|Approvals/Requirements Satisfied by eRADIMAGING Courses|
|~ ASRT accreditation for ARRT Category A credit (All Courses)||~ MDCB accreditation by the Medical Dosimetrist Certification|
|~ ARDMS and NMTCB accepted (All Courses)||~ CAMRT and Sonography Canada recognize the ASRT approval of these courses.|
|~ California CE requirements met for all radiography courses||~ Florida approval for all courses 1 credit or more|
Karen S. Bubb, AS, BSRT, RT(R), RVT, RDMS
*Manager, Outpatient Ambulatory Imaging Center, Oklahoma City, Oklahoma.
Address correspondence to: Karen S. Bubb, AS, BSRT, RT(R), RVT, RDMS, Manager, Outpatient Ambulatory Imaging Center, 1111 N Lee, Suite 334, Oklahoma City, OK 73103. E-mail: KarensBubb@cox.net.
Disclosure: Ms Bubb reports having no significant financial or advisory relationships with corporate organizations related to this activity.
Lower extremity venous insufficiency is a potentially debilitating condition that can negatively affect an individual's quality of life. There are several risk factors associated with the development of venous insufficiency symptoms. If these symptoms are left untreated, early venous insufficiency symptoms can continue to worsen until chronic venous insufficiency develops. The American Venous Forum developed a universal scoring system called the CEAP that takes into consideration the clinical, etiologic, anatomic, and physiologic factors that may affect the patient. The CEAP scoring system allows clinicians to categorize and quantify the severity of venous disease in order to determine the best possible treatment for each patient. Diagnosis of venous insufficiency must include a thorough history and physical, a comprehensive knowledge of the venous system, and state of the art diagnostic imaging equipment. This article provides a brief overview of venous anatomy, physiology, and pathology; a description of the CEAP system; and an explanation of the most common imaging methods used to diagnose venous insufficiency.
n North America, approximately 25% to 30% of adult females and 10% to 20% of adult males suffer from varicose veins.1 According to the Framingham Study, nearly 2.5% of the female population and nearly 2% of the male population are diagnosed with varicose veins every year. The most common risk factors associated with the development of venous disease are obesity, lack of exercise, hypertension, post-menopausal state, smoking, and cardiovascular disease.2 Other risk factors include prolonged body posture such as sitting or standing for long periods of time, genetic inheritance, heavy lifting, congenital defects, pregnancy, previous trauma, post-thrombotic syndrome, and hypercoagulable states.3 The presence of varicose veins should direct the clinician to investigate the possible development of a condition called venous insufficiency.
Lower extremity venous insufficiency is a condition in which the normal venous blood flow return coming from the lower extremities to the right atrium of the heart is disrupted, causing venous blood to flow backwards (retrograde) and collect in the lower leg. This retrograde venous flow increases the venous blood pressure in the lower extremities, eventually causing venous hypertension. Early symptoms of venous insufficiency include leg cramping, leg pain or heaviness during prolonged standing, skin itching, tingling, and swelling. If the condition is not corrected or properly treated, the severity of symptoms can escalate into the development of chronic skin changes around the ankles such as redness, hyperpigmentation, and skin thickening. Dilated cutaneous (skin) veins such as telangectasias (spider veins), large reticular veins, and varicose veins also begin to appear. Eventually, as the condition worsens, venous stasis changes can lead to dermatitis, lipodermatosclerosis, leg edema, and ulcerations. Over time, the result is a condition known as chronic venous insufficiency (CVI).4 Venous hypertension is the predominant underlying contributing factor that leads to the development of CVI.5
In the past, CVI was often overlooked and its severity was often underestimated due the clinician's lack of familiarity about the condition. However, CVI is no longer considered just a cosmetic problem. In fact, poor cosmesis is actually the result of a real and debilitating underlying disease. The prevalence and impact of CVI on patient populations varies in the literature due to discrepancies in the diagnostic evaluation and diagnosis of CVI and due to discrepancies in the exact definition of what is considered CVI in different areas of the world.6 For this reason, a classification and scoring system for CVI was developed by the American Venous Forum. This system provides classification categories for quantifying venous disease based on the severity, cause, site, and specific abnormality. This universal scoring system is known as CEAP ("C" represents clinical manifestations such as absence or presence of symptoms; "E" represents etiologic factors or causes that may arise from primary, deep, or congenital abnormalities; "A" represents anatomic distribution of the disease such as deep, superficial, or perforators; and "P" represents the underlying physiologic findings such as venous hypertension or obstruction).
The basic CEAP classification method is listed in the Table.7 An example case demonstrating the basic CEAP scoring method would consist of a patient presenting with visible varicose veins, leg pain, and lower leg dermatitis. A duplex ultrasound study reveals multiple incompetent perforator veins in the lower leg and primary reflux of the great saphenous vein. The CEAP scoring for this example patient would be: C 4a (lower leg dermatitis), S (symptomatic), Ep (primary), As (superficial),p (perforator), Pr (reflux), which would be abbreviated as C4aSEpAs,p.7 CVI is a term reserved and used for patients who have chronic changes caused by long-term venous insufficiency and fall into clinical classification categories C3 to C6.8
Venous Anatomy and Physiology of the Lower Extremity
To gain a better understanding of CVI and the importance of its treatment and management, it is important to review normal venous anatomy and physiology. Veins carry oxygen-depleted blood away from the tissues of the body toward the right atrium of the heart. The lower extremity contains fascia, a thin layer of fibrous tissue that separates different layers of tissue and covers the muscles, bones, nerves, etc.9 There are 2 distinct fascial compartments in the lower extremity, superficial and deep compartments. Normal venous anatomy is divided into 3 venous systems—deep, superficial, and perforating.
The superficial compartment contains structures located between the skin and the anterior surface of the muscular fascia, to include multiple layers of small veins that pass through it. The superficial compartment contains the subpapillary venous plexus in the dermal (skin) layer where venous blood collects from the tissues. This blood travels to the reticular venous plexus in the subcutaneous layer just below the skin, which in turn carries the blood to the superficial venous system. Two key veins form the majority of the superficial venous system. They are the small and great saphenous veins (SSV and GSV respectively). Even though the saphenous veins occupy the superficial compartment, they are encased in a subcompartment of fascial tissue called the saphenous compartment. The saphenous veins are covered by a thin saphenous fascia anteriorly and the thicker muscular fascia posteriorly.10 This encasement of fascia surrounding the saphenous vein provides a landmark for accurate identification of the saphenous vein and is termed the "saphenous eye" (Figure 1).11 On occasion, duplication of the saphenous vein is encountered. These veins are commonly called accessory saphenous veins and are typically found coursing parallel to the true saphenous veins. However, unlike the true saphenous veins, the accessory saphenous veins do not typically occupy the saphenous compartment.12
The deep compartment contains structures from the posterior surface of the muscular fascia to the bone to include the deep veins and arteries. The deep veins carry the venous blood one way toward the right atrium of the heart.
Perforator veins are a vital pathway for carrying the venous blood out of the superficial venous system and into the deep venous system. Perforating veins are small connecting veins that cross through the muscular fascial plane in order to connect the superficial veins to the deep veins. Perforator veins literally "perforate" the muscular fascia, hence their name. It is important not to confuse these veins with communicating veins and tributaries. Perforating veins course in a diagonal or semivertical plane and cross through the muscular fascia, while communicating and tributary veins travel horizontally along the superficial compartment and do not cross the muscular fascia (Figure 2).12 The majority of perforating veins are found in the medial (inner) aspect of the leg. They are typically spaced approximately 6 cm apart from the level of the ankle to the upper thigh.13
The deep, superficial, and perforator veins in the lower extremity contain multiple bicuspid (2 cusp), unidirectional valves (Figure 3). These valves are typically located from the level of the common femoral vein down to the level of the ankle. The veins in the foot as well as the veins in the pelvis and abdomen do not normally contain valves. The purpose of the valves in the lower extremity is to ensure that the blood flows only one way, antegrade, from the superficial system into the deep system and eventually into the right atrium of the heart. Venous valvular distribution varies. There are usually more venous valves located below the knee to accommodate the higher venous pressures below the knee. The valves work in conjunction with the muscular contractions of the calf muscles. When the calf muscles contract, they compress the deep veins, which forces the venous blood to flow up the leg. During calf muscle contraction, the valves open to allow the blood to flow up the leg and during calf muscle relaxation, the valves close to prevent the blood from refluxing back down the leg. 14 This calf muscle pump action is commonly called the "pseudo heart."
When a person sits or stands, pressure builds in the veins as the volume of venous blood in the column of veins from the level of the heart to the foot increases. This pressure is commonly called hydrostatic pressure. Normal venous standing pressure is approximately 80 to 90 mm Hg. In a normal individual, the hydrostatic pressure drops approximately 50% with calf muscle exercise and the leg refills with blood slowly. However, when one valve does not close properly, the venous blood refluxes back down the leg in a retrograde fashion (Figure 4). This causes the weight of the refluxed blood on the other valves in the lower part of the leg to increase. Over time, a domino effect can result with many more valves eventually failing due to the increased pressure on the valve cusps. When calf muscle exercise fails to decrease the hydrostatic pressure by 50% and the leg refills with blood rapidly, venous hypertension results due to increased capillary pressure from the accumulated blood in the lower extremity (above 90 mm Hg).14 As mentioned previously, venous hypertension is the predominant underlying contributing factor that leads to the development of CVI. Most deep veins can withstand an elevated pressure gradient because the muscular fascia that surrounds the deep veins is rigid and does not allow the deep veins to expand very much. However, the superficial veins do not have a muscular fascia to keep them from dilating. The stretchy, expandable tissues near the skin allow the superficial veins to dilate, resulting in large visible varicose veins.15
Extrinsic Causes of Lower Extremity Varicosities
Lower extremity varicosities do not always originate from abnormalities in the extremities themselves. They can occur due to an abnormality in the pelvis or abdomen. Although these cases are not as common as typical lower extremity venous insufficiency cases, they are important to document and treat. There are several types of pelvic and abdominal abnormalities that can cause the development of lower extremity varicose veins. These extrinsic abnormalities include vulvoperineal varicosities, round ligament varicosities, Klippel-Trenaunay syndrome (KTS), persistent sciatic vein incompetence, congenital venous malformations,16 May-Thurner syndrome, inferior vena caval occlusion,17 and pelvic masses.
Vulvoperineal varicosities are the most common extrinsic cause of lower extremity varicosities, occurring in 4% to 8% of cases.16 These varicosities are often associated with pelvic congestion syndrome (PCS). PCS is a condition in which the ovarian veins cannot empty, subsequently causing increased venous pressure. Over time, this pressure causes the vein walls and valves to weaken and engorge with blood, resulting in a condition called venous stasis. PCS occurs most often during pregnancy due to physiological changes that take place such as weight gain, increased fluid retention, and pressure from the growing uterus. Other factors such as an increase in estrogen, which weakens the vein walls, and anatomic differences in certain women can also cause PCS.18 Once the veins are damaged, the varicosities remain even after pregnancy. Over time, periovarian varicosities develop. Round ligament varicosities can also develop as mass-like structures near the inguinal region.16 As these varicosities progress in size, they begin to stimulate nearby nerves and cause symptoms such as pelvic pain, pelvic pressure, and heaviness. Eventually, as the condition progresses, venous pressure from the pelvic varicose veins causes vulvar, buttock, and posterior or lateral thigh varicosities to appear. These varicosities may or may not communicate with the saphenous veins of the lower extremity.18
Klippel-Trenaunay syndrome, persistent sciatic vein incompetence, and congenital venous malformations are other possible extrinsic causes of lower extremity varicosities.16 KTS is a congenital defect primarily affecting one leg, although other sites have been reported. Three signs of this syndrome are typically present: a port-wine stain (a capillary malformation), varicose veins or venous malformations, and hypertrophy of the limb involved. Most of the varicose veins associated with KTS are located on the lateral side of the leg originating from the foot and traveling upwards until reaching the thigh, buttock, or pelvic region. Most of these varicosities are not associated with the saphenous veins, but they can affect the entire venous system.19
A persistent sciatic vein is commonly associated with KTS, but has been found in patients without KTS. It is a congenital anomaly in which the embryonic axial vein fails to involute and develops into a persistent sciatic vein instead. These veins are categorized into 3 groups based on their anatomic location. The complete category extends from the popliteal veins to the internal iliac veins and passes through the sciatic notch. The upper category extends from the upper thigh to the pelvis and passes through the sciatic notch. The lower category is located in the mid to distal thigh and communicates with the deep femoral veins or the superficial veins.16
Venous malformations are congenital abnormalities typically found in patients with KTS, but they also occur in unrelated cases. Venous malformations may be localized or relatively extensive and can be found in the skin of the extremities and body. However, they can also be found internally in the abdominal viscera, skeletal muscles, and even in the bones. They are low-flow lesions that can engorge with blood and cause pain, swelling, and abnormal bleeding. They also have a tendency to thrombose.20
May-Thurner syndrome is an anatomic variant in which the right common iliac artery crosses over the left common iliac vein in such a way that it compresses the left common iliac vein. Over time, the left common iliac vein walls thicken, resulting in iliac vein stenosis and eventual thrombosis.17 The blood return from the left lower extremity slows down causing venous stasis and edema of the left lower extremity. Ultrasound of the left common femoral vein often reveals a patent deep venous system with decreased spectral wave velocities, phasicity, and spontaneity when compared to the contralateral right common femoral vein.21
Inferior vena caval occlusion is often caused by thrombus, renal cell carcinoma, retroperitoneal fibrosis, radiation therapy, aortic aneurysm, ascites, trauma, surgery, or filter placement. Symptoms usually present as bilateral leg edema that cannot be relieved with leg elevation. Other symptoms such as elevated venous pressure causing a heavy or full sensation in the groin, leg aches, and leg ulcerations are also present. The blood return from the lower extremities slows down and collateral veins and varicosities typically develop due to the elevated venous pressure in the legs.21
Diagnostic Techniques and Protocols
When a patient presents with symptoms of venous insufficiency, the first step in the diagnostic process is to conduct a thorough history and physical examination. Once the history and physical examinations are conducted, diagnostic testing should be carried out. A brief overview of the diagnostic techniques and protocols to assess CVI is presented below.
Duplex sonography, also called ultrasound, is considered the gold standard of testing for the diagnosis and monitoring of CVI.14 Sonographic imaging of CVI involves direct visualization of the vessels with the use of real-time duplex imaging combined with spectral and color Doppler imaging. A sonographic examination of the lower extremity venous system can provide useful information regarding variations of the venous anatomy such as the presence of accessory saphenous veins, intersaphenous communicating veins, and junctional variations. It can also provide the precise anatomic location of incompetent vein segments and identify and locate incompetent perforator veins. Sonography also can be used for guidance during treatment and as a device to monitor patients during follow-up examinations post treatment.22
Direct sonographic testing for the diagnosis of CVI should begin with a brief examination of the deep venous system to determine whether there is deep venous reflux and to rule out deep vein thrombosis (DVT). Images should include compression and spectral Doppler waveforms of the common femoral vein, proximal GSV, femoral vein, popliteal vein, posterior tibial veins, anterior tibial veins, and peroneal veins. After the deep system is evaluated, the superficial system is thoroughly examined. When examining the superficial and perforator venous systems, the patient should either be positioned standing or in a gravity-dependent reverse trendelenberg position, with their feet below the level of their heart. Patient physical condition and tolerance will determine the best method. Once the examiner reaches the knee level, the patient may be seated with their legs in a dependant position below the level of their heart. Representative images should be taken from proximal, mid, and distal vein segments. Images should include transverse and longitudinal B-mode images, as well as spectral and color Doppler images with maneuvers such as valsalva, augmentation, and proximal compression to evaluate flow characteristics and venous valvular reflux.23 Clinically significant venous reflux demonstrated on a spectral Doppler waveform is considered 1.0 seconds in the deep veins (femoral and popliteal), 0.5 seconds (500 ms) in the saphenous veins, and 0.35 seconds in the perforating veins (Figure 5).24 All 3 chambers of the calf (anterior, posterior, and lateral) should be scanned to identify incompetent perforator veins (IPV).23 IPVs typically cross the muscular fascia and demonstrate reflux. Perforator vein diameters should be measured at the point where they cross the muscular fascia. Most IPVs measure 3.9 mm or more in diameter, however smaller yet significant IPVs have been reported. Documentation of IPVs should include their location and distance from the sole of the foot (Figure 6).9
The use of sonography for the diagnosis of CVI has some limitations. The examination is highly operator dependant and it is imperative that the vascular sonographer obtain a thorough knowledge of superficial venous anatomy and physiology. Dysfunction and or abnormalities of the pelvis and abdominal venous structures are not well demonstrated with sonography. The examination is also time-consuming with the average complete bilateral examination taking approximately 60 to 90 minutes. Many vascular sonographers are reporting stress injuries related to poor examination ergonomics. To help eliminate this situation, a special tilt table or other standing platform should be used. This will allow the patient to stand comfortably and safely and enable the sonographer to better reach the patient's legs while simultaneously viewing the monitor and operating the equipment. For these reasons, adjunct imaging modalities should also be considered.
Plethysmography is an indirect testing method that can be used as an adjunct device to duplex sonography. The use of plethysmography in the diagnosis of CVI helps determine the effect venous reflux has on the body's overall circulation. Plethysmography is a non-invasive, indirect test used to measure physiological changes in blood volume and pressure. Indirect testing provides information about the physiologic hemodynamics involved. The term hemodynamics refers to the study of how the blood is actually moving or flowing inside the body based on the forces that affect its movement. It is typically measured by pressure and volume measurements.25 There are 2 general types of plethysmography, electrical and mechanical. Electrical plethysmography units use different types of transducers to measure blood volume changes. Mechanical plethysmography devices measure the amount of air or water that is displaced, which determines blood volume changes. Electrical plethysmography devices are much easier to operate than mechanical plethysmography devices and have replaced most mechanical plethysmography devices. Several types of electrical plethysmography devices can be used to evaluate CVI such as photo, strain gauge, and impedance plethysmography.26
Photoplethysmography (PPG) is a type of electrical plethysmography that uses a light emitting diode that can measure blood volume and pressure changes based on the absorption and reflection of light through the skin. The most common PPG instrument is a pulse oximeter. In venous testing, a PPG transducer is placed on the patient's foot or toe and the calf-muscle pump is exercised to empty the blood from the limb. Once the leg is emptied, the time it takes for the leg to refill with blood to approximately 90% of its original volume is recorded. Normal venous refill time should be 20 seconds or longer. Shorter refill times suggest the presence of venous reflux disease. Tourniquets can be used to assess deep versus superficial refill times. The use of PPG for the diagnosis of venous insufficiency is nonspecific in that it only provides information to verify the presence or absence of venous insufficiency, but not specific location or severity of the disease.1
Strain gauge plethysmography (SGP) is another type of electrical plethysmography. It can be used to determine maximum venous outflow, venous volume, maximum venous incremental volume, maximum venous reflux volume, and maximum venous reflux flow. When evaluating a patient for CVI, a small tube-like transducer filled with a conductive substance (eg, gallium or mercury) is wrapped securely around the largest part of the calf and connected to a current. The legs are elevated to a level above the patient's heart. A blood pressure cuff, acting as a tourniquet, is applied to the thigh and inflated above arterial systolic pressure (up to 300 mm Hg) to impede all blood flow. A second cuff placed below the first cuff is also rapidly inflated to approximately 50 mm Hg. The purpose of the second cuff inflation is to try to force the venous blood to flow distally, thus testing the valves for incompetence. As blood fills the extremity, the circumference of the extremity is altered creating a signal. Expansion of the limb indicates venous reflux. SPG is not accurate with the presence of partial DVT or post-thrombotic states.26
Impedance plethysmography (IPG) is also a type of electrical plethysmography that measures a voltage change directly corresponding to a change in blood flow and volume. The more volume of blood in the leg, the better the current conducted through the leg. A thigh tourniquet and 2 circumferential electrodes are placed on the calf, 10 cm apart. The leg is raised approximately 20 cm above the level of the heart. A weak, imperceptible alternating current is then applied and a pre-fill voltage is recorded. The tourniquet is tightened to approximately 60 mm Hg, enough to impede venous flow, but still allow arterial flow to continue. After approximately 45 to 120 seconds, once peak venous volume is achieved, a plateau filling voltage is recorded. The tourniquet is quickly released and a 3-second post tourniquet voltage is recorded. Normal venous return is indicated by a quick voltage drop back to the prefill voltage. Abnormal venous return is indicated by a long delay before the voltage drops or by no voltage change at all, indicating poor venous emptying.1 The drawback in using IPG for the diagnosis of CVI is that the presence of DVT and post-thrombotic states may also exist, hindering the diagnosis.
Other Imaging Modalities
As mentioned previously, lower extremity duplex sonography is considered the gold-standard imaging modality for most venous insufficiency studies. However, because lower extremity varicosities do not always originate from abnormalities in the extremities themselves, other complimentary imaging modalities can provide useful diagnostic information. Conventional venography, computed tomographic venography, and contrast-enhanced 3-dimensional (3D) magnetic resonance (MR) venography are useful for determining the precise cause of varicose veins and related symptoms.
Conventional venography and varicography, also called phlebography, is an invasive examination that involves injecting a contrast agent into the veins under fluoroscopic guidance.27 There are 2 types of conventional venography, ascending and descending. Ascending venography involves placing one tourniquet above the ankle and a second one above the knee. The patient is placed in a steep reverse trendelenberg (60 degrees). A small venous catheter is inserted into a vein on the top of the foot and X-ray contrast is injected into the vein under fluoroscopic imaging. The tourniquets are placed to prevent the contrast from entering the superficial venous system. The deep veins fill with contrast and are observed for occlusion, irregular filling of the lumen, and collaterals. Perforating veins are also observed for valve abnormalities that may represent insufficiency. Ascending venography is used today mainly as a preoperative mapping tool.
Descending venography is also performed with the patient in a steep reverse trendelenberg position. A venous catheter is inserted into the common femoral vein and contrast is injected while the patient performs a valsalva maneuver. If valve incompetence is present in the deep system, the contrast will reflux down the leg. The severity of reflux is classified based on the amount of reflux. Descending venography can also help determine whether the incompetent deep valves can be repaired with valvuloplasty. The images are recorded with fluoroscopy and radiographs. 28 Conventional venography is valuable in differentiating between primary and secondary venous disease, identifying an obstruction in the common femoral and iliac veins, and in determining the severity and level of reflux in the deep system.29 It is also useful in diagnosing and treating PCS. During a venography procedure, ovarian vein coil embolization can be performed to block the blood flow to the pelvic veins involved in PCS. Coil embolization is a process in which a tiny coil is inserted through the catheter in the vein and advanced into the ovarian vein. The coil triggers thrombus formation in the ovarian veins, subsequently blocking further accumulation of blood in the veins (Figure 7).16
Computed tomographic venography
Until recently, computed tomographic (CT) venography was not considered a reliable diagnostic method for evaluating venous disease. Conventional CT venography resulted in considerable false-positive diagnoses of venous thrombosis. The reason for the false-positive diagnostic errors was the inability of the contrast to mix easily with the venous blood. Venous blood flow is non-laminar (turbulent rather than streamlined), therefore when a contrast bolus was injected directly into the vein and a scan was immediately conducted, some of the blood would not mix with the contrast, resulting in partial or non-opacification of the veins. Attempts at trying to wait on the contrast to circulate through the patient's entire system before conducting the scan also resulted in timing errors.30
The use of multidetector CT (MDCT) and 3D reconstruction has significantly increased the reliability of CT venography. During MDCT venography, 2 separate injections are administered to the patient rather than 1 single contrast injection. The first injection consists of a bolus of undiluted contrast; the second consists of a saline flush or a very dilute mixture of contrast and saline. Each injection is administered with a power injector at specific time intervals. Image acquisition sequences are performed at specific time delays to obtain peak venous enhancement (typically 60, 90, and 180 seconds post injections).16,30 The delay in time allows excellent contrast enhancement without artifact. 3D reconstruction is done by smoothing the axial images and conducting interactive volume rendering of the axial, sagittal, and coronal images.31 MDCT venography with 3D volume rendering is especially useful in demonstrating pelvic and vulvoperineal varicosities causing distal varicosities in the lower extremities.21 It also provides an excellent map of the lower extremity venous system to include all superficial veins, perforating veins, and any varicose veins present (Figure 8).31
When comparing MDCT venography to duplex sonography, MDCT venography examinations were noted to be much faster than duplex sonography examinations and were more easily reproduced with much less operator dependence. MDCT venography provided an important outline map of the entire venous system to include all of the perforating veins.31 This map allowed the vascular surgeon to better visualize the exact anatomic morphology.30 Because MDCT venography is performed with the patient supine rather than upright, the hydrostatic pressure is significantly reduced in the supine position. Therefore, MDCT cannot provide accurate functional information such as perforator vein reflux. However, MDCT venography can provide useful morphological data to suggest venous insufficiency, such as increased vein diameters above 6 mm. In a recent research study by Lee et al, MDCT venography vein diameters demonstrated a strong correlation to sonographic vein diameters. These diameter measurements yielded 98% sensitivity and 83% specificity for the diagnosis of GSV insufficiency.31 Other morphologic findings such as the presence of varicosities, asymmetric tortuous vessels, and direct communication with varicosities also provide important clues to the functionality of the vessels.31 Contraindications to MDCT venography include adverse reactions to the contrast material and exposure to ionizing radiation. If the patient is allergic to the contrast agent and/or is pregnant, MDCT cannot be performed.
Duplex sonography is still a key imaging modality in evaluating and monitoring for perforating vein insufficiency. For this reason, both modalities should be utilized when evaluating for venous insufficiency. Ideally, conducting an MDCT examination first would provide an outline map of the entire venous system to include the perforating veins. Next, a targeted duplex sonography examination would be directed at the perforating veins to test for insufficiency, thus drastically reducing the sonographic examination time.31
Magnetic resonance venography
Similar to MDCT venography, MR venography image quality and scanning protocols have drastically improved and are now commonly used as an adjunct imaging modality to duplex sonography. MR venography is noninvasive and does not require exposure to ionizing radiation. MR images are easy to reproduce and are much less operator dependant than sonography. The use of MR allows for 2-dimensional (2D) or 3D visualization of the entire venous system with excellent visualization of the deep veins, superficial veins, perforating veins, and varicose veins.32 It also demonstrates post-thrombotic changes. 3D MR venography is valuable in surgical planning because it provides a morphological map of the entire venous system. Recent clinical studies indicate that varicose vein changes of the GSVs and SSVs were detected with a sensitivity of 94% and a specificity of 96% and post-thrombotic changes were diagnosed with 100% sensitivity and 98% specificity.33
A research study by Müller et al describes the typical performance of a direct contrast enhanced 3D MR venography study as follows: it is typically performed using a 1.5-Tesla MR scanner equipped with a 3-station phased array peripheral vascular surface coil.32 This coil enables visualization of the veins from the ankle to the inferior vena cava. The patient is positioned supine, feet first going into the bore of the magnet. A 2D spin-echo scout view sequence is performed in the transverse plane from the lower legs to the pelvis. Next, a 3D spoiled gradient recalled echo sequence is performed (Figure 9).33 Then, a direct contrast injection method is performed by placing a tourniquet around the patient's ankle. Contrast is injected continuously into a superficial vein on the dorsal part of the foot (if the study is bilateral, both legs should be injected and imaged at the same time). It is important to note that the tourniquet is essential because it routes the contrast into the deep venous system rather than allowing it to spill into the superficial venous system. After a time delay of approximately 40 seconds into the injection, image acquisition at each station is initiated. Once the data are acquired, the tourniquet is removed to allow filling of the superficial venous system and a second set of images is immediately acquired.32
The limitations of MR venography are similar to those of MDCT venography. Because the examination is performed with the patient supine, the hydrostatic pressure is reduced and functional information such as reflux is not obtainable. However, similar to MDCT venography, MR venography relies on morphologic data to indicate the presence of venous insufficiency. The presence of varicose veins with diameters above 3 mm suggests diagnostically significant superficial venous disease on MR venography. Contraindications of MR venography include the use of contrast material with the possibility of allergic reaction, the possibility of the presence of ferromagnetic material or devices such as neurostimulators and pacemakers, and individuals suffering from claustrophobia.32
Both duplex sonography and MR venography should be utilized when evaluating for venous insufficiency. Performing an MR venography examination first would cut down on the time needed to perform a duplex sonogram by providing a detailed map of the entire venous system so that a targeted duplex sonography examination of the perforating veins could be performed.
Lower extremity venous insufficiency is a potentially debilitating condition if left untreated. The first step in recognizing symptoms and diagnosing venous insufficiency is to gain a thorough knowledge of the venous system to include normal venous anatomy of the deep, superficial and perforating systems, anatomical variations, venous physiology, and pathology. The universal CEAP scoring system should be used to standardize the classification of disease and recommend the best possible treatment approach for each patient. Several diagnostic studies can be used to evaluate the extent of venous insufficiency. Duplex sonography remains the gold standard for lower extremity venous insufficiency imaging. However, determining which modalities to use should be based on the patient's history and symptoms as well as on the skill level of the technical staff, equipment availability, patient tolerance, cost, and time constraints. The use of dual modalities such as a combination of duplex sonography and MDCT venography provide the clinician with functional information as well as a reproducible outline of the entire venous system for future clinical treatment planning, periodic monitoring, and post-treatment follow-up.
1. Nicolaides A. Investigation of chronic venous insufficiency. Circulation. 2000;102:e126-e163. Available at: http://circ.ahajournals.org/cgi/reprint/102/20/e126. Accessed March 25, 2010.
2. Brand F, Dannenberg A, Abbott R, Kannel W. The epidemiology of varicose veins: The Framingham Study. Am J Prev Med. 1988;4:96-101. Abstract available at: http://www.ncbi.nlm.nih.gov/pubmed/3395496. Accessed April 25, 2010.
3. Venous Disease Coalition. Chronic venous insufficiency: what is it? Venous Disease Coalition Web site. Available at: http://www.spotaclot.org/. Accessed April 25, 2010.
4. US National Library of Medicine. Venous insufficiency. Medline Plus web site. Available at: http://www.nlm.nih.gov/medlineplus/ency/article/000203.htm. Accessed March 26, 1020.
5. Bergan JJ, Pascarella L. Perforating veins. In: Bergan JJ. The Vein Book. Burlington, MA: Elsevier, Inc. 2006;58:535-538.
6. Eberhardt R, Raffetto J. Chronic venous insufficiency. Circulation. 2005;111:2398-2409. Available at: http://circ.ahajournals.org/cgi/content/full/111/18/2398. Accessed April 25, 2010.
7. Meissner M, Gloviczki P, Bergan J, et al. Primary chronic venous disorders. J Vasc Surg. 2007;46(suppl S):54S-67S.
8. Pascarella L, Mekenas L. Ultrasound examination of the patient with primary venous insufficiency. In: Bergan JJ. The Vein Book. Burlington, MA; Elsevier, Inc. 2006;18:171-180.
9 Meissner M. Chronic venous disorders. In: Zierler G. Strandness's Duplex Scanning in Vascular Disorders. 4th ed. Philadelphia, PA: Lippincott, Williams, and Wilkins; 2009;18:3075-3081.
10. Mozes G, Gloviczki P. Venous embryology and anatomy. In: Bergan JJ. The Vein Book. Burlington, MA: Elsevier, Inc. 2006;2:20-24.
11. Cavezzi A, Labropoulos N, Partsch H, et al. Duplex ultrasound investigation of the veins in chronic venous disease of the lower limbs-UIP consensus document. Part II. Anatomy. Eur J Vasc Endovasc Surg. 2006;31:288-299.
12. Owen C. The role of ultrasound in endovenous ablation of varicose veins—before, during and after treatment. GE Healthcare Online CME Course. 2008:1-12. Available at: www.gehealthcare.com/usen/ultrasound/education/products/cme_end_abl.html. Accessed December 12, 2008.
13. Somjen G. Anatomy of the superficial venous system. Dermatol Surg. 1995;21:35-45.
14. Eberhardt R, Raffetto J. Chronic venous insufficiency. American Heart Association. Circulation. 2005;111:2398-2409. Available at: http://circ.ahajournals.org/cgi/content/full/111/18/2398. Accessed January 12, 2009.
15. Raines J, Almeida J. Role of physiologic testing in venous disorders. In: Bergan JJ. The Vein Book. Burlington, MA: Elsevier, Inc. 2006;5:45-50.
16 Jung S, Lee W, Chung J, et al. Unusual causes of varicose veins in the lower extremities: CT venographic and Doppler US findings. RadioGraphics. 2009;29:525-536. Available at: http://radiographics.rsna.org/content/29/2/525.long. Accessed May 8, 2010.
17. Nachreiner R, Bhuller A, Dalsing M. Surgical repair of incompetent venous valves. In: Dalsing MC. The Vein Handbook. Beverly, MA: American Venous Forum. 2008;16. Available at: http://veinforum.org/index.php?page=hbk16a. Accessed February 23, 2010.
18. Pelvic congestion syndrome. VeinDirectory.org. 2009. Available at: http://www.veindirectory.org/content/pelvic-congestion-syndrome.asp. Accessed May 5, 2010.
19. Janniger C. Klippel-Trenaunay-Weber Syndrome. eMedicine Web site. 2010. Available at: http://emedicine.medscape.com/article/1084257-overview. Accessed April 28, 2010.
20. Podda S, Duffy F. Vascular, venous malformations. eMedicine Web site. 2008. Available at: http://emedicine.medscape.com/article/1296303-overview. Accessed April 28, 2010.
21. Boyd D. Unilateral Lower Extremity Edema in May-Thurner Syndrome. Association of Military Surgeons of US. redOrbit Web site. 2004. Available at: http://www.redorbit.com/news/health/113570/unilateral_lower_extremity_edema_in_maythurner_syndrome/index.html. Accessed April 16, 2010.
22. Allan P. Role of ultrasound in the assessment of chronic venous insufficiency. Ultrasound Quarterly. 2001;17:3-10.
23. Society of Vascular Ultrasound. Lower Extremity Venous Insufficiency Evaluation—Vascular Technology Professional Performance Guidelines. Lanham, MD: Society for Vascular Ultrasound; 2007. Available at: http://www.svunet.org/files/positions/LEVenousInsufficiencyEvaluation.pdf. Accessed December 10, 2009.
24. Zygmunt J Jr. What is new in duplex scanning of the venous system? Perspect Vasc Surg Endovasc Ther. 2009;21:94-104.
25. What is hemodynamics? International Hemodynamic Society Web site. 2000. Available at: http://www.hemodynamicsociety.org/hemodyn.html. Acessed May 2, 2010.
26. Graham AA. Plethysmography: safety, effectiveness, and clinical utility in diagnosing vascular disease. National Library of Medicine. AHCPR. 1996. Available at: http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=hsarchive&part=A42071. Accessed May 2, 2010.
27. Chronic venous insufficiency. Epocrates online 2010. Avaiable at: https://online.epocrates.com/u/2934507/Chronic+venous+insufficiency/Diagnosis/Tests. Accessed May 2, 2010.
28. Nicolaides A. Pathophysiology of chronic venous disease [abstract]. Presented at: Arctic Fjords Conference and Workshops on Chronic Venous Disease. 2007. Avaiable at: http://www.europeanvenousforum.org/files/arctic_f_conf/Arct_Fjords_abstr_pres.pdf. Accessed May 6, 2010.
29. Guidelines for Diagnostics and Treatment of Venous Leg Ulcers. European Dermatology Forum. 2004. Available at: http://www.euroderm.org/content/guideline_on_venous_leg_ulcers.htm. Accessed May 8, 2010.
30. Meyer C, Vagal A. New CT protocol yields improved venous images. RSNA News. 2008. Available at: http://www.rsna.org/Publications/rsnanews/jan08/upload/RSNANews_Jan08_CT_Venous.pdf. Accessed May 10, 2010.
31. Lee W, Chung J, YinY, et al. Three-dimensional CT venography of varicose veins of the lower extremity: image quality and comparison with Doppler sonography. AJR Am J Roentgenol. 2008;191:1186-1191. Available at: http://www.ajronline.org/cgi/content/full/191/4/1186. Accessed May 10, 2010.
32. Müller M, Mayer D, Seifert B, et al. Recurrent lower-limb varicose veins: effect of direct contrast-enhanced three-dimensional MR venographic findings on diagnostic thinking and therapeutic decisions. Radiology. 2008;247:887-895. Available at: http://radiology.rsna.org/content/247/3/887.long. Accessed May 10, 2010.
33. Ruehm S, Wiesner W, Debatin J, et al. Pelvic and lower extremity veins: contrast-enhanced three-dimensional MR venography with a dedicated vascular coil—initial experience. Radiology. 2000;215:421-427. Available at: http://radiology.rsna.org/content/215/2/421.full. Accessed May 10. 2010.
|What did you think of this article?
|»||Comment From: TabbyG||» Posted on: 06/28/2010 14:48 PM|
|Great article - very informative!|
|»||Comment From: ARUBA00||» Posted on: 12/07/2010 12:29 PM|
|GOOD INFORMATION. RESULTS PROVEN BY MANY MODALITIES|
|»||Comment From: Donna||» Posted on: 10/28/2011 11:15 AM|
|Easy to follow article and test. More importantly the information didn't go deeper than what I would normally use in the clinical setting.|
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