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| Discussion |
Case Report:
A 40-year-old man presented with a long standing history of pain and swelling of both the lower limbs. He had history of a bilateral chronic deep venous thrombosis (DVT).
Clinical examination: revealeds edema of both the lower limbs. His per-abdominal examination showed a firm non pulsatile, non tender abdominal mass in the right para umbilical region - not moving with respiration
Ultrasonography of the abdomen revealed a well circumsribed cystic mass lesion measuring approximately 8 x 6 x 5 cms with hyperechoic organized debris within. The mass was seen in close proximity to the IVC with suspicious communication with it. The IVC below the lesion was thrombosed on Doppler imaging.
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Color Doppler confirmed chronic DVT with no filling of the calf, popliteal, femoral or iliac veins on either side.
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CT scan of the abdomen was performed. This confirmed the mass lesion. On plain CT scan, the mass was hyperdense.
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Fig. 6 |
It was seen in to be in the retroperitoneum in close proximity to the IVC and not separate from it. The mass was seen to displace the right renal vein superiorly and the pancreas and duodenum to their periphery. No bone erosion or extension into the neural foramina was seen. The mass showed no calcification and no post contrast enhancement or any enhancing solid component. However, post contrast delayed images revealed thrombosis of the infralesional IVC and of both the common iliac veins.
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MR imaging of the abdomen revealed a well circumscribed mass lesion in the retroperitoneum measuring approx. 8 x 6 x 5 cms. The mass was seen in close proximity to the transrenal IVC and the right psoas muscle. Obvious communication was seen with the IVC and mass effect was seen on the renal pedicles.
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Fig. 10 |
The suprarenal IVC was normal and the infrarenal IVC was seen to be thrombosed. The azygous system was hypertrophied. The head of the pancreas and the right kidney were compressed and displaced due to the mass. The mass display hypointense signal on T1 gradient images and display intermediate signal intensity on T2W images. The capsule displays hyperintense signal on T1W images
Based on the obvious communication seen between the “mass” and the IVC, a diagnosis of thrombosed aneurysm of the IVC was made.
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At laparotomy, the mass was seen to be arising from the IVC and it was diagnosed as a saccular aneurysm. The IVC was controlled proximally and distally and the aneurysm was punctured and an old organised thrombus was seen within the mass and extending into the IVC, which extended proximally. No venous reconstruction was attempted, as it was felt that due to the chronic nature of the thrombus, sufficient collaterals should have developed, and the venotomy was primarily closed.
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Post-operatively, the patient recovered well and was discharged with compression stockings. Histological examination of the aneurysm demonstrated a thickened venous wall with dilatation and thrombosis of its lumen.
DIAGNOSIS:
Thrombosed saccular aneurysm of transrenal IVC with bilateral lower limb DVT.
Aneurysms of the IVC are a diverse group of anomalies with distinct anatomic and clinical characteristics. They may be saccular or fusiform, with saccular being slightly more common. The cause is unknown although it has been suggested that they develop in the anastamoses between the embryological venous systems and that they may be associated with other congenital cardiovascular abnormalities.
Two different classification systems for IVC aneurysms have been defined in the literature.
Thompson and Lindenauer classification: Three types are recognized (I) congenital (II) acquired (III) Secondary to arteriovenous fistula. Acquired aneurysms may be secondary to trauma or disease processes in the affected vessel wall. Although the cause usually remains unclear, most of these aneurysms are believed to be congenital or acquired.
The Gradman and Steinberg classification defined four types: type I, aneurysms of the suprahepatic IVC without venous obstruction; type II, aneurysms associated with interruption of the IVC above or below the hepatic veins; type III, aneurysms confined to the infrarenal IVC without associated venous anomaly; and type IV, miscellaneous.
There are a range of reported presentations including pain, rupture and thromboembolism. Thrombosis usually presents with bilateral leg swelling. In type II and III aneurysms, surgical repair is advised due to the high incidence of developing symptoms. In type I aneurysms, as there is a high morbidity and mortality associated with surgery in the thorax and the low incidence of developing symptoms, asymptomatic non-enlarging venous aneurysms can be safely followed-up.
If surgical intervention is required complete excision is recommended with primary venous closure, as was done in this case. Reconstructive surgery with synthetic or vein graft may be necessary to re-establish caval flow if severely symptomatic, but there is a high risk of vena caval graft thrombosis. Reconstruction may not be technically possible if the proximal IVC is thrombosed. In these cases a suprarenal caval filter should be considered.
In conclusion, IVC aneurysm, although rare, should be considered in the differential diagnosis of retroperitoneal tumours. When the lumen is completely thrombosed, the diagnosis can be very difficult to make pre-operatively even with multiple imaging modalities, hence laparotomy may be the only method of definitive diagnosis. Finally, surgical treatment of abdominal venous aneurysms is advisable in symptomatic cases. In asymptomatic cases, surgery should be considered in fit patients who can undergo a relatively straightforward operation or in cases where the aneurysm is enlarging.