Minimally invasive treatments for venous compression syndromes

Abstract

The management of venous compression syndromes has historically been reliant on surgical treatment when conservative measures fail. There are, however, several settings in which endovascular therapy can play a significant role as an adjunct or even a replacement to more invasive surgical methods. We explore the role of minimally invasive treatment options for three of the most well-studied venous compression syndromes. The clinical aspects and pathophysiology of Paget-Schroetter syndrome (PSS), nutcracker syndrome, and May-Thurner syndrome are discussed in detail, with particular emphasis on the role that interventionalists can play in minimally invasive treatment.

Keywords: Endovascular procedures; May-Thurner syndrome; renal nutcracker syndrome; thrombolytic therapy; upper extremity deep vein thrombosis (UEDVT).

Figure 1

Compression ultrasonography showing an acute deep vein thrombosis (DVT) of the brachial and subclavian vein in cross-sectional and longitudinal views. (A) Longitudinal view of the brachial vein (v) showing hyperechogenicity and lack of color Doppler flow. Adjacent brachial artery (a) demonstrates antegrade flow; (B) cross-sectional view of the subclavian vein showing hyperechogenicity, lack of color Doppler flow, and lack of compression, consistent with acute DVT. Adjacent subclavian artery (a) demonstrates normal color Doppler flow.

Figure 2

Axial contrast-enhanced computed tomography (CT) of the chest showing an enlarged left axillary vein (arrow) with a large amount of surrounding fat stranding. The engorged vessel with surrounding inflammatory changes indicates an acute development of venous hypertension as a result of more central venous obstruction and thrombosis, in this case at the level of the thoracic inlet. The lack of collateralized vessels also suggests an acute presentation. The contralateral axillary vein (arrowhead) is shown for comparison.

Figure 3

Digital subtraction venography (DSV) of the left upper extremity and chest following local injection of iodinated contrast material through a sheath within the left brachial vein. (A) Prior to thrombolysis, there is abrupt termination of flow within the axillary vein at the level of the thoracic inlet (arrow), with redistribution of flow towards a multitude of collateral vessels within the neck (arrowhead); (B) following 24 hours of catheter-directed thrombolysis, there is restoration of flow within the subclavian and innominate veins extending to the superior vena cava. There is persistent stenosis (*) at the thoracic inlet, prompting referral to vascular surgery for decompression.

Figure 4

Axial ultrasonography with color Doppler of the left renal vein (LRV). (A) Greyscale ultrasound demonstrating significant decrease in caliber of the LRV as it crosses between the aorta (Ao) and superior mesenteric artery (SMA) towards the inferior vena cava (IVC). Liver, portal vein (PV) and vertebra are notated for anatomic reference; (B) color Doppler of the same anatomic region shows normal antegrade flow proximal to the aortomesenteric region shows significant turbulence (*) and elevated peak velocity.

Figure 5

Axial and sagittal computed tomography angiography (CTA)/computed tomography venography (CTV) with three-dimensional (3D) reconstruction at the level of the aortomesenteric angle. A split-bolus technique was used to opacify both the arterial and venous structures in the same phase. (A) Axial CTA/CTV shows significant decrease in diameter of the left renal vein as it crosses between the aorta and superior mesenteric artery (*); (B) sagittal CTA/CTV shows a very acute aortomesenteric angle (arrow) measured at 15 degrees, with resultant compression of the left renal vein (arrowhead); (C) left anterior inferior oblique view of the nutcracker phenomenon using 3D reconstruction of the same CTA/CTV. The celiac axis has been removed from the viewing plane to facilitate evaluation of aortomesenteric compression.

Figure 6

Axial computed tomography venography (CTV) images of May-Thurner syndrome, with acute left common iliac vein thrombosis extending to the left external and internal iliac veins. (A) Axial CTV at the level of the common iliac vein confluence, demonstrating the left common iliac vein (long arrow) to be unopacified and enlarged compared to the right common iliac vein (short arrow). The proximal aspect of the left common iliac vein is severely compressed and barely visualized, directly posterior to the right common iliac artery (arrowhead) and anterior to the vertebral body; (B) axial CTV on the same patient acquired inferior to the iliac bifurcation demonstrates an enlarged, heterogeneously hypodense left external iliac vein (long arrow) and a normal right external iliac vein (short arrow). The external iliac arteries can be seen directly anterior to their respective external iliac veins. The left internal iliac vein (curved arrow) is enlarged and hypodense, with a significant amount of perivenous inflammatory fat stranding.

Figure 7

Digital subtraction venography (DSV) of the left common iliac vein prior to and following stent placement for May-Thurner syndrome. (A,B) Transjugular venography prior to stent placement demonstrates abrupt termination of flow (arrow) within the left common iliac vein just prior to the inferior vena cava (IVC) confluence. A large ascending lumbar vein (arrowhead) is seen as well as deep pelvic varices (*). There is no flow within the IVC (location indicated by the descending transjugular venous catheter). Incidental note is made of a Greenfield IVC filter; (C) repeat venography following stent placement (arrow) shows restoration of patency to the left common iliac vein, with normal flow of contrast into the IVC and right common iliac vein.