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Inferior vena caval thrombosis

Represents a subset of deep vein thrombosis.

Relates to Virchow’s triad of venous stasis, blood vessel injury and hypercoagulability.

Frequency in patients with deep vein thrombosis is 4-15%.

Estimated 6600-74,000 cases per year in the U.S.

Etiology mirrors that of DVT.

Associated with malignancies, particularly renal cell carcinoma, as the tumor extends from the renal vein into the inferior vena cava with subsequent partial or complete occlusion of the IVC.

Other genitourinary malignancies that may be associated with IVC thrombosis include seminoma and teratoma.

Adrenal cortex cancer, retroperitoneal sarcomas, renal angiomyolipoma all reported associated with IVC thrombosis.

May be associated with hepatic hemangioma.

Malignancy increases the risk of DVT, which is a risk factor for extension into the IVC.

Can be caused by extrinsic compression distorting normal caval anatomy with venous stasis and blood flow turbulence by non malignant processes: aneurysms of the abdominal aorta, hepatic abscesses, polycentric renal disease, pancreatic pseudocysts, and acute pancreatitis.

Can be caused by extrinsic compression distorting normal caval anatomy with venous stasis and blood flow turbulence by non malignant processes: aneurysms of the abdominal aorta, hepatic abscesses, polycentric renal disease, pancreatic pseudocysts, and acute pancreatitis.

Compression may be associated with the presence of hematoma adjacent to the IVC and can be related to psoas hematomas and other retroperitoneal hematomas.

Direct trauma to the IVC by blunt or penetrating injury can lead to IVC thrombosis.

May be associated with the nephrotic syndrome with hypercoagulability.

May be caused iatrogenically with hepatic transplantation, dialysis access, femoral venous catheters, pacemakers wires, and the presence of inferior vena caval filters.

May be associated with pregnancy, oral contraceptives, developmental abnormalities and retroperitoneal fibrosis.

Patients may present after having a pulmonary embolus.

Classic presentation includes bilateral lower extremity edema with dilated abdominal veins.

Up to 60% of patients do not have bilateral lower extremity edema.

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