Figure 1a: Transverse sectional cut through the abdomen at the level of T10, showing a clot in the IVC (white star) just at the point of entry into the right atrium.

(Click on image to enlarge)

Figure 1b: Transverse sectional cut through the abdomen at the level of T12, showing a clot in the IVC (white star) with the 'Polo Mint sign'.  

(Click on image to enlarge)

Figure 1c: Computer generated coronal section through level of IVC showing an extensive clot in the IVC (white arrow) arising just above the origin of the left renal vein.  

(Click on image to enlarge)




The incidence of IVCT is largely uncertain because of the clinical variability in presentation and its association with other primary pathologies. However, studies in the USA, have shown that the incidence of IVCT is estimated at 4-15% in those diagnosed with Deep Venous Thrombosis (DVT).

The aetiologies of IVCT are fairly similar to that of DVT in that the factors leading to activation of the coagulation cascades are contributed by the Virchow’s triad of hypercoagulability, Haemodynamic (stasis, turbulence) and endothelial injury/dysfunction. However specific situations relate to IVCT only:



        Tumours - Numerous malignancies have been associated with IVCT but the most common is the Renal Cell Carcinoma which can invade into the renal vein, and extend into the IVC causing stasis and obstruction and hence thrombosis. Other reported malignancies include seminomas, teratomas, retroperitoneal leiomyosarcoma, adrenal cortical carcinoma, renal angiomyolipoma and hepatic hemangiomas, either through direct invasion of IVC or external compression. Most malignancies are a risk factor for DVT through Virchow’s triad and hence is also a risk factor for IVCT.

        Dysfunctional coagulation system - Nephrotic syndrome has been reported to cause IVCT. Other causes to be considered includes antiphospholipids syndrome, Protein S and Protein C deficiences.

        Iatrogenic - Recent medical intervention particularly endovascular involving the IVC has led to an increased recognition of IVCT, such as long line dialysis catheter, prolonged femoral venous catheters, porta-catheters, intravenous pacing wires, IVC filters and hepatic transplantation.

        Medication - oral contraceptives pills.


EXTERNAL AETIOLOGY (via extrinsic compression)

    Tumours - Most tumours described above can cause extrinsic ompression  of the IVC, leading to IVCT.

    Extrinsic compression by expanding nearby structures such as AAA, iliac aneurysms, hepatic abscesses (ameoba or echinococci), polycystic kidneys, pancreatic pseudocysts and acute pancreatitis have been reported to cause IVCT.

    Heamatoma/Trauma - Enlarging retroperitoneal, psoas or hepatic hematoma adjacent to the IVC as well as direct trauma to IVC (endothelial injury - one of Virchow’s triad)

    Pregnancy - the enlarging pregnant uterus can potentially compressed on the IVC causing extrinsic obstruction and hence IVCT.

    Congenital absence of IVC - Incidence of anomalies of IVC is reported at 0.6 - 2% in the presence of other cardiovascular defects. Individuals tend to present with DVT at a young age.



As shown in Figure 1a, 1b and 1c (CT scan), the thrombus occupies almost 90% of the lumen with a peripheral ring of blood flow as indicated by the contrast (Figure 1b), a sign know as the ‘Polo Mint Sign’. In this patient, the thrombus continue upwards into the right atrium (Figure 1c) and is at risk of embolisation into the pulmonary vasculature causing PE.


Images contributed by

Dr Ian Bickle, Department of Radiology,RIPAS Hospital

Text prepared by

Dr Chong Chee Fui, Thoracic Unit, Department of Surgery, RIPAS Hospital

All images are copyrighted and property of RIPAS Hospital.