Peripheral venous evaluation


On completion of this chapter, you should be able to:

  • Describe the anatomy encountered during a venous duplex imaging examination

  • Understand venous physiology as it relates to the development of peripheral venous disease

  • List the risk factors, signs, and symptoms of venous disease

  • Outline the proper instrument control settings used during venous duplex imaging

  • Describe the characteristics of venous Doppler signals obtained during venous duplex imaging

  • Describe the imaging characteristics of a normal venous system

  • Discuss the imaging characteristics associated with deep vein thrombosis and venous reflux

Venous disease may be categorized as an acute or a chronic process and can present in the upper and lower extremities. Due to ultrasound’s ability to conduct dynamic, nonionizing, and portable imaging in real-time, it is an ideal radiologic modality for the interrogation of venous pathology. Among these advantages is its ability to perform color and spectral Doppler imaging, which allow for an anatomic and physiologic evaluation of the venous system to be made. To this end, ultrasound imaging is tasked with conducting a variety of venous imaging examinations, spanning multiple areas of the body.

Venous pathology can take many forms; however, deep vein thrombosis (DVT) has a high prevalence and is arguably the most medically concerning. Characterized by a thrombus, or blood clot, in a deep vein(s), DVT can occur in both the upper and lower extremities. Although the exact incidence or prevalence of DVT in the United States is unknown, due to many going undetected, it has been estimated that DVT affects more than 600,000 individuals annually. The concerning nature of this disease arises from a complication that can occur when a thrombus dislodges from the venous lumen and propagates to the arteries of the lungs. This is known as a pulmonary embolism (PE) or venous thromboembolism (VTE) while describing both the DVT and PE. VTE is the third most common cardiovascular disorder in the United States and maintains a fairly high mortality rate. Thus a timely and accurate diagnosis of DVT is imperative.

The signs and symptoms of DVT are common and nonspecific, meaning they may have several other possible causes (e.g., musculoskeletal disorders, ruptured Baker’s cyst, cellulitis), making its diagnosis based on signs and symptoms alone unreliable. This, coupled with the importance of an accurate DVT diagnosis, has caused the venous duplex examination to become one of the most commonly ordered vascular sonograms.

Besides a PE, other less severe complications of DVT can often result. Postthrombotic syndrome (PTS) consists of chronic leg pain, inflammation, redness, and ulcers. Deep and superficial venous insufficiency, varicose veins, and recurrent DVT are also common manifestations of PTS. Ultrasound imaging is also often used for the evaluation of these DVT complications. Therefore it is necessary to understand and recognize the presentation of a wide variety of venous diseases, as the versatility and advantages of ultrasound imaging makes it the radiologic modality that is often used for venous pathology detection and evaluation.

Anatomy for peripheral venous duplex imaging

The peripheral venous portion of the circulatory system is located in the upper and lower extremities and consists of the deep, superficial, and perforating (communicating) veins located within them. The main function of the peripheral venous system is to return deoxygenated blood from organs and tissues back to the heart. In the periphery, deoxygenated blood leaving the capillaries enters the venules of venous microcirculation. From the venules, venous blood drains into the superficial veins and from there to the deep veins. Perforating veins provide a channel between superficial and deep veins.

Like arteries, veins are made up of three layers: (1) tunica intima (innermost), (2) tunica media (middle), and (3) tunica adventitia (outermost). However, these layers differ between arteries and veins, in that the tunica media layer in veins is poorly developed. Because the tunica media is the muscular layer of the lumen and it provides the vessel with stability, veins are more elastic than arteries.

The presence of venous valves is another unique feature of the venous system. Venous valves are bicuspid and unidirectional folds that arise from the tunica intima. These valves serve to maintain antegrade venous blood flow (from the peripheral to central veins, toward the heart). These one-way valves are necessary due to the effects that hydrostatic pressure places on the blood flowing within peripheral veins. Hydrostatic pressure, also known as gravitational pressure when standing upright, is defined as the pressure placed on a fluid in a column as a result of gravity. Because the heart is located above many of the peripheral veins, the blood traveling upward in the peripheral venous system must flow against the pressure placed on it from the weight of the column of blood that exists above it. To this end, the further a peripheral vein is from the heart, the more hydrostatic pressure the blood in it must overcome. It is for this reason that venous valves increase in quantity in the distal portions of the lower extremities.

Lower extremity

Deep veins.

​As the name suggests, lower extremity deep veins are located deep within the muscles of the legs and serve as the primary route of drainage for the leg ( Figure 40-1 ). Consequently, deep veins are typically larger than superficial veins, as they must support a larger blood volume. Lower extremity deep veins also have corresponding arteries located in close proximity to them.


​Diagram of the deep veins of the lower extremity.

Beginning distally, the anterior tibial veins (ATVs) are a set of paired veins that drain blood from the dorsum of the foot (dorsalis pedis veins) and the anterior compartment of the calf. Originating near the tibia at the level of the ankle, the ATVs are located anterior to the interosseous membrane, as they ascend the lower leg with the anterior tibial artery. Ultimately the ATVs join the posterior tibial veins to form the popliteal vein .

The posterior tibial veins (PTVs) are a set of paired veins that drain the posterior compartment of the lower leg and originate from the plantar veins (superficial and deep) of the foot. The PTVs ascend along the medial calf beginning at the level of the medial malleolous, parallel to the posterior tibial artery. In the proximal calf, the PTVs combine with the peroneal veins to form the tibial-peroneal trunk, just before uniting with ATVs to form the popliteal vein.

The peroneal veins (also known as the fibular veins) are another set of paired veins that drain blood from the lateral compartment of the lower leg. The peroneal veins parallel the path of the PTVs, located deep to the soleus and gastrocnemius muscles along the fibula. Also traveling with the peroneal veins is the peroneal artery (also known as the fibular artery). In the proximal calf, the peroneal veins join the PTVs to form the tibial-peroneal trunk.

The final deep veins of the lower leg are the soleal sinuses and the gastrocnemius (sural) veins. These veins are located deep within the muscular compartments of the soleus and gastrocnemius muscles, respectively. The soleal sinuses are large reservoirs of venous blood that drain to the PTVs or peroneal veins. The gastrocnemius veins are a set of paired veins that, accompanied by the gastrocnemius artery, ascend the leg in the medial and lateral gastrocnemius muscles, before draining directly into the popliteal vein.

The popliteal vein drains the blood of the lower leg and originates from the confluence of the ATVs with the peroneal and PTVs (tibial-peroneal trunk). The popliteal vein is located in the popliteal fossa (area behind the knee), in close proximity to the popliteal artery. In the lower popliteal fossa, the popliteal vein is medial and superficial to the artery. As they ascend the popliteal space, the popliteal vein remains superficial but moves lateral to the artery. The popliteal vein and artery continue to ascend until they pass through the adductor canal (Hunter’s canal) at the approximate level of the knee joint. Here they become the femoral vein and artery. A duplicated popliteal vein is present in approximately 36% to 44% of the population. ,

The femoral vein (FV) originates from the popliteal vein in the distal thigh at the hiatus of the adductor magnus muscle, at the level of the adductor (Hunter’s) canal. The FV is accompanied by the femoral artery, to which it courses deep throughout the medial thigh. The FV terminates in Scarpa’s (femoral) triangle at its confluence with the deep profunda femoris (deep femoral) vein. A duplicated FV is present in up to 33% of the population. Recognition and thorough evaluation of a duplicated FV system is imperative, as 20% of all lower extremity DVTs are isolated to the FV. It is important to note that the FV is often referred to as the superficial femoral vein. This began as a method of differentiating the FV from the profunda femoris (also referred to as the deep femoral vein). However, adding superficial to the name brought about confusion among clinicians. This resulted in DVTs located in the FV being left untreated, as they were mistakenly thought to be in the superficial system . In 2004 an international interdisciplinary committee of physicians met to discuss issues regarding terminology of the lower limb veins. The committee concluded that the word superficial be omitted, and only the term femoral vein be used. Similarly, the same nomenclature is applied to the femoral artery.

The profunda femoris vein, also known as the deep femoral vein, drains the deep muscles of the proximal thigh. Similar to other deep veins of the leg, the profunda femoris travels in proximity to the profunda femoris artery. The profunda femoris vein ascends the upper leg until it joins the FV to form the common femoral vein. The confluence of these two veins is distal to the bifurcation of the common femoral artery.

The common femoral vein (CFV) is formed by the confluence of the FV and profunda femoris vein. The CFV also receives the great saphenous vein at the level of the saphenofemoral junction. The CFV lies in Scarpa’s triangle, medial to the common femoral artery. The CFV terminates at the level of the inguinal ligament, where it becomes the external iliac vein.

The external iliac vein originates at the level of the inguinal ligament as a continuation of the CFV. The external iliac ascends parallel to the external iliac artery, before it joins the internal iliac vein to become the common iliac vein. The internal iliac vein travels with the internal iliac artery and serves to drain the pelvis, before it joins the external iliac vein.

The common iliac vein is formed by the confluence of internal and external iliac veins. Further proximal, the union of the right and left common iliac veins forms the inferior vena cava (IVC). The left common iliac vein is oriented obliquely and lies medial to the left common iliac artery. While they ascend, the left common iliac vein must cross beneath the right iliac artery to join the right common iliac vein at their confluence to form the IVC. This anatomic feature of the left common iliac vein crossing beneath the right iliac artery causes mild compression of the vein and has been cited as the reason for slightly greater prevalence of left-side DVT. Continued compression can result in the venous entrapment disorder known as May-Thurner syndrome, which is characterized by the compression of the left common iliac vein by the right common iliac artery. If vein narrowing is identified, left common iliac vein stenting may be necessary to ensure its patency and prevent DVT formation. The right common iliac vein is shorter than the left and oriented vertically as it ascends posterior and then lateral to its companion artery.

Superficial veins.

​The superficial veins of the lower extremities are superficial to the deep veins, located between two layers of superficial fascia in the subcutaneous tissue. Superficial veins serve to drain blood from the tissues and transport it to the deep system. These veins transport far less blood volume than deep veins and are therefore typically smaller in size. Unlike deep veins, the veins of the superficial venous system are not paired with an artery. Superficial veins also do not travel through muscle tissue; therefore muscle contraction plays a minimal role in the movement or pumping of blood through them. This makes it more difficult for venous blood in superficial veins to overcome hydrostatic pressure. To counteract this, venous valves, which aid in maintaining antegrade venous flow, are more prevalent in the veins of the superficial system than the deep, as they play a much more significant role. This is also why venous insufficiency is much more common in superficial than deep veins.

The great saphenous vein (GSV), also known as the long saphenous vein, originates on the dorsum of the foot and travels anterior to the medial malleolus, and ascends the anteromedial side of the calf and thigh. In the proximal thigh the GSV terminates as it joins the CFV at what is known as the saphenofemoral junction ( Figure 40-2 ). The GSV is the longest vein in the body and has between 10 and 20 valves. Because of its length, this vein is often harvested for use as an arterial graft. The small saphenous vein (SSV), also known as the lesser saphenous vein, originates on the dorsum of the foot, travels posterior to the lateral malleolus, and ascends along the midline of the posterior calf. The SSV terminates as it joins the popliteal vein in the popliteal fossa ( Figure 40-3 ). The level of entry of the SSV into the popliteal vein is variable; it has even been visualized to enter the FV in the mid thigh. The SSV has approximately 6 to 12 valves.


​Diagram of the great saphenous vein and perforators. The great saphenous vein is a superficial vein that travels along the anteromedial portion of the thigh and calf. Many perforators join the great saphenous vein.


​The small saphenous vein, also referred to as the lesser saphenous vein, is a superficial vein that travels along the midline portion of the posterior calf. The small saphenous vein typically drains into the popliteal vein in the popliteal fossa.

The posterior arch vein (vein of Leonardo) arises posterior to the medial malleolus and courses parallel and posterior to the GSV before it terminates into the GSV just below the knee. It also communicates with the PTV, mainly through the Cockett perforator located in the gaiter area (region above the medial malleolus) of the leg. The posterior arch vein drains blood from the medial ankle.

Perforating veins connect the superficial to the deep venous system. Perforating veins originate in the superficial fascia and penetrate the deep fascia. Like other veins, they contain one-way valves that permit unidirectional flow from superficial to deep. Many perforators exist throughout the lower extremity, with a greater number in the calf than thigh. Common perforators are Cockett’s, Boyd’s, Dodd’s, and Hunterian. Cockett’s perforators largely communicate with the posterior arch vein and are found in the lower leg. Boyd’s perforators are located around the level of the knee, Dodd’s in the distal thigh, and Hunterian in the proximal thigh.

Upper extremity

Deep veins.

​Like the deep veins of the lower extremity, the deep veins of the upper extremity are located within the musculature of the arms, travel in close association with a corresponding artery, and serve to transport deoxygenated blood from the superficial to central venous system ( Figure 40-4 ).


​Diagram of the deep veins of the upper extremity.

Beginning distally, the deep and superficial palmar venous arches in the hands form the paired sets of the radial and ulnar veins. This occurs on the lateral and medial sides of the arm, respectively. These veins are the primary source of venous drainage for the hand. The paired radial veins accompany the radial artery, and the paired ulnar veins accompany the ulnar artery as they ascend the forearm. Near the level of the antecubital fossa, the radial and ulnar veins join to form the brachial veins.

The brachial veins are a paired set of veins that originate from the confluence of the radial and ulnar veins near the antecubital fossa. From this location, the brachial veins ascend the upper arm on each side of the brachial artery. Just proximal to the axilla, at the inferior border of teres major, the brachial veins join the basilic vein and form the axillary vein.

The axillary vein is a single vein accompanied by the axillary artery, which originates from the confluence of the basilic and brachial veins in the upper arm. It drains blood from the upper arm supplied by the brachial, basilic, and cephalic veins, as well as the lateral portion of the thorax and the axilla. The axillary vein terminates beneath the clavicle at the outer border of the first rib, where it becomes the subclavian vein.

The subclavian vein is a continuation of the axillary vein. Accompanied by the subclavian artery, it extends from the outer border of the first rib to the inner end of the clavicle. Here it joins the internal jugular vein to form the innominate (brachiocephalic) vein. The subclavian vein is also joined by the external jugular vein, just distal to its anastomosis with the internal jugular vein. The subclavian vein is located deep to the clavicle and is inferior and anterior to the subclavian artery.

The innominate vein (brachiocephalic vein) is formed by the confluence of the subclavian and internal jugular veins. This is the most proximal vein of the upper extremity peripheral venous system, as the right and left innominate veins join just below the first rib to form the superior vena cava of the central venous system. Although present on both sides, the right and left innominate vary greatly. The superior vena cava terminates in the right atrium of the heart, located to the right of midline. Therefore the right innominate vein is considerably shorter than the left, as it is in closer proximity to the right atrium. Furthermore, the right innominate vein courses almost vertically downward, and is located superficial and to the right of the innominate artery. The right innominate vein receives the right vertebral, internal mammary, and inferior thyroid veins. As mentioned, the left innominate vein is longer than the right, as it must travel across midline from the left to the right side of the chest, where it joins the right innominate vein to form the superior vena cava. The left innominate vein courses beneath the sternum at a slight downward angle and receives the left vertebral, internal mammary, inferior thyroid, and left superior intercostal veins.

The external jugular vein (EJV) drains many outer structures of the head and face. Originating in the parotid gland, the EJV courses down the neck posterior to the mandible, before it crosses the sternomastoid muscle and terminates into the subclavian vein, just distal to its confluence with the internal jugular vein.

The internal jugular vein (IJV) drains the majority of the cerebral vessels and portions of the face. The IJV originates at the base of the skull in the jugular foramen, and courses down the neck just lateral to the internal and then common carotid artery. At its termination, it joins with the innominate vein to form the superior vena cava.

Superficial veins.

​In the upper extremity, the superficial venous system drains venous blood into the deep system for its return to the heart ( Figure 40-5 ). The superficial veins are located between two layers of superficial fascia, but outside of the deep investing fascia.


​Diagram of the superficial veins of the upper extremity.

The cephalic vein begins on the lateral side of the dorsum of the hand and travels along the outer border of the biceps muscle and deltopectoral groove. The cephalic vein penetrates the deep fascia at variable levels, to join the axillary vein just deep to the clavicle. The basilic vein originates on the medial side of the dorsum of the hand. The basilic vein is large, and courses medially along the inner side of the biceps muscle until it pierces the deep fascia and joins the brachial veins in the upper arm.

Venous physiology

Veins function to return deoxygenated blood to the heart once it has passed through the arterial system and capillaries (microcirculation). The arterial system is characterized as a closed, high-pressure system. This is due to the large amount of kinetic energy applied to it by cardiac contractions. These contractions create a pressure gradient that forces oxygenated blood through the arteries of the body, and then into microcirculation, consisting of arterioles and capillaries. While in microcirculation, blood flow encounters a large amount of hemodynamic resistance due to the reduction in vessel diameter. To overcome this resistance, much of the kinetic energy supplied by the heart is exhausted, causing the blood to have a small amount of remaining kinetic energy on its entry into venous circulation. It is for this reason that the venous system is characterized as a low-pressure system, and why normal venous flow is nonpulsatile.

Instead of the heart, the venous system relies on the muscles surrounding the veins to propel blood forward. On contraction, the muscle will tighten and squeeze the vein within it, propelling venous blood in an antegrade direction. This is made possible by the elasticity of vein walls. In the lower extremity, this is known as the calf muscle pump, which aids in venous blood flow during ambulation. Similarly, the diaphragm contracts and descends, causing intraabdominal pressure to rise during inhalation. This pressure increase compresses a distal portion of the IVC and impedes venous outflow from the legs. With expiration, the diaphragm rises, causing intraabdominal pressure to decrease and allowing venous flow from the legs to increase toward the IVC. It is for this reason that normal venous flow changes with respiration. This is called respiratory phasicity.

The venous system contains approximately two thirds of the body’s total blood volume at a given time. Veins do not contain a fully developed tunica media (muscular layer of the lumen) as arteries do. Therefore vein walls are more elastic, which allow them to appear in a variety of shapes. The cross-sectional shape of a vein is determined by transmural pressure. Transmural pressure is equal to the difference between the pressure inside the vein (intravascular) and the external pressure (interstitial pressure) placed on the vein from the surrounding tissue. Therefore a vein experiencing low transmural pressure will be somewhat collapsed and take on an elliptical appearance in a transverse plane, whereas a vein experiencing high transmural pressure will appear more rounded when imaged transversely. In the lower extremities, high transmural pressure is expected when standing or in a reverse Trendelenburg position, whereas a low transmural pressure is normally exhibited while in a supine position.

Venous pathology and treatments

Deep venous thrombosis

Deep vein thrombosis (DVT), also known as a thrombus or blood clot, is characterized by the abnormal coagulation of red blood cells. This occurs in response to a wide variety of stimuli in which elements within the blood become altered, causing abnormal red blood cell coagulation, resulting in a thrombus. Leg thrombi frequently originate on venous valves or within the soleal sinuses of the calf. Thrombi can be isolated to a single vein or extensive (present in multiple veins). DVT can occur in the upper and/or lower extremities, but upper extremity DVTs are much less common, making up only 10% of DVT findings. DVTs can present in an acute or chronic stage and must be appropriately characterized as such, as management may greatly differ between them.

Venous thromboembolism (VTE) is a condition in which a venous thrombus dislodges from the vein wall, propagates to the arteries of the lungs, and causes a pulmonary embolism (PE). Venous thromboembolism is the third most common cardiovascular disorder in the United States, with an incidence estimated between 1 and 2 in 1000, resulting in 300,000 to 600,000 cases annually. , Venous thromboembolism also maintains a high mortality rate of approximately 100,000 to 180,000 deaths annually. This exceeds the death rate of myocardial infarction.

Because of its high prevalence and potential to be life threatening, venous duplex examinations are often used as a diagnostic tool for the detection of DVT. In suspected cases of thrombosis, venous duplex imaging has emerged as the imaging modality of choice, as it is more accurate than other noninvasive techniques (nonimaging Doppler, impedance plethysmography), and unlike venography has no associated risks. , Symptoms commonly associated with DVT and PE are listed in Box 40-1 .

BOX 40-1

Symptoms and Signs Associated with Deep Vein Thrombosis and Pulmonary Embolism

Deep vein thrombosis

  • Persistent calf, leg, or arm swelling

  • Pain or tenderness of the leg (usually the posterior calf) or arm-shoulder region

  • Venous distention

  • Increased temperature and redness

  • Superficial venous dilation

  • Homan’s sign (calf discomfort on passive dorsiflexion)

Superficial venous thrombosis

  • Local erythema

  • Tenderness or pain

  • Palpable subcutaneous “cord”

Pulmonary embolus

  • Dyspnea (shortness of breath)

  • Chest pain

  • Hemoptysis (spitting up blood)

  • Sweats

  • Cough

Risk factors.

​In 1856 Rudolph Virchow presented classic concepts on the causes of thrombus formation within the venous system, which are still largely accepted today. The three factors associated with thrombus formation (Virchow’s triad) are (1) a hypercoagulable state, (2) venous stasis (blood pools in the veins), and (3) vein wall injury (endothelium of the vein is damaged, exposing the subendothelium to blood and triggering platelet adhesion and aggregation, which promotes blood coagulation). The interplay of these three factors creates the most likely setting for the development of DVT. A more detailed list of DVT risk factors can be found in Box 40-2 . An individual with a large amount of risk factors is at greater risk of developing a DVT.

BOX 40-2

Risk Factors for Deep Vein Thrombosis

  • Age (greater than 40 years old)

  • Malignancy (cancer)

  • Previous deep venous thrombosis or pulmonary embolism

  • Immobilization (bed rest, paralysis of legs, extended travel)

  • Fracture of the pelvis, hip, or long bones

  • Myocardial infarction, stroke

  • Congestive heart failure or respiratory failure

  • Pregnancy and postpartum

  • Oral contraceptives and hormone replacement therapy

  • Extensive dissection at major surgery (especially orthopedic surgery)

  • Trauma (multiple)

  • Hereditary factors (antithrombin deficiency, protein C and protein S deficiencies)

  • Obesity

  • Central venous lines, pacemakers

  • Intravenous drug abuse

Acute deep venous thrombosis.

​Acute DVT is typically defined as a thrombus that is no more than a week old. Acute thrombi are characterized by a soft or spongy appearance and may or may not envelop the entire cross section of the vein. Acute DVTs may be may be symptomatic or asymptomatic. Severe symptoms of lower extremity DVT include phlegmasia alba dolens (swollen, painful white leg) and phlegmasia cerulea dolens (swollen, painful cyanotic leg). Both of these affect arterial inflow and are limb threatening. More common symptoms include pain, warmth, erythema (redness), and edema. Acute DVTs have low densities, which cause their sonographic appearance to be low in echogenicity, or anechoic. Distention of the vein or visualization of the thrombus itself may also be seen.

Because of their soft nature, acute thrombi are more likely to dislodge from the vein wall, and propagate. Therefore the risk of PE in cases involving acute DVTs is heightened. The risk of PE is further increased the more proximal the DVT is located. Therefore management of acute DVT is typically much more aggressive that that of a chronic DVT and aims to dissolve or remove the thrombus. Management can be done in a variety of ways.

Conservative treatments consist of elevation, compression stockings, and/or bed rest. However, medical management is most commonly used to treat acute DVTs by anticoagulation or antiplatelet, agent administration, and/or thrombolytic therapy. Anticoagulation agents can be administered orally, intravenously, or subcutaneously, and aim to prevent further clot development by affecting coagulation factors. Common anticoagulants include heparin, warfarin, and lovenox. Antiplatelet agents prevent further clot formation by decreasing platelet aggregation. Common antiplatelet medications include aspirin, thienopyridines, and ticlopidine. Thrombolytic therapy is used to dissolve or break down an existing thrombus, known as thrombolysis. Common thrombolytic agents include tissue plasminogen activators (tPAs), urokinase, and streptokinase. In more severe cases, a variety of surgical interventions collectively referred to as a venous thrombectomy can be performed to remove the thrombus. Surgical placement of an IVC filter can also be done, which prevents propagating thrombi from reaching the lungs.

Chronic deep venous thrombosis.

​DVTs greater than a week old are often characterized as chronic. Unlike acute DVT, chronic DVTs are more dense and often calcified. This allows chronic DVTs to be visualized much easier sonographically, as they are typically much more echogenic, and also cause diffuse wall thickening. They are typically adhered firmly to the vessel wall and therefore do not have a large risk for propagating and causing a PE. Chronic DVTs are often obstructive and can cause the formation of collateral vessels and varicose veins. Individuals with a chronic DVT typically present with symptoms that involve the entire extremity, such as edema ( Figure 40-6 ), hyperpigmentation (brown discoloration), limb heaviness, varicose veins, and, in more severe cases, venous ulcerations.


​Edema is seen in the tissue surrounding and superficial to a chronically thrombosed pair of posterior tibial veins (PTV). The posterior tibial artery (PTA) is seen located between the two PTVs.

Severe chronic DVTs can lead to a process known as postthrombotic syndrome, which is caused by increased ambulatory venous pressure, also known as venous hypertension. Venous hypertension occurs when venous blood is unable to overcome hydrostatic pressure, resulting in blood stasis in the lower leg. This will lead to ulceration if left untreated. Venous hypertension can be a result of the venous obstruction (chronic DVT) and/or incompetent venous valves. Over time, the presence of a thrombus on or around venous valves can damage them, making them incompetent. This leads to deep venous insufficiency and subsequent venous hypertension. Additionally, varicose veins may occur. Varicose veins are dilated, elongated, tortuous superficial veins. Primary varicose veins are congenital, stemming from an inherent weakness of the venous walls, and occur without coexisting deep venous disease. Secondary varicose veins occur secondary to pathology (chronic DVT) of the deep venous system.

Treatment options for chronic DVT are similar to treatments used in acute DVT. Chronic DVT management, however, tends to involve more conservative treatment options, as risk of a PE occurrence is low. Therefore treatments typically aim to diminish patient symptoms through limb elevation, compression stockings, and in some cases bed rest.

Superficial venous thrombosis.

​A clot formation that exists in the superficial venous system is known as a superficial venous thrombosis (SVT). These are typically found in the GSV and SSV, but can present in varicose veins. Just as in the deep system, a common location for SVT is on or around venous valves. For this reason, the presence of chronic SVT can cause valvular incompetence, leading to insufficiency of the superficial venous system. Unlike chronic DVTs, symptoms of SVTs are typically localized to the area in which they are located. Common SVT symptoms include localized erythema and tenderness, and in some cases they can be palpated as a hard subcutaneous “cord.” Treatment for SVT typically includes limb elevation, compression stockings, and application of heat to the area.

Venous insufficiency

Venous insufficiency, also known as venous reflux, is caused by incompetent venous valves. Competent valves aid venous blood in overcoming hydrostatic pressure, allowing it to flow in an antegrade direction. In their absence, venous blood is not able to efficiently overcome hydrostatic pressure, resulting in retrograde flow within the vein. This leads to venous stasis and venous hypertension in the lower limbs. Venous insufficiency can occur in the deep or superficial system, as well as in perforating vessels. This can be caused by a previous DVT that has damaged the venous valves and rendered them incompetent. Venous reflux can also develop in veins that have experienced high levels of hydrostatic pressure for prolonged periods of time. This typically occurs from pregnancy or standing for long periods of time. Genetic predisposition also increases the likelihood of venous reflux development. Venous reflux is common, as one review states that lower extremity venous insufficiency and subsequent varicose veins is the seventh most common indication for referral in the United States, with the overall prevalence estimated to be as high as 25% in women and 15% in men. , Symptoms of venous insufficiency include chronic leg swelling, induration (hard, firm, almost leather-like appearance of the skin around the ankles), varicose veins, and venous stasis ulcerations in severe circumstances. In cases of superficial venous insufficiency, noninvasive treatments include limb elevation and compression stockings. Invasive treatments consist of surgical intervention, including ultrasound-guided venous ablation, varicose vein phlebectomies, and sclerotherapy. All interventions aim to reduce venous pressure in the afflicted limb.

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May 29, 2019 | Posted by in ULTRASONOGRAPHY | Comments Off on Peripheral venous evaluation
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