusion due to congestive heart failure is also seen.
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Figure 22b. Aortocaval fistula in a 67-year-old man with rapid onset of dyspnea and pedal edema. (a) Coronal reformatted CT image shows a large, infrarenal saccular aortic aneurysm (*) with aortocaval fistulous communication (arrow), resulting in simultaneous enhancement of the aorta (A) and IVC (V). The infrarenal IVC is compressed and displaced by the aneurysm. (b) CT scan shows the reflux of dense contrast material into the hepatic veins (small white arrows), abdominal wall collateral vessels (large white arrows), and azygous-hemiazygous veins (black arrows). The intrahepatic IVC is dilated, and bilateral pleural effusion due to congestive heart failure is also seen.
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The various collateral pathways seen in superior vena cava obstruction can result in early enhancement of the IVC. Collateral vessels following the azygous-hemiazygous and vertebral venous plexus routes drain directly into the IVC. Collateral vessels arising from the internal mammary and lateral thoracic veins drain first into the portal vein (cavoportal collateral route), resulting in abnormal liver enhancement, and then via the hepatic veins into the IVC (Fig 23). Two cavoportal pathways have been described (63–65):
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Figure 23a. Cavoportal collateral pathways in a 53-year-old man with lung carcinoma. (a) Contrast-enhanced CT scan shows a large anterior mediastinal mass causing superior vena cava obstruction (arrow). The azygous vein is dilated (arrowhead). (b) Contrast-enhanced CT scan shows paraumbilical collateral vessels (white arrow) that communicate with the left branch of the portal vein (black arrow), resulting in abnormal enhancement of the left hepatic lobe (*). (c) Contrast-enhanced CT scan shows collateral vessels that connect with the subcapsular branches of the portal vein (arrow), resulting in abnormal enhancement of the left lobe and segment VII of the liver with early enhancement of the right hepatic vein (arrowhead) and IVC (*).
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Figure 23b. Cavoportal collateral pathways in a 53-year-old man with lung carcinoma. (a) Contrast-enhanced CT scan shows a large anterior mediastinal mass causing superior vena cava obstruction (arrow). The azygous vein is dilated (arrowhead). (b) Contrast-enhanced CT scan shows paraumbilical collateral vessels (white arrow) that communicate with the left branch of the portal vein (black arrow), resulting in abnormal enhancement of the left hepatic lobe (*). (c) Contrast-enhanced CT scan shows collateral vessels that connect with the subcapsular branches of the portal vein (arrow), resulting in abnormal enhancement of the left lobe and segment VII of the liver with early enhancement of the right hepatic vein (arrowhead) and IVC (*).
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Figure 23c. Cavoportal collateral pathways in a 53-year-old man with lung carcinoma. (a) Contrast-enhanced CT scan shows a large anterior mediastinal mass causing superior vena cava obstruction (arrow). The azygous vein is dilated (arrowhead). (b) Contrast-enhanced CT scan shows paraumbilical collateral vessels (white arrow) that communicate with the left branch of the portal vein (black arrow), resulting in abnormal enhancement of the left hepatic lobe (*). (c) Contrast-enhanced CT scan shows collateral vessels that connect with the subcapsular branches of the portal vein (arrow), resulting in abnormal enhancement of the left lobe and segment VII of the liver with early enhancement of the right hepatic vein (arrowhead) and IVC (*).
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- Internal mammary or lateral thoracic veins communicate with periumbilical collateral vessels that drain into the left portal vein. This pathway results in abnormal enhancement of the left hepatic lobe around the fissure for the ligamentum teres hepatis (Fig 23).
- The internal mammary vein is directly connected with the inferior phrenic vein that communicates with the intrahepatic portal venous system via its capsular branches, resulting in hyperenhancement of the subdiaphragmatic portion and bare area of the liver (Fig 23).
Hepatic venous invasion occurs in up to 26% of cases of HCC (66) and can also result in early enhancement of the IVC due to arteriovenous shunting (Fig 24).
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Pitfalls in Imaging of the IVC
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Pitfalls in imaging of the IVC are primarily due to a flow-related phenomenon or partial volume averaging artifact. A pseudo filling defect due to a flow-related phenomenon is most often seen at the level of the renal veins in the corticomedullary or portal venous phase, since enhanced blood in the renal veins flows parallel to the unenhanced venous return from the lower part of the body (Fig 25). This artifact can be seen at both contrast-enhanced CT and contrast-enhanced MR imaging and usually resolves on the delayed postcontrast image, which is most reliable in distinguishing true thrombus from pseudothrombus (Fig 25) (67). Other MR imaging sequences, including a balanced steady-state gradient-echo (true FISP) sequence and T1- and T2-weighted sequences, are also prone to flow-related artifactual signal in the IVC at the level of the renal veins (Fig 25).
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Figure 25a. Pseudothrombus due to dense return from the renal veins in a patient with pheochromocytoma. (a) Gadolinium-enhanced corticomedullary phase T1-weighted MR image shows an apparent IVC filling defect. Arrow indicates pseudothrombus, * indicates pheochromocytoma. (b, c) Coronal reformatted image (b) shows dense return from the renal veins flowing along the IVC, and a nephrographic phase T1-weighted MR image (c) shows resolution of the filling defect, findings that confirm the artifactual nature of the lesion. * in c indicates pheochromocytoma. (d–f) Axial turbo spin-echo T2-weighted (d), gradient-echo T1-weighted (e), and true FISP (f) MR images show flow-related enhancement (arrow in d) and signal void due to phase dispersion (arrow in e and f) at the point where the two streams of blood with different velocities meet. * in d and f indicates pheochromocytoma.
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Figure 25b. Pseudothrombus due to dense return from the renal veins in a patient with pheochromocytoma. (a) Gadolinium-enhanced corticomedullary phase T1-weighted MR image shows an apparent IVC filling defect. Arrow indicates pseudothrombus, * indicates pheochromocytoma. (b, c) Coronal reformatted image (b) shows dense return from the renal veins flowing along the IVC, and a nephrographic phase T1-weighted MR image (c) shows resolution of the filling defect, findings that confirm the artifactual nature of the lesion. * in c indicates pheochromocytoma. (d–f) Axial turbo spin-echo T2-weighted (d), gradient-echo T1-weighted (e), and true FISP (f) MR images show flow-related enhancement (arrow in d) and signal void due to phase dispersion (arrow in e and f) at the point where the two streams of blood with different velocities meet. * in d and f indicates pheochromocytoma.
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Figure 25c. Pseudothrombus due to dense return from the renal veins in a patient with pheochromocytoma. (a) Gadolinium-enhanced corticomedullary phase T1-weighted MR image shows an apparent IVC filling defect. Arrow indicates pseudothrombus, * indicates pheochromocytoma. (b, c) Coronal reformatted image (b) shows dense return from the renal veins flowing along the IVC, and a nephrographic phase T1-weighted MR image (c) shows resolution of the filling defect, findings that confirm the artifactual nature of the lesion. * in c indicates pheochromocytoma. (d–f) Axial turbo spin-echo T2-weighted (d), gradient-echo T1-weighted (e), and true FISP (f) MR images show flow-related enhancement (arrow in d) and signal void due to phase dispersion (arrow in e and f) at the point where the two streams of blood with different velocities meet. * in d and f indicates pheochromocytoma.
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Figure 25d. Pseudothrombus due to dense return from the renal veins in a patient with pheochromocytoma. (a) Gadolinium-enhanced corticomedullary phase T1-weighted MR image shows an apparent IVC filling defect. Arrow indicates pseudothrombus, * indicates pheochromocytoma. (b, c) Coronal reformatted image (b) shows dense return from the renal veins flowing along the IVC, and a nephrographic phase T1-weighted MR image (c) shows resolution of the filling defect, findings that confirm the artifactual nature of the lesion. * in c indicates pheochromocytoma. (d–f) Axial turbo spin-echo T2-weighted (d), gradient-echo T1-weighted (e), and true FISP (f) MR images show flow-related enhancement (arrow in d) and signal void due to phase dispersion (arrow in e and f) at the point where the two streams of blood with different velocities meet. * in d and f indicates pheochromocytoma.
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Figure 25e. Pseudothrombus due to dense return from the renal veins in a patient with pheochromocytoma. (a) Gadolinium-enhanced corticomedullary phase T1-weighted MR image shows an apparent IVC filling defect. Arrow indicates pseudothrombus, * indicates pheochromocytoma. (b, c) Coronal reformatted image (b) shows dense return from the renal veins flowing along the IVC, and a nephrographic phase T1-weighted MR image (c) shows resolution of the filling defect, findings that confirm the artifactual nature of the lesion. * in c indicates pheochromocytoma. (d–f) Axial turbo spin-echo T2-weighted (d), gradient-echo T1-weighted (e), and true FISP (f) MR images show flow-related enhancement (arrow in d) and signal void due to phase dispersion (arrow in e and f) at the point where the two streams of blood with different velocities meet. * in d and f indicates pheochromocytoma.
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Figure 25f. Pseudothrombus due to dense return from the renal veins in a patient with pheochromocytoma. (a) Gadolinium-enhanced corticomedullary phase T1-weighted MR image shows an apparent IVC filling defect. Arrow indicates pseudothrombus, * indicates pheochromocytoma. (b, c) Coronal reformatted image (b) shows dense return from the renal veins flowing along the IVC, and a nephrographic phase T1-weighted MR image (c) shows resolution of the filling defect, findings that confirm the artifactual nature of the lesion. * in c indicates pheochromocytoma. (d–f) Axial turbo spin-echo T2-weighted (d), gradient-echo T1-weighted (e), and true FISP (f) MR images show flow-related enhancement (arrow in d) and signal void due to phase dispersion (arrow in e and f) at the point where the two streams of blood with different velocities meet. * in d and f indicates pheochromocytoma.
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The angulation and narrowing of the suprahepatic IVC just before it opens into the right atrium makes it prone to partial volume averaging artifacts at CT and MR imaging.Pseudolipoma of the IVC is a partial volume averaging artifact caused by juxtacaval fat above the caudate lobe, rather than a true intraluminal lesion (Fig 26) (51, 68). It has an association with cirrhosis, possibly because a shrunken right hepatic lobe not only tilts the IVC further but also accentuates pericaval fat collection (69). The morphologic appearance of pseudolipoma may vary with inspiratory effort (68). As in pseudolipoma, partial volume averaging of pericaval fluid can mimic bland thrombus of the IVC at axial imaging (Fig 27).
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Figure 26a. Pseudolipoma in a 46-year-old alcoholic patient with cirrhosis. (a) Axial T1-weighted MR image reveals a hyperintense lesion within the IVC (arrow), a finding that is suggestive of fat. (b) On a three-dimensional fat-suppressed volume-interpolated breath-hold T1-weighted MR image, the lesion (black arrow) mimics a filling defect. Note that the shape of the lesion and its location within the IVC are different on the two images, a feature that is typical of pseudolipoma. A widened gallbladder fossa is noted, along with subtle liver surface nodularity (white arrow) due to underlying cirrhosis.
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Figure 26b. Pseudolipoma in a 46-year-old alcoholic patient with cirrhosis. (a) Axial T1-weighted MR image reveals a hyperintense lesion within the IVC (arrow), a finding that is suggestive of fat. (b) On a three-dimensional fat-suppressed volume-interpolated breath-hold T1-weighted MR image, the lesion (black arrow) mimics a filling defect. Note that the shape of the lesion and its location within the IVC are different on the two images, a feature that is typical of pseudolipoma. A widened gallbladder fossa is noted, along with subtle liver surface nodularity (white arrow) due to underlying cirrhosis.
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Figure 27a. Pseudothrombus due to a pericaval fluid collection in a patient who had undergone cholecystectomy. Contrast-enhanced CT scans show a biloma (arrow in a) and fluid around the IVC mimicking thrombus (arrow in b).
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Figure 27b. Pseudothrombus due to a pericaval fluid collection in a patient who had undergone cholecystectomy. Contrast-enhanced CT scans show a biloma (arrow in a) and fluid around the IVC mimicking thrombus (arrow in b).
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Conclusions
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The IVC is host to a wide array of congenital anomalies and pathologic conditions. Imaging allows precise diagnosis of congenital variants and membranous obstruction of the intrahepatic IVC and is accurate in depicting the presence and extent of thrombus. Other imaging findings such as flat IVC and early enhancement of the IVC are useful in limiting the differential diagnosis. Radiologists should be aware of the various pitfalls of IVC imaging and able to differentiate true from pseudo filling defects.
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Footnotes
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Abbreviations: BCS = Budd-Chiari syndrome, FISP = fast imaging with steady-state precession, Gd-BOPTA = gadolinium benzyloxypropionic tetraacetate, HCC = hepatocellular carcinoma, IVC = inferior vena cava
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References
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Abstract
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