Imaging Evaluation of the Inferior Vena Cava
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.
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.
■ Identify IVC involvement in malignancy and its potential impact on surgical planning.
■ Describe the appearance of the IVC after intervention and in the context of trauma or infection.
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.
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).
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
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).
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 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).
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 left-sided 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).
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 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 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).
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.
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). Extraluminal 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 malignancy 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. 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).
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). 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 intra-atrial 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 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 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 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.
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).
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 transverse-to-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 two-thirds 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 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.
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 first-line modality if a caval pathologic condition is suspected, because Doppler US can be used to evaluate IVC thrombus without the risk of radiation exposure.
Recipient of a Certificate of Merit award for an education exhibit at the 2013 RSNA Annual Meeting.
For this journal-based SA-CME activity, the authors, editor, and reviewers have disclosed no relevant relationships.
- 1. . Imaging the inferior vena cava: a road less traveled. RadioGraphics 2008;28(3):669–689. Link, Google Scholar
- 2. . Imaging of the inferior vena cava with MDCT. AJR Am J Roentgenol 2007;189(5):1243–1251. Crossref, Medline, Google Scholar
- 3. . From the archives of the AFIP. Leiomyosarcoma of the retroperitoneum and inferior vena cava: radiologic-pathologic correlation. RadioGraphics 1992;12(6):1203–1220. Link, Google Scholar
- 4. . Spectrum of congenital anomalies of the inferior vena cava: cross-sectional imaging findings. RadioGraphics 2000;20(3):639–652. Link, Google Scholar
- 5. . Embryology, normal anatomy, and anomalies. In: Ferris EJ, Hipona FA, Kahn PC, Phillips E, Shapiro JH, eds. Venography of the inferior vena cava and its branches. Baltimore, Md: Williams & Wilkins, 1969; 1–32. Google Scholar
- 6. . Congenital absence of inferior vena cava. Eur J Vasc Surg 1993;7(2): 201–203. Crossref, Medline, Google Scholar
- 7. . Congenitally absent inferior vena cava presenting in adulthood with venous stasis and ulceration: a surgically treated case. J Vasc Surg 1996;23(1):141–146. Crossref, Medline, Google Scholar
- 8. . Complete absence of the inferior vena cava presenting as a paraspinous mass. Thorax 1980;35(10):798–800. Crossref, Medline, Google Scholar
- 9. . Absence of the infrarenal inferior vena cava with preservation of the suprarenal segment as revealed by CT and MR venography. AJR Am J Roentgenol 1999;172(6):1610–1612. Crossref, Medline, Google Scholar
- 10. . Congenital absence of inferior vena cava. J Belge Radiol 1990;73(6):516–517. Medline, Google Scholar
- 11. . Occult cancer in patients with deep venous thrombosis: a systematic approach. Cancer 1991;67(2):541–545. Crossref, Medline, Google Scholar
- 12. . Absence of hepatic segment of the inferior vena cava with azygous continuation. J Comput Assist Tomogr 1980;4(1):112–114. Crossref, Medline, Google Scholar
- 13. . Anomalous inferior vena cava with accessory hemiazygos continuation. Radiology 1976;119(1):51–54. Link, Google Scholar
- 14. . Accessory hemiazygos continuation of left inferior vena cava: CT demonstration. J Comput Assist Tomogr 1984;8(4):777–779. Crossref, Medline, Google Scholar
- 15. . Anomaly of the vena cava inferior; report of fatality after ligation. J Am Med Assoc 1951;146(14):1321–1322. Crossref, Medline, Google Scholar
- 16. . Membranous obstruction of the inferior vena cava and its causal relation to hepatocellular carcinoma. Liver Int 2006;26(1):1–7. Crossref, Medline, Google Scholar
- 17. . Budd-Chiari syndrome: hepatic venous web outflow obstruction treated by percutaneous placement of hepatic vein stent. Semin Intervent Radiol 2007;24(1):100–105. Crossref, Medline, Google Scholar
- 18. . Congenital absence of the portal vein: two cases and a proposed classification system for portasystemic vascular anomalies. J Pediatr Surg 1994;29(9):1239–1241. Crossref, Medline, Google Scholar
- 19. . Congenital hepatic shunts. RadioGraphics 2004;24(3):755–772. Link, Google Scholar
- 20. . Ultrastructural analysis of the liver with portal vein agenesis: a case report. Ultrastruct Pathol 1998;22(6):477–483. Crossref, Medline, Google Scholar
- 21. . Congenital extrahepatic portocaval shunts: the Abernethy malformation. J Pediatr Surg 1997;32(3):494–497. Crossref, Medline, Google Scholar
- 22. . Leiomyosarcoma of the inferior vena cava: three case reports and review of the literature. Ann Diagn Pathol 2005;9(5):259–266. Crossref, Medline, Google Scholar
- 23. . Neoplasms of the inferior vena cava: pictorial essay. Can Assoc Radiol J 2005;56(3):140–147. Medline, Google Scholar
- 24. . Obstruction of the inferior vena cava: a multiple-modality demonstration of causes, manifestations, and collateral pathways. RadioGraphics 1992;12(2):309–322. Link, Google Scholar
- 25. . Inferior vena cava filling defects on CT and MRI. AJR Am J Roentgenol 2005;185(3):717–726. Crossref, Medline, Google Scholar
- 26. . Imaging of leiomyosarcoma of the inferior vena cava: comparison of 2 cases and review of the literature. Cancer Imaging 2010;10:80–84. Crossref, Medline, Google Scholar
- 27. . Leiomyosarcoma of the inferior vena cava. Can J Surg 2005;48(3):252–253. Medline, Google Scholar
- 28. . International registry of inferior vena cava leiomyosarcoma: analysis of a world series on 218 patients. Anticancer Res 1996;16(5B):3201–3205. Medline, Google Scholar
- 29. . Leiomyosarcoma of the inferior vena cava: a case report and review of literature. Int Surg 2005;90(5):262–265. Medline, Google Scholar
- 30. . Surgical aspects in the therapy of primary sarcoma of the vena cava. J Am Coll Surg 2006;202(3):559–562. Crossref, Medline, Google Scholar
- 31. . Imaging primary and secondary tumor thrombus of the inferior vena cava: multi-detector computed tomography and magnetic resonance imaging. Curr Probl Diagn Radiol 2006;35(3):90–101. Crossref, Medline, Google Scholar
- 32. . The role of radical surgery for renal cell carcinoma with extension into the vena cava. J Urol 2000;163(6):1671–1675. Crossref, Medline, Google Scholar
- 33. . Spectrum of the inferior vena cava: MDCT findings. Abdom Imaging 2007;32(4): 495–503. Crossref, Medline, Google Scholar
- 34. . Current concepts in the diagnosis and management of renal cell carcinoma: role of multidetector CT and three-dimensional CT. RadioGraphics 2001;21(Spec No):S237–S254. Link, Google Scholar
- 35. . Renal cell carcinoma: presentation, staging, and surgical treatment. Semin Oncol 2000;27(2):160–176. Medline, Google Scholar
- 36. . Adrenocortical carcinoma: diagnosis, evaluation and treatment. J Urol 2003;169(1):5–11. Crossref, Medline, Google Scholar
- 37. . Hepatocellular carcinoma with intra-atrial tumor thrombi: a report of three cases responsive to thalidomide treatment and literature review. Oncology 2004;67(3-4):320–326. Crossref, Medline, Google Scholar
- 38. . Transatrial stent placement for treatment of inferior vena cava obstruction secondary to extension of intracardiac tumor thrombus from hepatocellular carcinoma. J Vasc Interv Radiol 2003;14(10):1339–1343. Crossref, Medline, Google Scholar
- 39. . Renal vein thrombosis in transitional cell carcinoma. Australas Radiol 2007;51(Spec No):B62–B63. Crossref, Medline, Google Scholar
- 40. . Transitional cell carcinoma of the renal pelvis forming tumor thrombus in the vena cava. Int J Urol 2001;8(10):575–577. Crossref, Medline, Google Scholar
- 41. . Surgical treatment of inferior vena cava invasion in patients with renal pelvis transitional cell carcinoma by use of human cadaveric aorta. Korean J Urol 2012;53(4):285–287. Crossref, Medline, Google Scholar
- 42. . Evaluation of diagnostic performance of CT for detection of tumor thrombus in children with Wilms tumor: a report from the Children’s Oncology Group. Pediatr Blood Cancer 2012;58(4):551–555. Crossref, Medline, Google Scholar
- 43. . Testicular tumors manifested as inferior vena cava thromboses: case reports. Acta Radiol 2003;44(1):24–27. Crossref, Medline, Google Scholar
- 44. . Autopsy findings in 154 patients with germ cell tumors of the testis. Cancer 1982;50(3):548–551. Crossref, Medline, Google Scholar
- 45. . Metastases from testicular carcinoma: study of 78 autopsied cases. Urology 1976;8(3):234–239. Crossref, Medline, Google Scholar
- 46. . Intravascular ultrasound-guided mesocaval shunt creation in patients with portal or mesenteric venous occlusion. J Vasc Interv Radiol 2012;23(1):136–141. Crossref, Medline, Google Scholar
- 47. . Symptomatic hydronephrosis caused by inferior vena cava penetration by a Greenfield filter. J Vasc Interv Radiol 1996;7(1):99–101. Crossref, Medline, Google Scholar
- 48. . Postoperative imaging in liver transplantation: what radiologists should know. RadioGraphics 2010;30(2):339–351. Link, Google Scholar
- 49. . Surgical management of malignant tumours invading the inferior vena cava. Eur J Cardiothorac Surg 2014;45(3):537–542; discussion 542–543. Crossref, Medline, Google Scholar
- 50. . Inferior vena cava resection and reconstruction for retroperitoneal tumor excision. J Vasc Surg 2012;55(5):1386–1393; discussion 1393. Crossref, Medline, Google Scholar
- 51. . Traumatic aortocaval fistula from gunshot wound, complicated by bullet embolization to the right ventricle. Radiol Case Rep 2012;7(4):1–4. Crossref, Google Scholar
- 52. . Imaging of postpartum ovarian vein thrombosis. Case Rep Obstet Gynecol 2012;2012:134603. Medline, Google Scholar
- 53. . A calcified lesion within the inferior vena cava presenting as recurrent pulmonary emboli. J Vasc Surg 2011;53(1):204–205. Crossref, Medline, Google Scholar
Article HistoryReceived: Apr 3 2014
Revision requested: July 10 2014
Revision received: Aug 4 2014
Accepted: Aug 13 2014
Published online: Mar 12 2015
Published in print: Mar 2015