Inferior Vena Caval Thrombosis Clinical Presentation

Updated: Aug 01, 2017
  • Author: Luis G Fernandez, MD, FACS, FASAS, FCCP, FCCM, FICS, KHS; Chief Editor: John Geibel, MD, DSc, MSc, AGAF  more...
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Presentation

History

Patients with inferior vena caval (IVC) thrombosis (IVCT) may present with a spectrum of signs and symptoms. Patients may be asymptomatic, or they may present only after complications occur.

This variability is a significant part of the challenge of diagnosis. Using a classification system may help the clinician make the correct diagnosis. Thus, 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 IVC and on the location between the iliac confluence and the right atrium.

Patients who have IVCT may present only after having pulmonary embolism (PE). 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 PE with no symptoms of deep vein thrombosis (DVT). Thus, PE may be the first sign of IVCT.

In patients with complete absence of the IVC, symptoms associated with severe venous hypertension (eg, bilateral lower-extremity edema, varicose veins, nonhealing venous ulcers, caput medusae, or other manifestations of collateral venous system hypertension/dilatation) may be varied in their manifestation and, in some cases, may not be apparent until later in life.

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Physical Examination

The classic presentation of IVCT includes bilateral lower-extremity edema with dilated, visible superficial abdominal veins. Intuitively, this constellation makes sense, though 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.

Occlusive thrombus of the IVC at the juxtarenal level can affect renal function by altering renal perfusion.

It is hypothesized that blood return with an absent IVC is inadequate, despite adequate collaterals, resulting in chronic venous hypertension in the lower extremities and causing venous stasis that precipitates thrombosis.

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Budd-Chiari syndrome

Budd-Chiari syndrome merits specific attention, though a discussion of the entire syndrome is beyond the scope of this article. The essentials of this condition 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 it is at the hepatic venous level, two or three 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.

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