Chapter 13. Sonography of the Peripheral Veins
George L. Berdejo, Joshua Cruz, and Evan C. Lipsitz
ANATOMY OF BLOOD VESSELS1–8
Blood vessels act as the conduits through which blood is pumped by the heart. The vessels fall naturally into three general categories:
1. Arteries are vessels that convey blood away from the heart and toward the tissues. According to size and structure, large, medium, and small arteries (arterioles) are recognized. A transition vessel between arteries and capillaries is formed by the meta-arteriole. Because of the content of smooth muscle in their walls, medium and smaller arteries play an important role in the regulation of blood pressure and blood flow.
2. The capillaries permeate the body organs and tissues and act as the vehicles for exchange of materials between blood and cells.
3. Veins convey blood from the tissues and toward the heart. They act as volume conduits rather than pressure vessels.
Capillaries are composed of an endothelial tube supported by a few reticular fibers. They measure about 7–9 microns in diameter and are the most numerous of the body’s blood vessels. There are quite literally miles of capillaries in the body, and they present a very large surface area to the flow of blood. Because of their extreme thinness, capillaries serve as the vessels through which exchange of materials between cells and blood occurs. The large surface area of the capillaries ensures a slow flow of blood through vessels, permitting time for exchanges to occur.
Venules, or small veins, drain the capillary beds. These vessels typically have two layers of tissue in their walls: endothelium and a surrounding layer of collagenous connective tissue. Mediumsized veins acquire a thin media containing scattered smooth muscle cells and a prominent adventitia. Large veins are almost always adventitia. Veins have little pressure to withstand and are easily collapsed. Veins of the arms, legs, and viscera are provided with valves to ensure blood flow toward the heart. Medium and large vessels of both types possess a system of blood vessels that nourish the tissue in their walls. These constitute the vasa vasorum: literally blood vessels to blood vessels.
The vessels of the arterial and venous systems are basically tubes. The largest of these tubes have walls composed of three layers, or coats. The walls of the next largest consist of two of these coats. The walls of the smallest vessel consist of only one coat that is so thin that it is composed of a single layer of cells. The layers are given the same names in both the arterial and the venous system, but their size, strength, and composition are somewhat different.
The outermost layer of the vessel wall is called the tunica adventitia. Tunica is the Latin word for coat; adventitia is Latin for extraneous or coming from abroad. Although tunica adventitia is the form most commonly used to describe the outside layer, some anatomy books use the term tunica externa.
We are accustomed to thinking of blood vessels as conduits that carry blood to or away from other structures. However, blood vessels are composed of living tissue, so they also require nourishment. The adventitia of both veins and arteries is nourished by minute vessels called vasa vasorum.
The middle of the vessel wall consists of a layer called the tunica media. The name of this layer is easy to remember. It comes from the same Latin root as the word medium, which means in the middle. The innermost layer of a blood vessel is called the tunica intima, coming from the Latin word for within.
Although the three layers of the venous walls have the same names as those of the arteries, there are some differences in structure. In a vein, the adventitia is considerably thinner and much less strong. The tunica media of veins is also much thinner and weaker than the arterial media, and it contains far less elastic tissue. This makes sense, as arteries must withstand the pulsations of the heart, while veins are usually non-pulsatile and need less elasticity (Fig. 13–1).
FIGURE 13–1. Cross sectional image of a vein and artery. Note the differences in the 3 layers of the vessel walls.
The venous and the arterial tunica intima consists of a single-celled endothelium. However, the major difference between the venous and the arterial tunica intima is the presence of vein valves.
The most significant feature of venous structure is the presence of bicuspid valves (Fig. 13–2). These valves are oriented to permit blood to flow in a cephalad direction only. When functioning properly, they do not allow retrograde flow down the leg. Valves in the perforating veins direct blood from the superficial to the deep system only. Just cephalad to and surrounding the valve cusps, the vein is dilated to form a small sinus. This aids the function of the valve by facilitating their closure. Without the dilated area, the valves when open would be closed approximated to the venous wall. Because blood flow at the base of the valve cusp is relatively stagnant, venous thrombi tend to form in the valve sinuses. Valves are much more numerous in the veins below the knee than in the more proximal veins. The vena cava and the common iliac veins have no valves. Only about one-fourth of the external iliac veins contain a valve and about three-fourths of the femoral veins have a valve. One to four valves are present in the superficial femoral vein, one to three in the popliteal, about seven in the peroneal, and nine in the anterior and posterior tibial veins. A valve is constantly present in the profunda femoris vein just before it joins the femoral vein to form the common femoral vein. Within the terminal 2–3 cm of the great saphenous vein, there are one or two valves. The remainder of this vein contains 10–20 valves, most of which are below the knee. The small saphenous vein has 6–12 valves.
FIGURE 13–2. Vein valve closed (left). Vein valve open (right).
The veins are the back half of the closed loop circulatory system. Blood flows through the veins toward the heart and that is how we will trace the course of each system of the venous circulation, starting with the periphery and working back toward the heart. As veins join with other veins, they get bigger.
In discussing the venous portion of the peripheral systemic circulation, we will deal with three different groups or systems: the deep veins, the superficial veins, and the perforating or communicating veins (Fig. 13–3).
FIGURE 13–3. Venous flow pattern in the lower extremity.
The deep veins are so called because of where they are in relation to skin and muscle. All veins lie under the skin, but some veins are more deeply situated than others. The deep veins are those that lie under both skin and fascia. The major deep veins are analogs of the corresponding arteries.
In the extremities, deep veins are surrounded by muscle, a fact that is important to the flow of venous blood. Deep veins of the body lie next to the major arteries and almost always share their names. There are four exceptions to the arterial/deep venous similarity and three of them occur more or less as a group in the upper half of the body. There are two exceptions in name and two in number. The two name exceptions are the internal jugular vein/common carotid artery equivalent and the vena cava/aorta equivalent. Number exceptions are one innominate artery versus two innominate veins and one infrapopliteal artery on each side versus two or more infrapopliteal veins (Fig. 13–4).
FIGURE 13–4. Transverse sonogram of the tibial veins. White arrows pointing to arteries with adjacent deep veins.
Anatomy of the Upper Extremity. Blood returning from the digital or finger veins empties into a venous network in the hand called the palmar arch. Just as in the arterial system, there is both a deep and a superficial arch in the hand and these unite to form the beginning of the radial and ulnar veins of the forearm. The radial (thumb side) and ulnar (pinky side) veins move proximally in the forearm next to the arteries and they generally join in the area just below the antecubital fossa to form the brachial vein (Fig. 13–5). The brachial vein has no superficial component, and therefore, some anatomists consider it to be the first of the true deep veins of the upper extremity. It courses up the arm beside the brachial artery gradually increasing in size as it goes along.
FIGURE 13–5. Deep venous anatomy of the upper and lower arm.
Where the brachial vein enters the axilla or armpit, it takes on the name of its new location and becomes the axillary vein (Fig. 13–6). As it emerges from the axilla and crosses the outer border of the first rib, it is called the subclavian vein. The subclavian vein courses underneath the clavicle to the base of the neck where the first of the artery/deep venous exceptions is encountered.
FIGURE 13–6. Veins in the axillary region.
In the arterial circulation, there is a vessel on each side of the neck called the common carotid artery. In the deep venous circulation, there is no carotid vein to correspond with that artery. Instead, the right and left internal jugular veins run alongside the carotid arteries. On the right side, the right subclavian vein joins the right internal jugular vein to form the right innominate vein. On the left side where there is no equivalent innominate artery however, the left subclavian and left internal jugular veins form the left innominate vein. The right and left innominate veins anastomose to form the third of the arterial deep venous exceptions, the superior vena cava (Fig. 13–7).
FIGURE 13–7. Internal jugular veins, subclavian and central veins.
The two venae cavae are the venous equivalent of the aorta. Just as all blood supplied by the arterial system comes from the heart by way of the aorta, all blood drained by the venous system returns to the heart by way of the vena cava. The superior vena cava, which is formed by the anastomosis of the two innominate veins, is the larger of the two. The inferior vena cava, which drains the abdomen, will be discussed later. The superior vena cava is so named because it receives the venous return from the upper portion of the body (head, neck, thorax, and upper extremities) and is situated above or superior to the heart. The plural form, venae cavae, is generally used in speaking of the superior and inferior venae cavae together.
Anatomy of the Lower Extremity. To find the last arterial/deep venous exception, it is necessary to go to the distal lower extremity in the calf. In the foot, a deep and superficial arch structures receive venous drainage from the toes. At the ankle, we find the first of the exclusively deep veins. Just as in the arterial circulation, the leg contains anterior tibial, posterior tibial, and peroneal veins, but the arterial system has only one of each. The venous system has several of each; two, occasionally three, and sometimes four anterior tibial, posterior tibial, and peroneal veins may be found in the leg in normal individuals. This multiplicity of named deep veins in the leg contributes to the difficulty of assessing small deep venous thromboses in this area. These veins move proximally along the leg next to the arteries whose names they share. Large spindle-shaped veins called soleal sinusoids collect the venous drainage from the soleus muscle and terminate in the posterior and peroneal veins. The veins draining the gastrocnemius muscle are tributaries of the popliteal vein. These large muscular sinusoids are important physiologically because they act as the principal bellows of the muscle pump and pathologically because they are a favored site for the formation of thrombus (Fig. 13–8).
FIGURE 13–8. Superficial and deep veins of the lower extremities.
The joining of the leg veins is similar to the division of the infrapopliteal arteries. The popliteal artery first divides to form the anterior tibial artery and then the tibial peroneal trunk, which then divides to become the posterior tibial and peroneal arteries. In the venous system, the posterior tibial and peroneal veins come together first and are then joined by the anterior tibial veins. All these veins join to form the popliteal vein (Fig. 13–8).
The popliteal vein leaves the fossa and enters the thigh as the femoral vein. The femoral vein is a deep vein. It runs through the adductor canal along the medial side of the superficial femoral artery. As the femoral vein moves proximally, it joins the profunda or deep femoral vein and enters the region of the groin. There, it becomes the common femoral vein. The femoral vein in the thigh and the common femoral vein are always situated medial to the superficial femoral and common femoral arteries (Fig. 13–8).
Moving proximally to the level of the inguinal ligament, the common femoral vein becomes the external iliac vein. It then joins with the internal iliac or hypogastric vein to become the common iliac vein. Finally, at the level of the umbilicus, the right and left common iliac veins anastomose to form the beginning of the inferior vena cava (Fig. 13–9).
FIGURE 13–9. Demonstrating the anatomy of the venous system in the pelvis and lower abdomen.
The inferior vena cava and the abdominal aorta are paired vessels, both of which arise from paired vessels at their distal margins; however, there is only so much room in which the six major vessels can exist. The right common iliac artery actually lies atop the left common iliac vein so that the inferior vena cava and the aorta can lie side-by-side (Fig. 13–9). This position sometimes causes compression of the left common iliac vein (May Thurner syndrome) and may occasionally be a factor in certain noninvasive tests of the lower extremity.
The inferior vena cava moves proximally through the abdomen gathering returned blood from different visceral and pelvic veins. As it reaches the level of the heart, it joins with the superior vena cava to empty all the returning venous blood into the right atrium where it begins the circulatory cycle all over again.
The superficial veins are those that are located under the skin, but above the fascia. These veins can sometimes be seen beneath the skin, especially if they become distended as varicose veins.
Upper Extremities. In the hand, as already mentioned, there are superficial as well as deep venous structures called palmar arches. In the forearm, the superficial veins form a complex network spreading out over the circumference of the limb. In the arm, these four arm veins join to form two larger superficial veins.
The superficial veins running along the lateral aspect of the arm are called the cephalic veins, while those in the medial aspect are called the basilic veins. The pattern of distribution for the superficial veins of the upper extremity is different for each person and can differ from one side to the other in the same individual. The main trunk of the cephalic vein empties into the subclavian vein and the main trunk of the basilic veins empty into the deep venous system via the axillary; however, both these terminations can be variable (Fig. 13–10).
FIGURE 13–10. Demonstrating superficial veins of the arm and forearm.
Lower Extremities. The lower extremity also has two sets of superficial veins. Starting posterior to the lateral malleolus and running along the posterior aspect of the leg are the veins that form the small saphenous network. The posterior lateral and posterior branches of the small saphenous vein join, then move deep into the interior of the leg by perforating the fascia at the upper third of the calf. The small saphenous network empties into the popliteal vein usually at the middle portion of the popliteal fossa; however, this can vary and sometimes occurs well above the knee (Fig. 13–11).
FIGURE 13–11. Small saphenous vein and tributaries. Great saphenous vein and branches. (Reprinted with permission from Gray H. In: Goss CM, ed. Anatomy of the Human Body. Philadelphia: Lea & Febiger; 1973: 717, 718.)
Beginning again at the dorsum of the foot, but this time anterior to the medial malleolus is the great saphenous vein. This superficial vein is an extremely important one, especially in surgery where it is used as material for bypass grafts (lower extremity or coronary). Its branches or tributaries extend over the anterior medial and lateral aspects of the limb, but the course of its main trunk is reasonably well defined. After its origin in the foot, the great saphenous vein passes superiorly along the medial aspect of the leg. In the area of the knee, it swings toward the back of the limb. The great saphenous network connects with the deep venous system a few centimeters below the inguinal ligament. Like the small saphenous network, it must penetrate the fascia to reach the deep veins (Fig. 13–11). The greater saphenous vein is the longest vein in the body.
Draining into the saphenous veins are numerous tributaries, which lie more superficially in the subcutaneous tissue. One of these veins, the posterior arch vein, deserves special mention because it represents the superficial connection of the three ankle perforating veins, which are of major importance in the genesis of venous stasis ulceration. The posterior arch vein begins behind the medial malleolus and passes up the medial aspect of the calf to enter the great saphenous vein at the knee level. The confluence of the cephalad end of the great saphenous vein with the deep venous system is called the saphenofemoral junction. This junction is very important, as a thrombus in the greater saphenous vein may propagate into the deep venous system by means of the saphenofemoral junction.
In addition to their depths, the deep and superficial veins differ in another way, especially in the lower limbs. The walls of the saphenous veins are somewhat stronger than those of the deep veins in the leg. This makes sense when you consider their relative position. The deep veins are buried within the muscle masses of the lower limbs under the fascial layer and they are supported by these structures. The superficial veins have only a thin covering of skin for protection and support. However, the strength of the saphenous veins is limited; they cannot carry large amounts of blood at any one time.
Connecting the deep and superficial systems is a series of perforating or communicating veins. These perforating veins allow blood in the superficial veins to remain at manageable levels. These veins penetrate the fascia, hence, the name perforating. In the thigh, there is a constant perforating vein known as the Hunterian perforator that connects the femoral vein to the greater saphenous vein. More numerous and more important are the perforating veins in the calf.
When functioning properly, valves in the perforating or communicating veins direct the flow from the superficial veins toward the deep system only (Fig. 13–12).
FIGURE 13–12. Venous flow pattern. Superficial to deep veins via the perforators.
NORMAL VENOUS HEMODYNAMICS9, 10
In order to understand the changes that occur with disease, a general understanding of normal venous hemodynamics needs to be achieved. The pressure within any blood vessel is a result of, in part, the dynamic pressure produced by the contraction of the left ventricle. Unlike the arterial system, this component in the venous system is relatively low, around 15–20 mm Hg in the venules and 0–6 mm Hg in the right atrium. In any position other than horizontal, hydrostatic pressure plays a major role in determining the pressure within the veins. Hydrostatic pressure is due to the weight of the column of blood within the vessel. Hydrostatic pressure is equal to the density of the blood multiplied by the acceleration due to gravity multiplied by the height of the column of blood. In the human body, the level of the right atrium is used as the reference point by which to measure hydrostatic pressure. When supine, the arteries and veins are all approximately the same height as the heart. Therefore, the hydrostatic pressure is negligible and the pressure will approximate the dynamic pressure. The pressure within the veins at the level of the ankle is about 15 mm Hg. When standing, an individual who is approximately 6 feet tall will add a hydrostatic pressure of 102 mm Hg at the ankle level (Fig. 13–13).
FIGURE 13–13. Graph showing changes in venous pressure caused by changes in body position. (Reprinted with permission from Strandness DE. Sumner DS. Hemodynamics for Surgeons. New York: Grune & Stratton; 1975: 123.)
Because veins are collapsible tubes, their shape is determined by transmural pressure. Transmural pressure is equal to the difference between the pressure within the vein and the tissue pressure. At low transmural pressures (when a person is supine), a vein will assume a dumbbell shape. As the pressure within a vein increases, the vein will become elliptical. At high transmural pressures (while standing), the vein will become circular. As venous transmural pressure is increased from 0 to 15 mm Hg, the volume of the vein may increase by more than 250%. A small increase in pressure is required to change an elliptical vein into a high volume circular vein; however, a significant increase in pressure is required to stretch the venous wall once the vein has assumed a circular configuration.8–10
VENOUS PRESSURE AND FLOW
The first characteristic we associate with arterial flow is pulsatility; however, the direct influence of the pulsating heart on the venous system is minimal. Most veins do not yield pulsatile flow, but there are two full and one partial exceptions to that rule. Because of the proximity to the heart, the internal jugular vein and subclavian vein are normally pulsatile. The axillary vein may or may not be pulsatile depending on the individual. Pulsatility in the axillary vein is not considered abnormal but rather an individual variation. Non-pulsatility is normal in all but the great veins. The characteristic of flow typical of veins is called phasicity.
The term phasicity in reference to the venous system refers to the ebb and flow that occurs in normal veins in response to respiration. All deep veins normally exhibit phasicity, even those that are somewhat pulsatile. Respiration has this ebb-and-flow influence because unlike the strong-walled arteries, veins are collapsible.
The two phases of respiration are inspiration (breathing in) and expiration (breathing out). The way in which the blood moves in phase with respiration differs according to the part of the body affected and the position in which the body is placed.
When a body is standing upright, breathing produces pressure gradients that influence the movement of venous blood. As the lungs fill with air during inspiration, the thoracic cavity expands. When the thorax expands, the diaphragm drops, and consequently the abdominal cavity becomes smaller. The veins located within the chest and abdomen are affected by these changes in pressure. As the thoracic cavity gets larger, pressure within it decreases and pressure within the right atrium and the thoracic portion of the vena cava is also reduced. At the same time, the abdominal cavity is getting smaller, raising the pressure within the abdomen and the abdominal veins.
Fluids move from areas of high pressure to areas of low pressure. During inspiration, the result is collapse of the inferior vena cava and decreased or no flow from the lower extremities. With expiration, the process reverses itself; the intra-abdominal pressure decreases and the intrathoracic pressure increases, resulting in increasing venous blood flow to the heart from the lower extremities and in general decreased flow from the upper extremities.8, 9
Venous Return from the Upper Extremities
Respiration affects venous return from the upper extremities, but to a lesser extent than it affects the lower body. Again, phasicity in the upper extremity veins also can vary according to circumstances. In the brachial vein for instance, inspiration may produce either a reduced or an increased sound. If the lowered or negative intrathoracic pressure causes more blood to move from the brachial vein to the subclavian vein, flow from the brachial vein will increase. Sometimes, however, expansion of the lungs on inspiration will physically compress the subclavian vein. When this happens, less venous blood will move from the chest into the arms and the sound on the brachial vein will diminish. From a clinical standpoint, this is important in that phasic changes should be detectable in all deep veins in relation to breathing.
Venous Return from the Lower Extremities
In the presence of a deep venous thrombosis, venous pressure is increased due to an increase in venous resistance. The change in venous resistance will depend on the location of the obstructed venous segment, the length of the obstruction, and the number of veins involved. Oscillations in the venous flow from the leg may be reduced or absent and flow may become continuous.
Edema is a consistent sign of increased venous pressure. The Starling equilibrium equation describes the movement of fluid across the capillary. Forces that act to move fluid out of the capillary are the intracapillary pressure and the interstitial osmotic pressure. Forces that favor the reabsorption of fluid from the interstitium are the interstitial pressure and the capillary osmotic pressure. Normally, the forces are balanced so that there is little overall fluid loss out of the vascular space into the interstitial space. While standing, the increased capillary pressure is no longer balanced by the reabsorptive forces and fluid loss from the vascular system occurs. Edema formation is limited by the action of the muscle of the calf muscle pump. Contraction of the calf muscles acts to empty the veins and decrease venous pressure. In the presence of venous thrombosis, venous pressure is increased. This increased venous pressure will be transmitted back through the vascular system to the capillary level resulting in increased capillary pressure which will lead to edema formation. Use of compression stockings will decrease interstitial pressure, which will favor increased fluid reabsorption. This decreases edema formation. Elevating the legs will reduce the intracapillary pressure by reducing the hydrostatic pressure, which will also limit edema formation.8
VENOUS DYNAMICS WITH EXERCISE
The calf muscle pump aids in the return of blood from the legs against the force of gravity. The muscles act as the power source. The intramuscular sinusoids (especially the gastrocnemius and soleus) and the deep and superficial veins all play a part in this mechanism. The valves are necessary to ensure efficient action of the muscle pump. Closure of the valves in the deep veins decreases the length of the column of blood, which aids in reducing venous pressure. At rest, blood pools in the leg and it is only propelled passively by the dynamic pressure gradient created by the contraction of the left ventricle. Contraction of the calf muscles can generate pressures >200 mm Hg. This compresses the veins forcing blood upward in both the deep and superficial veins. The valves are closed in the perforating veins and in the veins in the distal calf to prevent reflux of blood. Upon relaxation, since these veins in the calf are empty, blood is drawn into this area from the superficial veins via perforators. More distal veins also help fill the calf veins upon relaxation.8, 10
When distended, the cross-sectional area of the vein is about three to four times that of the corresponding arteries. It is not surprising then that the extrapulmonary veins contain about two-thirds of the blood in the body. Nevertheless, it is somewhat surprising that despite their large diameter, veins offer about the same resistance to flow as arteries. This is explained by the collapsible nature of the vein walls. Veins are seldom completely full. In the partially empty state, they assume a flattened or elliptical cross-section, which offers a great deal more resistance to blood flow than a circular cross-section. The ability to go from an elliptical to a circular cross-section is distinctly advantageous. It permits the veins to accommodate a great increase in blood flow without an increase in the pressure gradient from the periphery to the heart. In other words, as the rate of flow increases, the vein becomes more circular, lessening resistance.
DEEP VEIN THROMBOSIS: MECHANISMS OF DISEASE AND PATHOLOGY
Etiology, Pathology, and Pathophysiology of Deep Vein Thrombosis11
Venous obstruction is almost always the result of venous thrombosis. Less frequently, extrinsic compression may lead to total obstruction, such as on the subclavian vein, sometimes due to a thoracic outlet issue, although this is rare. This is sometimes referred to as effort thrombosis or Paget-Schroetter syndrome12, 13 (Fig. 13–14). Compression can also occur in the area of the left common iliac vein (May Thurner syndrome14, 15). Deep vein thrombosis in the lower limbs is a relatively common condition and is particularly important because of the risk of pulmonary embolism. In the past, it was thought that deep venous thrombosis inevitably caused chronic edema, hyperpigmentation, and other changes of chronic venous insufficiency. Now, it is well known that approximately one-third of thrombi will lyse quickly. In vein segments that experience total lysis within 3–5 days, valvular function is often maintained.16Because of the risk for pulmonary embolization, urgent diagnosis is made by imaging techniques and treatment is by immediate anticoagulation. Acute anticoagulation is achieved with heparin and chronic anticoagulation with warfarin. Thrombolytic therapy may be used in special clinical situations.17–23
FIGURE 13–14. Sonograms demonstrating normal subclavian vein on the left image and compression with abduction of upper extremity on right image.
Deep vein thrombi can vary from a few millimeters in length to long tubular masses that fill the main veins. They can form in veins >1 or 2 mm in diameter and generally in large or medium sized vessels. Thrombi begin as microscopic nidi, and then grow by an additive process and become visible. Small thrombi are commonly found in valve pockets throughout various deep veins of the leg and thigh and in saccules of soleal veins. It is from these that the long tubular structures grow. Initially, there is propagation in the direction of the venous stream by deposition of successive layers of thrombus coagulum from the blood, the primary microscopic nidus thus becomes visible. Additional further layers, both longitudinally and circumferentially, increase the length and diameter of the thrombus. Such thrombi at first are attached to the vein only at their points of origin and float almost freely in the blood system (Fig. 13–15). If further propagation occurs, venous obstruction may result and this often leads to retrograde thrombosis back to the next patent vessel.24, 25
FIGURE 13–15. Sonogram with red arrows demonstrating thrombus within the lumen of a vein.
Pathophysiology of Calf Vein Thrombosis. Despite observations that most thrombi begin in the calf and that proximal thrombi are often an extension of calf vein thrombosis, limited data suggest that there are pathophysiological differences between proximal and isolated calf vein thrombosis. Patients with isolated calf vein thrombosis have fewer risk factors and a lower incidence of malignancy. Among 499 patients with an acute deep vein thrombosis, those with calf vein thrombosis had a median of one risk factor in comparison to two risk factors in those with proximal thrombosis.16 Consistent with these observations, patients with isolated vein thrombosis appear to be less hypercoagulable. Such data suggest the isolated calf vein thrombi are not simply early thrombi that have yet to propagate but rather reflect a more limited prothrombotic state.
Incidence of Deep Vein Thrombosis26, 27
Clinically recognized acute deep vein thrombosis has been estimated to have an incidence of up to 250,000–300,000 new cases per year in the United States. A number of studies have focused specifically on the epidemiology of venous thromboembolism (VTE). In these studies, involving predominantly Caucasian populations, the incidence of first-time symptomatic VTE directly standardized for age and sex to the U.S. population ranged from 71 to 117 cases per 100,000 population.27–32
Based on potential differences in the incidence of acute and chronic complications, these episodes are commonly defined as involving the proximal lower extremity veins, extending from the popliteal to the iliac vein confluence or isolated to the calf veins. Isolated calf vein thrombosis may involve the peroneal, posterior tibial or anterior tibial veins, the gastrocnemius veins, or the soleal veins. Although lower extremity deep vein thrombosis is thought to usually originate in the calf veins, most symptomatic thromboses involve the proximal veins. The incidence of isolated calf vein thrombosis has varied among series but has rarely been insignificant. As many as one-third of thrombi detected by duplex ultrasonography are isolated to the calf veins.16
Patient’s with one or more elements of Virchow’s triad (Table 13–1) are susceptible to thrombosis.33–35 Most cases arise during the course of another illness and a connection with confinement to bed and advancing age has been known for a long time. Post-trauma, orthopedic, gynecologic, obstetric, and surgical patients are at risk, but many medical patients such as those with heart attacks, congestive heart failure, acute strokes, and paraplegia are as well. Additionally, deep vein thrombosis occurs as a primary state in healthy ambulatory men and women without apparent cause, and it is now recognized as a hazard in patients taking therapeutic estrogen and in women taking oral contraceptives. Other recognized predisposing factors are obesity and previous thrombosis (Table 13–2).
TABLE 13–1 • Virchow’s Triad
TABLE 13–2 • Risk Factors for Venous Thromboembolism
Isolated iliac vein thrombosis is thought to be rare. However, it is well known that pregnancy and pelvic abnormality such as cancer, trauma, and recent surgery can also predispose to iliac vein thrombosis.36 The true incidence of isolated pelvic deep vein thrombosis in these patients, however, is not known, as duplex diagnosis of iliac thrombosis is often difficult and its accuracy, compared to the diagnosis of lower extremity deep vein thrombosis, is yet to be established.
While axillary-subclavian venous thrombosis represents a small fraction of all cases of deep vein thrombosis, in fact it is an important clinical entity. In the past, it was thought to be benign and self-limiting, and conservative measures were advocated. More recently, it has been recognized that considerable morbidity may occur and aggressive management is dominant in today’s practice.37 Similarly, in the past, spontaneous axillary-subclavian venous thrombosis, referred to as effort thrombosis, was associated with a variety of physical activities. Now because of central lines and pacemaker wires, a more frequent cause is traumatic and iatrogenic. In fact, this element of axillary-subclavian venous thrombosis is so common that it is felt that between one-third and two-thirds of patients with subclavian lines or catheters develop deep vein thrombosis. Some patients with upper extremity venous thrombosis will have abnormal clotting factors (Fig. 13–16).
FIGURE 13–16. Transverse sonogram of deep vein thrombosis in the upper extremity.
Symptoms and Physical Findings
Difficulty in diagnosing deep vein thrombosis is based on the presence of nonspecific symptoms in many patients. The clinical presentation of deep vein thrombosis can be totally asymptomatic or may progress to flagrant phlegmasia cerulea dolens and venous gangrene. The clinical diagnosis based on a physical examination is known to be notoriously inaccurate. Homans’ sign (calf pain with passive dorsiflexion of the foot) is also a poor predictor for the presence of deep vein thrombosis. This has led to the investigation and use of pretest probability algorithms. Wells et al. suggested an algorithm based on the determination of pre-test probability and compression ultrasound screening.38 When thrombi develop in the deep venous system of the lower extremity, the findings may include acute inflammation, pain, and/or swelling, or it may be an entirely bland pathologic process. While the thrombus can produce a venous occlusion, such blockage may be partial or so well compensated that the distal limb swelling does not occur. Therefore, definitive diagnosis remains elusive except by imaging techniques.
The findings of deep vein thrombosis will vary with the location of the thrombus as well as whether it occurs in isolated fashion or in multiple venous segments. It is the proximal iliofemoral veins that present the greatest risk for fatal pulmonary embolism and often produce the most dramatic manifestations (Fig. 13–17). There can be massive swelling, pain, and tenderness of the lower extremity. Phlegmasia cerulean dolens is a severe form of iliofemoral thrombus that causes significant obstruction to venous outflow. This is characterized by cyanosis, which rarely progresses to gangrene. Phlegmasia alba dolens is another form characterized by arterial spasm and a pale cool leg with diminished pulses. Thrombi in the distal or calf veins present the least risk for pulmonary embolus.39
FIGURE 13–17. Sonogram of an iliac vein thrombus. In lower right edge of the image is a corresponding CT scan with increased size of the right leg in this patient with phlegmasia.
Superficial Thrombophlebitis. The terminology describing this entity is appropriate because it truly describes an inflammatory process. It is commonly believed that thrombosis of the deep and superficial venous system represents the same process. However, there does not appear to be any evidence to support that theory.
Contributing Factors. The most common cause of superficial thrombophlebitis is intravenous infusions that inflict a chemical injury on the vein wall that leads to inflammation and then inevitably thrombosis of the involved vein or veins. In the lower limbs, superficial thrombophlebitis most commonly occurs in varicose veins. This commonly follows a traumatic event that may or may not be severe. The development of migratory superficial phlebitis may be the first sign of an underlying malignancy (Trousseau’s sign)40 and has also been associated with Buerger’s disease (thromboangiitis obliterans).41
Risk Factors and Clinical Manifestations. Varicose veins in the lower extremity and intravenous therapy in the upper extremity predispose a patient to phlebitis. The clinical presentation of superficial thrombophlebitis consists of severe pain, redness, inflammation, swelling, and pyrexia (fever). This is evident simply on physical examination of the involved area, and because the process leads to the development of thrombosis, a palpable cord is often seen.
Differential Diagnosis. The most common entities that can be confused with superficial thrombophlebitis are lymphangitis and cellulitis. In most case, the differential diagnosis is not too difficult, particularly if the examiner realizes that cellulitis and lymphangitis do not typically lead to thrombosis of the superficial veins.
Diagnostic Approach. Phlebitis in a superficial vein is readily diagnosed clinically. Physical diagnosis of superficial thrombophlebitis can be made by detecting an erythematous streaking in the distribution of the superficial veins. Tenderness is present and the extent of thrombus is identified by a palpable cord. Because superficial thrombophlebitis leads to thrombosis of the involved veins, continuous-wave Doppler is the ideal method for establishing the diagnosis. The finding of a patent vein in the area of inflammation rules out phlebitis. Although the diagnosis can be made by physical examination, accurate estimation of the proximal extent of the disease process or deep venous involvement is based on objective testing in the vascular laboratory. If there is any concern over the extent of the thrombosis, particularly whether it involves the deep venous system, it is important to use duplex scanning to depict both the thrombus and its proximal extent.
Clinical Implications. Although the initial diagnosis can be made clinically, it is now known that approximately 20% of patients with superficial vein thrombosis will have an associated occult deep vein thrombosis. Further, in approximately one-third of those who present with only superficial phlebitis initially, the thrombus will eventually extend into the deep venous system via the saphenofemoral junction or perforating vein. Phlebitis of the long saphenous vein above the knee is particularly susceptible to progression to deep vein thrombosis. Therefore, it is prudent to perform a duplex examination for deep vein thrombosis and in selective cases, a follow-up examination in patients with suspected or proven ascending superficial phlebitis.
Evaluation of the lower extremity venous system for deep vein thrombosis has revealed thrombosis of the great saphenous vein in approximately 1% of limbs. Thus, examination of the saphenofemoral junction should be part of the examination of the lower extremity venous system when deep vein thrombosis is suspected.
Upper Extremity Findings. Symptomatic patients with axillary-subclavian venous thrombosis often present with a swollen forearm, upper arm, and shoulder. A visible pattern of venous distention may be present across the anterior aspect of the shoulder and chest wall. There may be venous distention of the antecubital veins as well as those in the hand. If a tender palpable cord is present in the neck and/or axilla, this is due to a superficial thrombophlebitis accompanying the deep vein thrombosis. A bluish or cyanotic discoloration is commonly present in the hand and fingers and an aching pain in the forearm, exacerbated by exercise is also a common complaint.
Pulmonary embolism (PE) is a common medical condition that can contribute substantially to individual patient morbidity and mortality as well as global healthcare costs. There are an estimated 600,000 cases of PE each year in the United States, with an in-hospital case-fatality rate attributable to PE of approximately 2%.42, 43 These statistics clearly underestimate the extent of the problem, as this does not include patients with deep vein thrombosis, many more patients with PE die with PE (even if not from PE), and the mortality with these conditions continues to increase after hospital discharge. In fact, mortality rates from 3 months to 3 years after hospital discharge frequently range from 15% to 30%.43–45 For patients with hemodynamic compromise, the mortality with PE is substantially higher, in the range of 20% to 30%, while still in the hospital.42 Mortality rates are higher in men than women and in African-American individuals compared with Caucasian individuals, yet mortality rates overall are declining temporally.46–49
Ninety percent of PEs arise from deep vein thrombosis of the lower extremities and pelvis; the rest originate from the upper extremities, heart, or pulmonary arteries. While in most patients with established PE, diagnosis of deep vein thrombosis may be confirmed by noninvasive testing or venography, and only about 30% will present with clinical manifestations of venous thrombosis. In the appropriate clinical setting, suspicion usually is aroused by the sudden onset of chest pain, dyspnea, and hemoptysis and by low Po2.50–53 Findings, however, have almost no predictive value. Tachycardia, tachypnea, and low Pco2 are perhaps more indicative of pulmonary embolism.54, 55
The treatment of acute deep vein thrombosis is directed at preventing its primary complications, recurrent venous thromboembolism, and the post-thrombotic syndrome. Without appropriate treatment, 20–50% of patients with proximal thrombosis will sustain a pulmonary embolism. The data with respect to calf vein thrombosis is less sound, although the incidence of pulmonary embolism is thought to be significantly less than for proximal deep vein thrombosis.50–53
The embolic potential of isolated calf vein thrombosis continues to be debated; however, approximately 20% of such thrombi will propagate to a more proximal level at which point the risk for pulmonary embolus is increased. Although the incidence of post-thrombotic sequelae may be less than after proximal thrombosis, between one-fourth and one-half of patients will have mild to moderate symptoms 1–3 years later. Isolated calf vein thrombosis should, therefore, not be regarded as trivial and cannot be ignored.
Current consensus recommendations in patients without contraindications include antithrombotic treatment, including unfractionated heparin, warfarin, low-molecular-weight heparin, and thrombolytic agents presently to treat venous thromboembolic disease. However, improved anticoagulants are being developed. Gradient elastic stockings, filters, stents, and thrombectomies can also be used in the therapeutic armamentarium, when appropriate. Thrombolytic therapy is suggested for patients with massive iliofemoral deep vein thrombosis at risk of limb gangrene. Venous thrombectomy is suggested in related patients with massive iliofemoral deep vein thrombosis at risk of gangrene. These modalities are often employed in patients with massive, severely symptomatic phlegmasia cerulea or alba dolens. Placement of an inferior vena cava filter is suggested for patients with a contraindication for, or complication of, anticoagulant therapy as well as recurrent or progression of deep vein thrombosis despite adequate anticoagulation. Serial noninvasive follow-up to exclude proximal propagation is a reasonable alternative in patients with contraindications to anticoagulation.17
Lower Extremity Venous Duplex Ultrasound
Full diagnostic capabilities for the ultrasound evaluation and diagnosis of deep vein thrombosis include Doppler spectral analysis, color-flow Doppler imaging transducer compression, and high resolution B-mode imaging. Normal ultrasound findings include unidirectional flow, compressibility of the vein, and a lumen free of internal echoes. In order to demonstrate the compressibility of a normal vein, minimal external compression is needed with the transducer in the transverse position (Fig. 13–18). Unidirectional flow is best demonstrated with color-flow Doppler imaging. Doppler spectral analysis is beneficial in evaluating venous flow, which normally changes during the respiratory cycle as described above.
FIGURE 13–18. (A) schematic illustrating external compression with the transducer in the transverse position, (a) non-compression (b) compression. (B) Sonogram demonstrating the effect of non-compression and compression a normal vein. (C) Sonogram demonstrating the effect of compression on a vein with thrombus.
For the average person, a 5 MHz linear transducer is the scan head of choice. Often, transducers are changed during an examination depending on the depth of the vessel and the patient’s body habitus. For larger patients, a lower frequency transducer of 2.5 MHz or 3.75 MHz can be used with the tradeoff of slightly reduced resolution.
Examination Protocol. The following protocol has been described in detail in the Society for Vascular Ultrasound’s Vascular Technology Professional Performance Guideline.56 The routine protocol calls for careful examination of the common femoral vein, great saphenous vein, deep femoral vein origin, femoral vein in the thigh, popliteal vein, and the calf veins including the posterior tibial and peroneal veins.
The examination is performed with the patient in the supine position and the examination table in slight reverse Trendelenburg with the leg externally rotated (Fig. 13–19). This is the position of choice for viewing the common femoral vein, femoral vein in the thigh, deep femoral vein, great saphenous vein, popliteal vein, and the anterior and distal posterior tibial veins. The patient may be turned prone or lateral to view the popliteal vein, peroneal and proximal posterior tibial veins, and small saphenous and soleal veins.
FIGURE 13–19. (A) Examination table in reverse Trendelenburg position. (B) Patient lying down in a reverse Trendelenburg position.
When indicated, and if possible, the iliac veins are also evaluated. The anterior tibial veins are not routinely evaluated, as in the absence of symptoms in their distribution, their involvement in the thrombotic process is rare. The sonographer should carefully study all vessels using a combination of long-and short-axis images. Special care must be taken not to miss duplicated vessels. This is especially true of the femoral vein in the thigh and the popliteal vein below the knee (Fig. 13–20). Several reports have demonstrated that multiple femoral veins were present in 177 (46%) of 381 venograms, a much higher rate than the generally accepted frequency of duplication of 20–25%.57, 58
FIGURE 13–20. Duplex image of a duplicated popliteal vein.
Images with and without compression and using the color flow to detect directional flow are all useful. Doppler spectral analysis helps in assessing phasicity and augmentation responses and is particularly helpful as a secondary means of evaluating the patency of the iliac veins. Although the great saphenous vein is not included in the deep venous system, its origin is often visualized because of the risk of saphenous thrombophlebitis extending into the deep system.56–59
In this patient population, the vascular laboratory is accustomed to primarily evaluate for the presence of deep vein thrombosis. Incidental findings of other abnormalities have been reported; however, a search for these entities is neither routine nor standard protocol. A systematic search for alternative causes of the patient’s signs or symptoms and official reporting of these findings is beneficial to the patient and may avoid additional testing or prolonged hospitalization.
Some of the differential diagnoses that may be present in a patient with suspected deep vein thrombosis include cellulitis, true or false aneurysms, arterial venous fistulas and feeder sources for hematomas. In addition, the surrounding tissues may contain masses such as cysts and hematomas and enlarged lymph nodes may also be present.
Cellulitis is rarely associated with DVT.60 In these cases, the vascular laboratory may be asked to exclude deep vein thrombosis or evaluate for the presence of abscess formation. Soft tissue thickening and edema are a common finding in these patients. Abscess typically presents as a discrete fluid collection with variable echogenicity. There may be neovascularity of the wall.61
In the case of conspicuous swelling of the extremity, lymphedema can be suspected when markedly enlarged lymph nodes are visualized in the groin with normal venous hemodynamics. The inguinal nodes lie in the groin near the femoral vessels and appear enclosed in a dense fibrous capsule (Fig. 13–21). Lymphadenopathy is an enlargement of lymph nodes, which can be the result of an inflammatory or a neoplastic process. Swelling and localized tenderness can occur secondary to lymphatic obstruction or extrinsic venous compression. It may be possible to distinguish a benign enlarged lymph node from a malignant lymph node by shape and vascular patterns. A benign node generally will maintain an ovoid shape with bright echoes reflecting the hilum and surrounding hypoechogenic regions for the remainder of the node. Vascularity is seen entering in the hilar region. With malignancy, the node may become more spherical with loss of the echogenic hilum and more irregular vascularity.
FIGURE 13–21. Sonogram of a inguinal node near the femoral vessels.
A bursa is a sac of fluid. Dilated bursae communicating with the knee form cysts in the area of the popliteal fossa. These popliteal cysts commonly cause pain, swelling, and tenderness. Popliteal cysts are avascular, which may be helpful in the diagnosis of a structure in this region. They are found in patients with osteoarthritis, rheumatoid arthritis, and injury to the knee. Dilated bursae that lie between the gastrocnemius muscle and the semi-membranous tendons, posterior and medial to the knee joint are known as Baker’s cysts. Baker’s cysts have an oval and often septated appearance that is mostly hypoechoic in character and are typically located posteromedial to the popliteal vessel in the popliteal space. Ruptured cysts can dissect downward into the muscular fascial planes of the calf muscles producing irregular borders and pointed inferior end and may yield the appearance of a thrombosed vessel. Therefore, care should be taken to demonstrate that it is distinct from the vein and artery (Fig. 13–22).
FIGURE 13–22. Sonographic images demonstrating various shapes of Baker’s cyst.
Following trauma to an extremity, extravascular blood may accumulate. The resulting hematoma may appear quite similar to a Baker’s cyst yet can become more echogenic with time. Characteristically, they appear as heterogeneous areas within a muscle or between muscle planes, although their appearance can be quite variable (Fig. 13–23). Differentiation between a hematoma and abscess is not possible based on ultrasound alone and usually requires aspiration for a definitive diagnosis.
FIGURE 13–23. (A & B) Sonographic variations of hematomas.
Peripheral masses that develop acutely are usually accompanied by a history of previous trauma or surgical intervention. The incidence of pseudoaneurysm complication is 0.5–1.0% and the most common site is the common femoral artery. This mass is easily recognized by persistent circular swirling of blood between the site of rupture and the arterial lumen. False aneurysms are at risk for expanding, can cause localized compression of adjacent structures, and may rupture. True venous aneurysms are rare and obvious from their overtly large size. Arteriovenous fistulas (AVFs) are also common following catheter insertion and can be identified by high-velocity turbulent signals within the vein, high-velocity, low-resistance flow within the communicating neck, and an easily visible color Doppler bruit. Congenital AVFs are rarely seen and are usually diagnosed early in life. These entities are discussed in detailed in Chapter 14.
On rare occasions extravascular sources such as tumors can cause extrinsic compression and swelling. These masses are difficult to differentiate clinically from deep venous thrombosis. Sonographically, hypervascularization and enhanced color fill within these structures are suggestive of this problem and warrant further investigation. This phenomenon is often noted at the iliac vein level and should be suspected in patients with abnormally continuous venous flow within the common femoral vein when there is no evidence of deep vein thrombosis noted in the legs. These findings should prompt examination of the iliac veins to exclude a compression syndrome versus a thrombotic process or a combination of the two (Fig. 13–24).
FIGURE 13–24. (A) Extrinsic compression of the iliac vein. Spectral Doppler on lower right of image demonstrate a continuous flow. (B) White arrows pointing to a stent repair in a iliac vein. Bottom right image demonstrate normal phasic flow pattern.
DIFFERENTIATION OF ACUTE VERSUS CHRONIC DEEP VEIN THROMBOSIS
Duplex ultrasound is the most common method utilized today for the diagnosis of acute deep vein thrombosis.72 Three diagnostic criteria have been utilized to document the presence of acute deep vein thrombosis (Fig. 13–25).
FIGURE 13–25. Color Duplex image demonstrating acute deep vein thrombosis.
1. Intraluminal echoes are seen.
2. The vein is incompressible. The vein will sometimes be significantly distended (often the diameter of the vein will be up to twice that of the accompanying artery). Increased vein size is a very specific sign of an acute process; however, not all patients with acute deep vein thrombosis will present with this finding.
3. There is no Doppler (color or spectral) evidence of active blood flow.
In most laboratories, the result of the duplex scan is the basis for clinical decisions regarding the need for anticoagulant therapy in patients suspected of deep vein thrombosis.
The ability of duplex imaging to differentiate between acute and chronic disease is critical to its use in patients with symptoms of recurrent deep venous obstruction. In the lower extremity, the diameter of the vein appears to be an important factor. Van Gemmeren et al.73 compared duplex scan results to either histologic criteria or patient history and symptoms. A significant correlation was found between the age of thrombosis and the venous diameter. When thrombosis was less than 10 days old, the venous diameter was at least twice that of the diameter of the accompanying artery. Two other criteria, echogenicity and margin of the vein wall, were not reliable indicators.
To increase the utility of duplex imaging in patients with recurrent disease, a baseline follow-up study should be obtained in all patients with deep venous obstruction. Gaitini et al. recommended a follow-up study 6–12 months following an acute episode.74 An alternative approach is to obtain a baseline study at the time anticoagulant therapy is discontinued. If the patient presents with recurrent symptoms, it may be possible to interpret the results of the duplex examination without comparison to a baseline study75.
UPPER EXTREMITY VENOUS DUPLEX ULTRASOUND
After explaining the procedure to the patient, obtain a pertinent history and perform a physical examination of the extremities. Remove clothing so that access is not limited to the arm and neck on either side. If an indwelling catheter is in place, remove the bandages or dressings and cover the area with a sterile skin cover. The examination should be performed in a routine systematic fashion commencing at the internal jugular vein down to the innominate veins through the chest and into the arm and forearm if indicated. The asymptomatic side is always evaluated first. Comparison to the side contralateral to the involved symptomatic extremity at the same level with the patient in a similar position (supine or close to supine is best) is critical. Because the innominate, subclavian, and axillary veins are deep and protected by overlying anatomic structures and are in close proximity to the clavicle, compression ultrasound is not possible. Color and Doppler spectral flow patterns can used to assess patency of these veins. Compression techniques can be reserved to assess the more peripheral, easily compressed deep and superficial veins in the arm.
Spontaneous flow should be present in the innominate, subclavian, and internal jugular veins. In addition, the flow signals are pulsatile due to their proximity to the right atrium. Venous flow does not reduce as dramatically during expiration in the upper extremity (particularly medial to the clavicle) and phasicity normally seen in lower extremity veins may not be appreciated. Augmentation from compression maneuvers is reduced when compared to the lower extremity veins due to the smaller venous volume of the upper extremities.
Begin the scan with the patient in the supine position and the arm at the patient’s side. Using a 5 or 7 MHz linear-array transducer, the internal jugular vein is identified in the mid-neck in the transverse plane. This vessel should be examined from the level of the mandible to its confluence with the subclavian vein while compressing the vessel intermittently to assess it for the presence of intraluminal thrombus. Anatomic structures may prevent compressibility of the very proximal internal jugular vein. Spectral waveforms are obtained in the long axis carefully noting the direction and pattern of the venous flow as the internal and external jugular veins serve as major collateral pathways to shunt flow to the contralateral side in the presence of innominate vein occlusion. Venous flow is frequently pulsatile due to the proximity of this vein to the heart.
Using color Doppler, scan in a medial direction along the cephalad border of the clavicle and follow the subclavian vein into the innominate vein. This part of the scan is performed using a small footprint transducer with a 5 MHz imaging frequency. The right innominate vein is oriented vertically and the left assumes a more horizontal plane. Color flow should outline the flow channel even when the vessel walls are poorly seen. In some patients, the innominate vein may be followed to the superior vena cava, although most often only a small section of this vein may be visualized (Fig. 13–26).
FIGURE 13–26. (A) Transducer position at the suprasternal notch. (B) Sonogram of the superior vena cava (SVC) using the suprasternal notch approach.
The subclavian vein is then located inferior to the clavicle and followed to the outer border of the first rib where it becomes the axillary vein (Fig. 13–27). Compression maneuvers can be attempted; however, most often color and spectral Doppler will need to be used as these vessels may be resistant to compression despite the absence of clot. If the subclavian or axillary vein are not clearly seen, abduct the arm 90° from the torso and bend the arm in a pledge position to free the vessels from compression from surrounding structures. In the transverse and then longitudinal view, observe the vessel looking for the presence of internal echoes that may represent thrombus. Wall motion should also be observed as often as the vein walls will coapt in response to breathing.
FIGURE 13–27. Demonstrate transverse and sagittal approach to imaging the subclavian vein below the clavicle (left) with corresponding sonograms (right).
The axillary vein can be followed through the deltopectoral groove into the arm where it becomes the brachial vein. The brachial veins are adjacent to the brachial artery and may be difficult to see because of their small size. They are best imaged in the transverse plane and should be compressed in a manner similar to that of the lower extremity veins to their termination at the elbow.
The cephalic vein is imaged at its confluence with the axillary vein. This vessel is best imaged using a high-frequency (7 to 10 MHz) transducer and is evaluated for patency using the compression technique. It is often very small and too superficial to image unless it is thrombosed. An occlusive tourniquet can be placed proximally on the upper arm to dilate this vein and make it easier to see. If signs or symptoms of cephalic vein thrombosis are present, the symptomatic segments of the vein should be imaged. The basilic and the brachial veins are continuous with the axillary vein in the upper arm, allowing these vessels to be seen in the same scan plane. The basilic vein is more posterior and is closer to the skin; however, once it has penetrated the fascia, it will be as deep as the brachial veins.
The forearm veins may be evaluated if the patient is symptomatic in this region. These veins are small and often difficult and tedious to visualize and evaluate. They are best identified by using the color-flow scan to find the adjacent artery and then using augmentation techniques to confirm the presence of flow.
Photoplethysmography techniques assess reflux and differentiate between superficial and deep vein incompetency. These techniques provide indirect information about location and extent of venous insufficiency. These methods are less time consuming than the color-flow Doppler for screening the bilateral lower extremities and can be of great value when there are a large number of patients. Photoplethysmography (PPG) involves the use of a photoelectric cell placed above the medial malleolus. This photocell actually has an infrared light emitting diode and a photodetector that is attached to an amplifier and a strip chart recorder in the direct current (DC) mode. The patient is placed in a sitting position with the legs hanging in a dependent, non-weight-bearing position. Either the patient dorsiflexes the foot to contract the calf muscles or the calf is squeezed to empty the veins. The leg is allowed to relax and the refilling time of the veins is recorded. The normal venous refilling time is 20 seconds or greater. Less than 20 seconds indicates venous incompetency80 (Fig. 13–28). Venous incompetency can be confined to the superficial veins or involve the deep veins. It is important to discriminate which systems are involved since the superficial veins can be surgically corrected but the deep veins cannot be surgically corrected. If the initial examination is positive for incompetency the test is repeated with a tourniquet placed above the knee to occlude the superficial veins. If the test with the tourniquet is positive it indicates the deep system is also incompetent.
FIGURE 13–28. Images of photoplethysmography (PPG). Left upper photo demonstrate the feet in a resting position and the lower left photo demonstrate the feet in a dorsiflexion position in order to empty the calf. On the top upper right is a normal response to calf exercise. On the bottom right is an abnormal response to venous valvular incompetency.
Air plethysmography (APG)81, 82 is a technique that allows the measurement of limb volume changes with different maneuvers. The device consists of a cuff that is placed around the leg, a calibrated pressure transducer, and an analog chart recorder that provides a visual display. Parameters derived from performing various APG measurements with positional changes include the venous filling index, which quantitates venous reflux, the ejection fraction, which correlates with calf muscle pump function, and the residual volume fraction, which correlates with ambulatory calf venous pressure. Venous occlusion techniques allow the measurement of arterial flow into the limb and the venous outflow fraction, which can be used to evaluate venous obstruction. Differentiation of pathology in the deep venous system from that in the superficial venous system is possible. APG has been validated in the evaluation of venous insufficiency in the legs and has a place in the evaluation of symptomatic patients suspected of having deep venous thrombosis. The ability of the device to quantitate absolute arterial flow to the lower extremity makes it useful in evaluating operative results and following disease progression.
Venography (phlebography)83, 84 is defined as radiography of the veins after injection of contrast medium. It is now used infrequently because ultrasound studies are a less invasive way to get the needed diagnostic information. There are two types of venography ascending and descending depending on the injection site. Ascending venography will be injected into a peripheral vein and the contrast material carried centripetal by the venous flow. Descending venography will be injected into a proximal vein in the leg and the contrast media carried distally by induced retrograde venous flow.
The normal venogram of the lower extremity demonstrates the deep and superficial system, as well as the external and common iliac veins. In some instances, special maneuvers (compression or muscular contraction) may be required to delineate the venous structures fully. The veins are quite variable among different individuals but are usually shown as deep venous trunks that are well defined and easily recognized. The valves are best seen after muscular contraction. The perforators will be defined between the deep venous trunks and the superficial veins.
CHRONIC VENOUS DISEASE
Venous insufficiency can be conveniently divided into primary venous insufficiency (varicose veins, telangiectasias) and chronic venous insufficiency (skin changes, secondary venous dysfunction).85 About 10–30% of the US population has some variant of venous disease.86 The American Venous Forum has developed the CEAP classification to help define the different degrees of venous insufficiency by different categories: C (clinical state), E (etiology), A (anatomy), P (pathophysiology).
The major components of pathophysiology in venous insufficiency are obstruction and vascular incompetence. These components may lead to venous hypertension, which is presently thought to be responsible for significant signs and symptoms in this disease class.
Signs and Symptoms. Varicose veins are dilated veins within subcutaneous tissue, which can be divided into primary (normal deep system) and secondary (abnormal deep symptoms). Symptoms that may be associated with varicose veins include heaviness, itching, tiredness, burning, and cramps. Chronic venous insufficiency may be manifested by varicose veins alone or by hyperpigmentation, edema, ulceration, and lipodermatosclerosis (Fig. 13–29).85
FIGURE 13–29. Images of various manifestations of chronic venous insufficiency. (A) large varicose veins. (B) Hyperpigmentation. (C) Venous ulcerations.
History and physical examination as above can identify the diagnosis of venous insufficiency but in general cannot identify the presence, location, or extent of vascular incompetency or obstruction. Duplex scanning has become the single most important noninvasive adjunctive tool in answering these questions and, thus, provides the appropriate medical or surgical approach in this clinical setting.
The exam may be completed in two parts.87, 88 First, a supine protocol can be utilized to identify patency versus venous obstruction. In the second part of the exam, the proximal great saphenous can be evaluated with Valsalva in reversed Trendelenburg position, but the remainder of the exam should be completed in the standing position with the weight on the leg that is not being examined. In general, reflux >0.5 seconds, is consistent with the venous insufficiency, and this may further be classified into mild, moderate and severe, according to reflux duration (Fig. 13–30).89
FIGURE 13–30. Doppler image demonstrating venous reflux.
Management of venous insufficiency can be noninvasive or invasive, depending on the underlying condition of the patient. Noninvasive options include leg elevation, compression, and topical treatment. Invasive approaches include sclerotherapy, skin grafting, stripping of superficial veins, open subfascial perforator surgery, subfascial endoscopic perforator surgery (SEPS), and deep vein reconstruction.90 A relatively new development in the treatment of saphenous vein reflux is minimally invasive catheter directed endovenous obliteration.91
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