Conventional venography, also known as phlebography, refers to radiographic imaging of the veins after direct injection of the contrast material. Before the advent of cross-sectional imaging (ultrasonography, computed tomography [CT], and magnetic resonance imaging [MRI]), venography played significant role in the diagnosis of venous thrombosis. Currently, its role is limited to catheter-directed therapy of various venous disorders, venous sampling for hormonally active tumors, and dialysis access management.1,2,3 This chapter discusses the indications, techniques, and contraindications of venography and venographic appearances of normal anatomy and various pathologies affecting the veins. The subsections are divided into different regions to facilitate the discussion on technical aspects of venography.
Venography of the upper extremities has regained its importance because of the increasing number of dialysis-dependent patients and the availability of new therapeutic options for deep venous thrombosis (DVT).
Venous mapping for preoperative planning of dialysis access surgery (arteriovenous fistula or graft creation)3,4
As a part of pharmacologic, mechanical, or combined thrombolysis of DVT affecting the upper extremity veins (e.g., Paget Schroetter syndrome) and dialysis fistula or graft5
As a part of treatment for central venous occlusion secondary to long-term indwelling catheters, mediastinal fibrosis, thoracic malignancy, or radiotherapy6
As a part of treatment for venous stenosis in patients with arteriovenous fistula or graft
As a part of venous catheter placements (e.g., peripherally inserted central catheter [PICC], long-term central venous catheters, ports); superior vena cava (SVC) filter placement; and catheterization of the right heart, pulmonary arteries, and other systemic veins
Rarely, to diagnose congenital venous anomalies and venous vascular malformations
Relative contraindications include a history of anaphylaxis with iodinated contrast materials and renal dysfunction. In patients with allergy to iodinated contrast materials, alternative contrast materials, such as carbon dioxide or gadolinium, may be used for venography.7 Patients with renal dysfunction may be prepped with renal-protective algorithms with sodium bicarbonate infusion, hydration, and Mucomyst. Carbon dioxide can be safely used in patients with renal failure. Use of carbon dioxide as a contrast material necessitates digital subtraction angiography (DSA) for imaging.8
The patient is placed in the supine position, and the hands are positioned in supination and abduction. This positioning is important because it is the anatomic position and it reduces the incidence of axillary vein pseudostenosis caused by pressure form the tissue bulk. A superficial vein in the dorsum of hand is accessed with 18- or 20-gauge needle. A tourniquet is applied at the upper arm. This helps fill the deep veins with contrast material. Initially, 5 to 10 mL of iodinated contrast material is injected under fluoroscopy to rule out extravasation. Then diluted iodinated contrast material (240 mgI/mL) is injected, and multiple intermittent overlapping screen images are taken of the forearm and upper arm. After releasing the tourniquet, DSA of the central veins (subclavian and brachiocephalic veins and SVC) is performed under suspended respiration. Anteroposterior (AP) projections are anatomically optimum in most cases. In difficult cases, oblique views may be performed to evaluate the pathology. While performing venography for primary subclavian vein stenosis or thrombosis, it is important to perform runs in abduction with pectoral fixation because this will demonstrate pronounced stenosis or compression. Because this disease is often bilateral, venography of both upper extremities should be performed in such cases. SVC opacification may be improved by simultaneous injection of contrast material in both arms, cannulation of the antecubital veins, or direct catheterization of the central veins. Inflow from unopacified veins may appear as filling defects, so care should be taken not to misinterpret these as thrombi.
Contrast extravasation is the main complication. Contrast extravasation may lead to swelling, compartment syndrome with arterial and neurologic deficits, and skin necrosis. Another potential complication is an allergic reaction to contrast materials. Interventional procedures involve the risk of venous perforation, rupture, bleeding, and injury to the heart and pericardium.
Normal Anatomy. Anatomically, the upper extremity veins are divided into the superficial and deep groups. Unlike the lower extremity, the superficial veins provide the dominant venous drainage pathway in the upper extremity. The superficial veins join the deep veins at the level of the axilla. All of the veins in the upper extremity have valves albeit inconsistently.
In the forearm, the superficial system consists of the cephalic vein running along the anterior radial edge, the basilic vein running along the posterior ulnar edge, and the median vein running in the midline anteriorly. Just below the elbow in the antecubital fossa, the median cubital vein originates from the cephalic vein, running obliquely across to join the basilic vein. The median cubital vein receives drainage from the medial vein of the forearm.
In the arm, the cephalic vein runs in the groove between the biceps and brachialis muscles. On reaching the shoulder, it passes between the pectoralis and deltoid muscles before arching down along the medial aspect of pectoralis minor muscle to join the axillary vein. This curvature is known as the cephalic arch. The basilic vein runs along the medial border of biceps, superficial to the brachial fascia. At the junction of the middle and lower thirds of the arm, it pierces the brachial fascia and joins the deep brachial vein near the lower border of teres major, forming the axillary vein.
The deep veins are paired structures and are named after their accompanying arteries. They are ulnar, radial, and interosseous veins. In the antecubital fossa, they drain into the paired brachial vein, which run along with the brachial artery and median and radial nerves under the brachial fascia.
The axillary vein is the site for transition of dominance of drainage from the superficial veins to the deep veins. At the lateral edge of the first rib, it becomes the subclavian vein, which passes between the first rib and clavicle to combine with the internal jugular vein at the thoracic inlet to form the innominate vein. The right brachiocephalic is a short (2–3 cm) vein that runs vertically down. The left innominate is longer than the right and crosses the midline to join its counterpart in the anterior mediastinum, forming the SVC. The SVC is 6 to 8 cm in length and up to 2 cm in diameter and drains into the right atrium. The azygous vein drains into the SVC before it enters the pericardium and becomes an alternate route of drainage in cases with occlusion of the SVC distal to it.
Anatomic Variations. Left-sided SVC and double SVC are uncommon. The left SVC drains into the right atrium through the coronary sinus. It may be associated with partial anomalous pulmonary venous drainage and atrial septal defects.
Pathology. Pathologies involving the veins of the upper extremity and central veins include acute thrombosis, chronic thrombosis, thoracic outlet syndrome, SVC stenosis, and SVC syndrome. With the widespread use of central catheters, the incidence of thrombosis is on the rise. About 40% to 60% of patients with chronic indwelling subclavian venous catheters develop thrombus around the catheters, although only about 5% are symptomatic. On venography, thrombi appear as filling defects, often with a meniscus shape at the edge of the thrombus in acute cases (Figure 11-1). Chronic thrombosis may demonstrate filling defects or constriction or non-opacification of the vein. When the veins are occluded, collateral veins form an alternate pathway (Figure 11-2).
Peripheral venous stenosis or occlusion may develop in patients with arteriovenous fistula or graft (created for dialysis). Such stenoses or occlusions are best diagnosed on venography. Interventions to salvage the fistula or graft include angioplasty and stent placement.
In Paget-Schroetter syndrome, there is stenosis of the subclavian vein at the thoracic inlet (Figure 11-3). The stenosis is secondary to chronic irritation and compression of the vein between the first rib and the clavicle. The stenosis is markedly pronounced in abduction; as such, this entity is more often observed in patients who are actively involved in sports that require frequent abduction of the arm (e.g., horse riders, softball players). There may be associated thrombosis of the subclavian and axillary veins (see Figure 11-3). This is treated with pharmacomechanical thrombolysis followed by surgical resection of the first rib.9 Endovascular therapy of the subclavian stenosis with stents should be avoided because stents at this location tend to fracture.
SVC stenosis or occlusion can be caused by many diseases such as malignancy, chronic indwelling central venous catheters, mediastinal hematoma, mediastinal fibrosis, sarcoidosis, radiation therapy, and postsurgery (e.g., anastomotic stenosis after cardiac transplantation). Of these, bronchial carcinoma is the most common cause of SVC syndrome. Venography demonstrates severe stenosis of the SVC and the presence of multiple collateral veins in the chest wall and abdomen to reroute the venous drainage through the inferior vena cava (IVC) (Figure 11-4). Endovascular therapy with angioplasty, stenting, or both is the treatment of choice in these patients.6
Congenital aneurysms of the internal jugular vein have been reported. They appear as large focal dilatations of the veins with or without filling defects secondary to thrombosis.
The lower extremity venous drainage consists of superficial and deep systems. Unlike the upper extremity, the deep system is dominant drainage pathway with perforators connecting them with the superficial system. All of the veins consistently show valves, a mechanism to counteract gravity in bipeds. Diseases of the lower extremity veins are much more common than arterial pathology, although they have a limited range of pathology.
Historically, the most common indication for lower limb and pelvic venography is suspected DVT. Ultrasonography, color Doppler, and CT venography have replaced conventional venography for the diagnosis of DVT. The present indications for venography of the lower extremity and pelvis are:
As a part of catheter directed thrombolysis for DVT.1
Diagnosis and endovascular management of May-Thurner syndrome.10
Venous mapping before dialysis access creation in patients with no useful upper extremity veins.
When planning a venous bypass procedure for a chronic venous occlusion.
Pelvic venography is performed as a part of treatment for pelvic venous congestion syndrome. It is often performed when gonadal vein embolization fails.11
Suspected popliteal venous aneurysms and popliteal venous entrapment syndrome.
Anaphylaxis to iodinated contrast material is an absolute contraindication. Renal insufficiency is a relative contraindication. Alternative contrast materials such as carbon dioxide and gadolinium may be used.
Ascending Venography. The best positioning for this procedure is the reverse Trendelenburg position to 30 to 60 degrees. A support is provided for the nonexamined foot to rest the patient’s weight. A vein in the dorsum of foot is accessed using a 20- to 21-gauge needle with the tip, preferably directed towards the toe. A tourniquet around the ankle is helpful in directing the contrast material into the deep system. Initially, 5 to 10 mL of contrast material is injected under fluoroscopy to look for extravasation. Diluted contrast material (240 mgI/mL) is injected. Multiple overlapping images in three projections are acquired as screen shots. For patients with varicose veins, a radio-opaque ruler is placed adjacent to the leg, and tourniquets are used at multiple levels to compartmentalize the vein and identify the perforators. For imaging the iliac veins, a tourniquet is tied in the upper thigh, and 50 to 100 mL of contrast material is injected. With the patient placed in supine or a mild Trendelenburg position, the tourniquet is released, allowing the contrast material to flow into the iliac vein and proximal IVC. A squeeze in the thigh and continuous contrast material administration also help better opacify the iliac veins. After the study has been completed, normal saline is infused through the intravenous cannula to flush out the contrast material to prevent thrombophlebitis.
Descending Venography. This is performed for the evaluation of valvular incompetence. The common femoral vein (CFV) is accessed with an 18-gauge needle, and a short sheath is placed with its tip in the external iliac vein. The head is raised to 60 degrees, and 20 mL of contrast material is injected through the sheath. If the table cannot be tilted, the patient is asked to perform the Valsalva maneuver during contrast material administration. Patients with valve incompetency will show reflux (retrograde flow of the contrast material), which is graded depending on the distance it reaches from the injected site.
Extravasation of the contrast material is one of the common complications that can be avoided by practicing caution. Other complications are thrombophlebitis and allergic reactions.
Normal Anatomy. The veins of the pelvis are the common iliac, external iliac and internal iliac veins. The external iliac vein starts at the inguinal ligament and is the direct continuation of the CFV draining the lower extremity. It receives drainage from the inferior epigastric, circumflex iliac and pubic veins before joining with the internal iliac at the level of sacroiliac joint to form the common iliac vein (CIV). On the right, the external iliac vein lies medial to the external iliac artery and gets posterior to it before joining the internal iliac vein. The left external iliac vein remains medial to the left external iliac artery throughout its course. The CIVs are angled anteriorly and cranially and run vertically to meet the contralateral vein, forming the IVC at L5. The right CIV runs posterior, and the left CIV runs medial to their corresponding named arteries; thus, the left CIV has to cross under the right common iliac artery to meet the right CIV, resulting in broadening and at times causing functional compression, also called May-Thurner syndrome.
The lower extremity veins are divided into superficial and deep groups. Unlike the upper extremity, the deep veins are the dominant drainage system. The perforator veins direct blood from superficial to the deep system. The CFV is formed by the confluence of the deep femoral vein and femoral vein (also called the superficial femoral vein [SFV]), running in the femoral sheath lying medial to the femoral artery. It receives drainage from the long saphenous vein and medial and lateral circumflex femoral veins. The SFV extends from the inguinal canal to the adductor canal, where it is called the popliteal vein. It runs lateral and deep to the superficial femoral artery. The popliteal vein is formed by the joining of the tibial veins at the upper calf. The popliteal vein is superficial to the artery, thus lying closer to the skin. The small saphenous vein and gastrocnemius veins drain into the popliteal vein. The SFV may be duplicated or complex in 20% of cases. The popliteal vein is duplicated or complex in 35% of the population.
In the leg, the deep veins are paired structures running parallel to the corresponding arteries. The size of the veins corresponds to the area they drain; thus, the posterior tibial and peroneal veins are large. The veins of the plantar surface of the foot continue as posterior tibial veins, and the vein of the dorsum of the foot forms the anterior tibial veins. The peroneal veins are formed at the ankle and together with the posterior tibial veins receive the perforators and muscular branches.
The superficial veins are constituted by the long and small saphenous veins, both lying in the subcutaneous fat superficial to the muscles. The long saphenous vein originates at the medial edge of the foot, ascends along the medial aspect of the leg, and joins the CFV at the sapheno–femoral junction just below the inguinal ligament. Along its length, it communicates with the deep system through perforators. The perforator veins normally have valves, which, if disrupted, may lead to reflux and varicose veins. The tributaries of the long saphenous vein are the medial and lateral accessory saphenous veins. The small saphenous vein drains the lateral edge of the foot, ascends along the midline posterior in the calf between the two bodies of gastrocnemius, and joins the popliteal vein at the popliteal fossa just below the knee joint.
Pathology. Acute thrombus appears as a filling defect with enlargement of the vein (Figure 11-5). Often no collateral veins are visualized. A meniscus sign at the edge of the thrombus may be seen. With chronicity, the thrombus gets organized, and venography demonstrates venous stenosis and non-opacification of the veins and collaterals bypassing the occluded segment.
A combination of left CIV stenosis caused by compression by the right common iliac artery and left leg DVT is called May-Thurner syndrome. It is an underdiagnosed cause of left sided ileofemoral DVT. It can be diagnosed by venography with pressure measurement across the stenosed segment. Venography demonstrates narrowing and flattening or widening of the left CIV where the right common iliac artery crosses it and multiple enlarged retroperitoneal and cross-pelvic collateral veins (Figure 11-6). Endovascular therapy with stent placement has shown to be effective in preventing recurrent DVT in such patients.12
FIGURE 11-6.
May-Thurner syndrome. Venography performed through a left femoral vein catheter (block arrow) demonstrates extrinsic compression (arrow) over the left common iliac vein by the right common iliac artery. Multiple cross-pelvic collateral veins (arrowheads) are seen rerouting the blood through the right common iliac vein (curved arrow).
Ultrasonography and color Doppler provide functional information about valve closure times and have virtually replaced venography for the evaluation of valvular incompetency. On ascending venography, reflux can be detected and can be graded on the basis of the extent of reflux from the site of injection of contrast material.
Klippel-Trenaunay syndrome is a rare, congenital, noninheritable condition that characteristically shows hypoplasia or absence of the deep veins with persistent lateral embryonic and sciatic veins. Parkes-Weber syndrome is even rarer than Klippel-Trenaunay syndrome and is associated with high-flow arteriovenous malformations. Venous malformations result in rare congenital varicosities that are distinct from acquired ones. Venography is diagnostic.
Popliteal venous aneurysms (or varix) may be congenital or posttraumatic. They often present symptoms of DVT or PE caused by thrombus formation within the aneurysm. Rupture is rare.
Currently, venography of the IVC (cavography) is performed as a part of interventional procedures. Rarely, it is required to assess the anatomical variations relevant to surgery.
As a part of interventional procedures such as IVC filter placement or retrieval, pharmacomechanical thrombolysis of thrombosed IVC, treatment of extrinsic and intrinsic stenosis (e.g., IVC web, Budd-Chiari syndrome), and venous sampling procedures for suspected renal and adrenal tumors
To assess anatomical variations of the IVC in patients undergoing liver or kidney transplantation
To study the collateral pathways of venous circulation in the presence of chronic IVC occlusion
As a part of treatment for occluded portocaval, mesocaval shunts, and splenorenal shunts in patients with portal hypertension
Absolute contraindications are sepsis at the venous access site and severe anaphylaxis to contrast material.
Venous access to the IVC can be gained through the femoral or jugular or antecubital venous approach. A pigtail catheter is placed in the IVC at the level of iliac vein confluence. Iodinated contrast material (370 mgI/mL) is injected at a rate of 20 to 30 mL/s for a total volume of 30 to 40 mL. DSA of the IVC is obtained in AP and lateral projections at a frame rate of 2 to 3 per second for the entire IVC. It is important to opacify the inflow from the left CIV to confidently exclude presence of a duplicated IVC. Some advocate left CFV access for cavography to exclude duplicated IVCs. Cavagram should be evaluated for anatomical variations of the IVC and renal veins, location of the renal vein inflow, presence of thrombus, intrinsic or extrinsic stenosis, and occlusion.
Complications include hematoma, pseudoaneurysm, arteriovenous fistula and infection at the venous access site, and (rarely) rupture of retroperitoneal veins if they are inadvertently catheterized and a large volume of contrast material is injected.
Normal Anatomy. The IVC is formed through confluence of both CIVs. Major tributaries to the IVC include the renal veins (at the level of the L1–L2 vertebrae) and hepatic veins at the junction of the IVC and the right atrium. In addition, lumbar, right gonadal, adrenal, and accessory hepatic veins drain into the IVC. On cavagram, the IVC is seen as a tubular structure with a negative jet of inflow seen from the renal veins. The diameter of the IVC changes with blood volume, phase of respiration, and cardiac movement. The normal diameter of the IVC just below the level of the renal veins ranges from 13 to 30 mm.13
Anatomical Variations. Duplication of the IVC occurs in 0.2% to 3% of the population.14 This occurs because of persistence of both supracardinal veins. The left CIV continues superiorly along the left side of the aorta as the left IVC and joins the left renal vein, which in turn drains into a right-sided IVC. The suprarenal course of the IVC is normal. The left IVC results from persistence of the left supracardinal vein with regression of the right supracardinal vein. This prevalence of the left IVC varies from 0.2% to 0.5%. The left IVC joins the left renal vein, crosses to the right, and courses similar to normal right-sided IVC.
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