Idiopathic inferior vena caval obstruction

                            Most inferior vena caval thrombi originate in an adjacent vein and spread centrally. Thus a lower extremity venous thrombus can extend superiorly, or a renal malignancy, especially originating in the right kidney, not uncommonly invades and obstructs the inferior vena cava. Caval thrombosis is a complication of Crohn’s disease, systemic lupus erythematosus, andBehçet’s syndrome. In these settings caval obstruction should be suspected if hepatosplenomegaly, ascites, and lower extremity dependent edema develop. Imaging detects a thrombus as an intraluminal filling defect or simply as lack of caval filling with contrast. A primary thrombus and a neoplastic thrombus have a similar imaging appearance and can be differentiated only if thrombus neovascularity or other evidence of a neoplasm is detected. Noncontrast CT reveals an acute thrombus to be isodense or slightly hyperdense to blood.With age, a thrombus gradually becomes hypodense. The involved vessel diameter tends to be expanded focally, regardless of etiology. Gas within a thrombus is rare and suggests infection. Calcifications develop in some chronic thrombi. With incomplete obstruction, postcontrast CT identifies most thrombi as a hypodense tumor surrounded by contrast-opacified blood. A bland thrombus does not enhance postcontrast, while a tumor thrombus does. Complicating the issue is the occasional bland thrombus attached to a tumor thrombus. Still, caution is needed to differentiate a thrombus from incomplete mixing of opacified and nonopacified blood and a resultant transient artifact.
Collateral vessels are common with obstruction of the inferior vena cava. Lower extremity radionuclide venography reveals collateral flow; an occasional patient has diffuse hepatic uptake of the radionuclide. With superior vena caval obstruction, the azygos vein, hemiazygos vein, internal mammary veins, vertebral venous plexus, and lateral thoracic and some superficial thoracoabdominal veins enlarge and become collateral vessels. Because of these collaterals, after contrast injection into an upper extremity
CT can reveal enhancement of a liver segment or the inferior vena cava. Early and dense contrast enhancement of liver segment IV occurs due to segmental liver perfusion from epigastric and paraumbilical veins; such a pseudolesion in segment IV is a potential pitfall seen occasionally during both arterial portography and helical CT.
Magnetic resonance readily detects a caval thrombus. With SE sequences the vena cava contains a tumor rather than a signal void as seen with flowing blood. Slow-flowing blood, however, also results in loss of the caval signal void. With GRE sequences flowing blood appears hyperintense, and this technique appears more reliable in detecting a thrombus than a SE technique. In some patients incomplete obstruction simply results in hepatosplenomegaly and follows a relatively benign course, while others develop chronic liver disease and esophageal varices. Caudate lobe and left lobe hypertrophy, right lobe atrophy, and a nodular liver outline develop with intrahepatic inferior vena caval obstruction; peripheral linear or wedge-shaped hypodense defects are detected in some patients. Some chronic thrombi are associated with caval wall thickening; MR contrast enhancement extends from the vena cava into surrounding soft tissues, probably reflecting thrombophlebitis. Occasionally a caval thrombus regresses spontaneously.
Idiopathic inferior vena caval obstruction. A: A lateral view from a barium enema and cystogram reveals widening of the presacral soft tissues (arrows), a common finding with caval obstruction. B: Venogram identifies extensive collaterals veins and confirms lack of vena cava filling.
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