AUTHOR AND EDITOR INFORMATION

Section 1 of 7  

• Authors and Editors
• Introduction
• Workup
• Treatment
• Outcome And Prognosis
• Future And Controversies
• References

INTRODUCTION

Section 2 of 7  

• Authors and Editors
• Introduction
• Workup
• Treatment
• Outcome And Prognosis
• Future And Controversies
• References

Thrombosis of the inferior vena cava (IVC) is an underrecognized entity with a variety of clinical presentations. The general concepts of deep venous thrombosis (DVT) and thrombophlebitis are discussed in detail in Deep Venous Thrombosis and Thrombophlebitis. However, the implications and complexity of inferior vena caval thrombosis (IVCT) merit specific attention.

From a global standpoint, IVCT represents a subset of DVT. Virchow recognized and described the factors predisposing a patient to venous thrombosis. The triad of stasis, vessel injury, and hypercoagulability formulated by Virchow remain the foundation for our understanding of the pathophysiology of DVT in general and for IVCT in particular. As appreciation of the impact of these factors on the patient has improved, therapy has become more directed.

Problem

Understanding the anatomy of the IVC and its tributaries is essential to understanding the variability in the clinical presentations of patients with IVCT. The IVC is formed by the confluence of the left and right common iliac veins. Numerous paired segmental lumbar veins drain into the IVC throughout its length. The right gonadal vein empties directly into the cava, while the left gonadal vein generally empties into the left renal vein. The azygous system has connections with the IVC or the renal veins at the level of the renal veins. The next major veins encountered are the renal veins, followed by the hepatic veins. No valves are within the IVC. The cava enters the thoracic cavity through the tendonous portion of the diaphragm and terminates at its junction with the right atrium.

Several congenital anomalies of venous anatomy can involve the IVC, and their presence can increase the likelihood of IVCT. The symptomatology related to IVCT follows directly from the anatomic location of the thrombus and the degree of the lumen occupied by the thrombus.

Frequency

The exact number of patients who have IVCT remains elusive because of the clinical variability in presentation. By compiling information from several epidemiologic studies that investigated DVT prevalence, the following estimates can be generated:

• The DVT rate in the United States is 60-180 cases per 100,000 population per year.
• The frequency of IVCT in patients with DVT is 4-15%.
• In the United States, 165,000-493,000 cases of DVT occur each year.
• In the United States, 6600-74,000 cases of IVCT occur each year.

These numbers are estimates generated from various population-based studies. Various groups within the general population have a greater propensity for IVCT, as discussed in Etiology.

Etiology

To a large degree, the etiology of IVCT mirrors that of DVT in general. However, specific situations relate to the IVC only, but the wide variety of these situations all relate in one or more ways to Virchow's classic description.

Tumors

Numerous malignancies have been associated with IVCT. Perhaps the most familiar is renal cell carcinoma. The intravascular tumor extends from the renal vein and can propagate as far as the heart. The tumor can partially or completely occlude the IVC. Not all intravascular irregularities of the kidney represent tumor thrombus. One case has been reported of a patient who underwent radical nephrectomy for presumed renal cell carcinoma and was subsequently found to have only renal vein thrombosis. Other genitourinary tumors that reportedly cause IVCT include seminomas and teratomas.

Numerous other less common tumors reportedly involve the IVC. Intuitively, any structure that is anatomically related to the IVC can generate either direct compression or vascular invasion. Retroperitoneal leiomyosarcoma, adrenal cortical carcinoma, and renal angiomyolipoma have all been reported as presenting in association with IVCT. Even hepatic hemangioma has caused IVCT from extrinsic compression. Additionally, malignancy itself is a risk factor for DVT and thus represents a risk factor for the extension of DVT into the IVC.

Compression

Extrinsic compression may also result from nontumoral sources and increase the likelihood of IVCT. The distortion of the normal caval anatomy generates both venous stasis and turbulent flow. This situation facilitates the formation of thrombus. An activity as innocuous as bicycle riding has reportedly caused IVCT. The spectrum of medical diagnoses that can cause compression of the IVC is determined by those structures anatomically adjacent to the IVC.

Aneurysms of the abdominal aorta can compress the vena cava and cause thrombosis. Although this clinical situation is somewhat uncommon, the implications for surgical repair of the aneurysm are significant. The surgeon must be prepared for enlarged venous collaterals and the possibility of unusual configurations of the tissue planes. One reported case described incorporation of the IVC into the aneurysm. In this particular case, the wall of the IVC was actually part of the wall of the aneurysm. Knowing that abdominal aortic aneurysm is a risk factor for IVCT should heighten clinical suspicion in appropriate cases.

Hepatic abscesses, either from amebae or echinococci, can also generate thrombosis of the IVC from compression. Because of the propensity of these processes to evolve over time, patients may present without symptoms suggestive of IVC occlusion. They may only demonstrate evidence of the primary process or of collateral venous hypertrophy. The initial presenting symptom may even be pulmonary embolization.

Other retroperitoneal organ systems that have been shown to cause IVCT include the pancreas and the kidneys. Polycystic disease of the right kidney has reportedly been clinically associated with thrombosis of the IVC. Pancreatic pseudocysts have been observed to cause thrombosis of the IVC. Acute pancreatitis has also been found to generate thrombosis of the IVC. The pathophysiology of the evolution of the thrombosis may reflect either the local impact of inflammation of the pancreatic head or the impact of a hypercoagulable state on the IVC. Although IVCT in the setting of pancreatitis is uncommon, this clinical entity may account for an unexplained deterioration in the status of a patient with acute pancreatitis.

Hematoma/trauma

Other aspects of compression can be attributed to the presence of a hematoma adjacent to the cava or the iliac systems. Psoas hematomas and other hematomas of the retroperitoneum have been identified as causing IVCT. In one case, the hematoma was the result of a common iliac artery injury. Because the venous system was not involved, the presumed mechanism of compression of the cava by clot seems credible.

Unique among causes, trauma combines the limbs of the Virchow triad. Stasis, vessel injury, and hypercoagulability may all exist in the same clinical situation. Direct trauma to the IVC may be the result of either penetrating or blunt trauma. In the absence of venous laceration, blunt endothelial damage has been postulated to cause IVCT. Other mechanisms observed secondary to trauma include extension of hepatic venous thrombosis and thrombus formation after perihepatic packing.

Dysfunctional coagulation system

By necessity and function, the balance between the coagulation system and the fibrinolytic system is delicate and dynamic. Disorders that disrupt this balance can cause a situation in which IVC thrombus formation may occur. The nephrotic syndrome is a classic example. Patients with this syndrome have urinary protein losses. Both renal vein thrombosis and IVCT have been described. The exact mechanism of the hypercoagulability of patients with the nephrotic syndrome has not been fully delineated. However, these patients have massive urinary protein loss, and diminished levels of antithrombin III have been observed.

Iatrogenic

Patients with a recent history of medical care may present with iatrogenic IVCT. The expansion of endovascular technology has led to increased recognition of iatrogenic IVCT. Interventions that reportedly have identifiable rates of IVCT include (1) hepatic transplantation, (2) dialysis access, (3) femoral venous catheters, (4) pacemaker wires, and (5) vena caval filters.

Awareness of the association of these procedures with IVCT allows clinicians to make educated decisions. Recognizing the association allows an accurate risk-benefit assessment for a given procedure. Additionally, recognizing these factors may aid in determining a prompt diagnosis in patients who have postprocedural clinical changes.

Other

Numerous other clinical situations have been associated with IVCT. They may meet some classification criteria to be listed in one or more of the categories listed above; however, they are listed here for clarity and can include (1) developmental anomalies of the IVC, (2) retroperitoneal fibrosis, (3) pregnancy, and (4) oral contraceptives.

Although not all-inclusive, the foregoing information provides a review of many of the known clinical situations in which IVCT may be evident. Knowledge of the potential for thrombosis of the IVC increases physicians' level of clinical awareness in patients who present with the identified primary processes.

Clinical

Patients with IVCT may present with a spectrum of signs and symptoms. This variability is a significant part of the challenge of diagnosis. Using a classification system may help the clinician make the correct diagnosis. Patients may present with symptoms that are predominantly thrombotic in origin or predominantly embolic in nature. Additionally, the thrombotic findings are dependent on the degree of occlusion of the cava and on the location between the iliac confluence and the right atrium.

The classic presentation of IVCT includes bilateral lower extremity edema with dilated, visible superficial abdominal veins. Intuitively, this constellation makes sense, although it is not universally found. In one study, almost 60% of patients did not have bilateral leg edema. In addition, if the thrombus is confined to the cava and does not involve the iliac or femoral system, the collateral pathways form along the posterior abdominal wall. This scenario may have significant impact on surgical procedures involving this anatomic region.

Thrombosis occurring at the level of the renal veins raises the possibility of renal cell carcinoma. However, more commonly, thrombosis at this level suggests a nephrotic syndrome. Occlusive thrombus of the IVC at the juxtarenal level can affect renal function by altering renal perfusion.

Budd-Chiari syndrome merits specific attention. A discussion of the entire syndrome is beyond the scope of this article, but the essentials as they relate to IVCT are important. Patients typically have significant ascites, portal hypertension, hepatomegaly, collateral vein enlargement, and hepatic fibrosis. The pathophysiology of this syndrome centers on either IVC or hepatic venous thrombosis. If at the hepatic venous level, 2-3 of the major hepatic veins must be occluded before the syndrome can develop. Both hypercoagulable states and membranous venous webs have been postulated as the etiologic agents of Budd-Chiari syndrome.

Finally, patients who have IVCT may present only after having a pulmonary embolism. The lack of uniform symptoms and the significant number of asymptomatic patients contribute to this feature of IVCT. In one retrospective review of all patients who had cavography to document IVC thrombus, 20% had angiographically proven pulmonary embolism with no symptoms of DVT. Thus, pulmonary embolism may be the first sign of IVCT.

WORKUP

Section 3 of 7  

• Authors and Editors
• Introduction
• Workup
• Treatment
• Outcome And Prognosis
• Future And Controversies
• References

Lab Studies

• No specific laboratory test includes or excludes the diagnosis of IVCT.
• Assessing clotting and fibrinolytic systems may be helpful.
• • Confounding factors include variations caused by heparin and warfarin therapy.
  • Dynamic factors involved with acute thrombosis may also alter measured parameters because of the active consumption of factor by the thrombus.
• Protein C, protein S, antithrombin III, and anticardiolipin studies may all be helpful, but many of these assessments can only be made after the fact.

Imaging Studies

• Virtually all radiologic modalities have been applied to the diagnosis of IVCT. Although evidence of collateralization may be evident on plain radiographs, this modality should not be used as a primary diagnostic tool. Contrast venography, duplex scanning, CT scanning, and MRI all have defined roles in diagnosis.
• Contrast venography
• • This modality is the criterion standard for diagnosis of DVT.
  • Two access sites may be required in order to document extent of thrombus in situations of IVC occlusion by clot.
  • The caudal extent of clot may be overestimated because of preferential flow into collaterals.
  • Pros include (1) limited false-positive study results; (2) access for therapy, thrombolytic agents, or caval interrupting device; and (3) access for pulmonary angiography (if indicated).
  • Cons include (1) invasiveness, (2) possible need for more than one puncture, and (3) possible postprocedure DVT.
• Duplex scanning
• • Pros include (1) noninvasiveness; (2) portability; (3) efficacy in helping diagnose DVT at the femoral level and, to some extent, to the distal iliac level; (4) possible help in visualizing dilated collaterals, and (5) possibly more accurate assessment of extent of thrombus than venography.
  • Cons include (1) operator dependence, (2) anatomic limitations, (3) less reliable diagnosis within the abdomen because of greater difficulty in assessing venous compressibility, and (4) lost respiratory phasicity above the renal veins because of retrograde transmission of the cardiac cycle through the valveless IVC.
• CT scanning
• • CT scans are often obtained as part of the diagnostic evaluation for the primary process (eg, malignancy).
  • The use of intravenous contrast materials is typically required.
  • False-positive study results sometimes occur.
  • Pseudothrombosis, particularly of the infrarenal IVC, is generally thought to result from the variable amounts of contrast in the cava above and below the renal veins. It may also result from collapse of the IVC at the diaphragm while patients are supine.
• MRI
• • MRI allows for examination in multiple planes and for estimation of the thrombus age.
  • Reconstructive imaging technology can generate images similar to those seen with venography.
  • Pros include (1) noninvasiveness, (2) lack of any ionizing radiation, and (3) help in determining proximal extent of thrombosis.
  • Cons include (1) cost, (2) accessibility, and (3) turbulent flow that may be read falsely as clot.

Diagnostic Procedures

• Although other modalities may have a more primary role, IVCT may still be diagnosed intraoperatively in patients who were treated with laparotomy for their primary problem.

TREATMENT

Section 4 of 7  

• Authors and Editors
• Introduction
• Workup
• Treatment
• Outcome And Prognosis
• Future And Controversies
• References

Medical therapy

Treatment options for IVCT have evolved as understanding of the pathophysiological mechanisms has increased. Both surgical and medical options are available. The goals of therapy center on managing the primary impact of the DVT and the impact of embolization. Medical professionals are encouraged to investigate the most recent research to keep apprised of the latest information relating to the various risks and benefits of treatment modalities. Medical management can include anticoagulation therapy and thrombolytic agents.

Anticoagulation

Heparin or warfarin may be used to prevent propagation of thrombus. One group has reported no embolic events with this therapy, even with so-called free-floating IVCT. However, propagation may still occur. Therapy is usually converted to oral anticoagulation with warfarin, but the time course of warfarin therapy is somewhat empiric.

Thrombolytic agents

Most thrombolytic agents have been reported in the treatment of IVCT. The relative merits of thrombolytic therapy must be weighed against the risks of hemorrhagic complications.

Urokinase, tissue-type plasminogen activator (tPA), and streptokinase have all been used. Typically, delivery is catheter-directed with or without a pulse spray. Patients require concurrent heparin therapy; however, tPA protocols do not use concurrent heparin because of the risk of bleeding complications. Up to a 25% risk of pulmonary embolism during therapy has been reported. Some reports advocate using filters above the thrombolysis site; some do not. This therapy may play the greatest role as part of combination therapy with endovascular interventions.

Surgical therapy

In the broadest sense, surgical therapy encompasses caval interruption and thrombectomy. Currently, both of these modalities are being used less frequently.

Caval interruption

• Ligation
  • The proper level must be chosen.
  • Ligation effects a permanent, complete occlusion of the IVC.
  • The risk of recurrent pulmonary embolism is not zero.
• Filters
  • Filters are relatively noninvasive.
  • Filters allow central flow.
  • Thrombosis may occur at the insertion site or the site of the filter itself.
  • Numerous proprietary configurations are available.
  • Technology is constantly changing.
  • Data from older studies may not extrapolate to current devices.
  • Filters may be placed at several different anatomic levels as indicated by the clinical situation.

Thrombectomy

• Thrombectomy is often carried out for therapy of phlegmasia.
• Rethrombosis rates are significant.
• The procedure is typically performed in conjunction with a distal arteriovenous fistula to maintain high flow.
• The operative mortality rate is reportedly 2%; the morbidity rate is 30%.
• Thrombectomy often fails to completely remove the thrombus.
• The procedure may be required for cases of septic thrombus.

Endovascular interventions

• These techniques are particularly helpful to treat patients with IVCT that has arisen from iatrogenic causes. The numerous clinical scenarios that lend themselves to this approach can include (1) long-term venous access, (2) hemodialysis access, and (3) surgery on the IVC, including hepatic transplantation.
• Several interventional modalities are available to treat IVCT. The optimal result can often be obtained by using a combination of these options as follows: (1) percutaneous balloon angioplasty, (2) Wall stents, and (3) Z stents.
• The number and type of expandable stents are changing as product development continues. The various stents have limitations both in vessel diameter and length of available stent. Consulting with vascular surgeons, radiologists, and available literature to identify the locally available devices is encouraged and recommended.

Follow-up

For excellent patient education resources, visit eMedicine's Circulatory Problems Center. Also, see eMedicine's patient education article Blood Clot in the Legs.

OUTCOME AND PROGNOSIS

Section 5 of 7  

• Authors and Editors
• Introduction
• Workup
• Treatment
• Outcome And Prognosis
• Future And Controversies
• References

The outcome of patients who have IVCT is often determined by the underlying condition that initially caused the thrombosis. However, some general statements can be made. The impact and outcome of IVCT are as variable as the clinical presentation. In one study, only a third of patients had a correct diagnosis before venography. Adult patients with ligation of their vena cava reportedly have either no symptoms or mild edema after ligation.

A report on children who had IVCT unrelated to catheterization revealed that 50% had persistent IVCT. Symptoms of chronic limb pain and chronic abdominal pain were observed. Another series of pediatric patients with IVCT secondary to central venous access identified no sequelae unless concurrent superior vena cava thrombosis was present. Finally, the outcome of patients who have IVCT relates to the embolic risk associated with DVT overall. If the cava is occluded, pulmonary embolization does not present a significant risk. On the other hand, if a caval lumen remains, embolization may occur.

FUTURE AND CONTROVERSIES

Section 6 of 7  

• Authors and Editors
• Introduction
• Workup
• Treatment
• Outcome And Prognosis
• Future And Controversies
• References

IVCT remains a challenging process to diagnose and treat. In a recent list server based discussion among critical care physicians, surgeons, radiologists, and other physicians regarding IVCT, a lack of uniformity of opinion existed regarding the optimal diagnostic study. However, a general consensus existed among the discussion participants that contrast venography remains the criterion standard.

Patients may be asymptomatic, or they may present only after complications occur. Once the diagnosis has been confirmed, the clinician must choose an appropriate treatment regimen based on the underlying pathophysiology. With physician awareness of the possibility of IVCT in various situations, the patient is more likely to receive prompt diagnosis and subsequent intervention that minimizes ensuing sequelae.

REFERENCES

Section 7 of 7

• Authors and Editors
• Introduction
• Workup
• Treatment
• Outcome And Prognosis
• Future And Controversies
• References

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Article Last Updated: Sep 28, 2005