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150 Duplex ultrasound scanning for acute venous disease
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16. Mansour MA. Venous duplex ultrasound of the lower extremity in the diagnosis of deep venous thrombo­sis. In: AbuRahma AF, Bandyk DF, eds. Noninvasive Vascular Diagnosis: A Practical Guide to Therapy, 3rd Ed. London: Springer-Verlag, 2013, 473–81.
17. Merritt CRB. Ultrasonographic demonstration of portal vein thrombosis. Radiology 1979;133:425–7.
18. Benson CB and Frates MC. Ultrasound of the hepatoportal circulation. In: AbuRahma AF and Bandyk DF, eds. Noninvasive Vascular Diagnosis: A Practical Guide to Therapy, 3rd Ed. London: Springer-Verlag, 2013, 565–87.
19. Kearon C, Julian JA, Math M, Newman TE, and Ginsberg JS. Noninvasive diagnosis of deep venous thrombosis. Ann Intern Med 1998;128:663–77.
20. Laissy J-P, Cinqualbre A, Loshkajian A etal. Assessment of deep venous thrombosis in the lower limbs and pelvis: MR venography versus duplex Doppler sonography. Am J Roentgenol 1996;167:971–5.
21. Tessler FN, Gehring BJ, Gomes AS etal. Diagnosis of portal vein thrombosis: Value of color Doppler imaging. Am J Roentgenol 1991;157:293–6.
22. Sottiurai VS, Towner K, McDonnell AE, and Zarins CK. Diagnosis of upper extremity deep venous thrombosis using noninvasive technique. Surgery 1982;91:582–5.
23. Falk RL and Smith DF. Thrombosis of upper extrem­ity thoracic inlet veins: Diagnosis with duplex Doppler sonography. Am J Radiol 1987;149:677–82.
24. Sajid M, Ahmed N, Desai M, Baker D, and Hamilton G. Upper limb deep vein thrombosis: A literature review to streamline the protocol for management. Acta Haematol 20 07;118:10 –18.
25. Kearon C, Akl EA, Comerota AJ etal. Antithrombotic therapy for VTE disease: Antithrombotic therapy and prevention of throm­bosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest 2012;141:e419S–94S.
26. Zierler BK. Ultrasonography and diagnosis of venous thromboembolism. Circulation 2004;109(Suppl. I): I-9–I-14.
27. Strothman G, Blebea J, Fowl RJ, and Rosenthal G. Contralateral duplex scanning for deep venous thrombosis in unnecessary in patients with symp­toms. J Vasc Surg 1995;22:543–7.
28. Prandoni, P, Lensing AWA, Piccioli A, Bagatella P, and Girolami A. Ultrasonography of contralateral veins in patients with unilateral deep-vein thrombo­sis. Lancet 1998;352:786.
29. Pennell RC, Mantese VA, and Westfall SG. Duplex scan for deep vein thrombosis—Defining who needs an examination of the contralateral asymptomatic leg. JVasc Surg 2008;48:413–6.
30. Le Gal G, Robert-Edabi H, Carrier M, Kearon C, Bounameaux H, and Righini M. Is it useful to also image the asymptomatic leg in patients with sus­pected deep vein thrombosis? J Thromb Haemost 2015;13:563–6.
31. Heit JA, Mohr DN, Silverstein MD, Petterson TM, O’Fallon WM, and Melton LJ III. Predictors of recur­rence after deep vein thrombosis and pulmonary embolism: A population-based cohort study. JAMA Intern Med 2000;160:761–8.
32. Siragusa S, Malato A, Anastasio R etal. Residual vein thrombosis to establish duration of antico­agulation after a first episode of deep vein throm­bosis: The Duration of Anticoagulation based on Compression Ultrasonography (DACUS) study. Blood 2008;112:511–5.
33. Stephenson EJP and Liem TK. Duplex imaging of residual venous obstruction to guide dura­tion of therapy for lower extremity deep venous thrombosis. J Vasc Surg Venous Lymphat Disord 2015;3:326–32.
34. Carrier M, Rodger MA, Wells PS, Righini M, and Le Gal G. Residual vein obstruction to predict the risk of recurrent venous thromboembolism in patients with deep vein thrombosis: A system­atic review and meta-analysis. J Thromb Haemost 2011;9:1119–25.
35. Donadini, MP, Ageno W, Antonucci E et al. Prognostic significance of residual venous obstruc­tion in patients with treated unprovoked deep vein thrombosis. Thromb Haemost 2014;111:172–9.
36. Kyrle PA and Eichinger S. Clinical scores to pre­dict recurrence risk of venous thromboembolism. Thromb Haemost 2012;108:1061– 4.
37. Hamadah A, Alwasaidi T, Le Gal G etal. Baseline imaging after therapy for unprovoked venous throm­boembolism: A randomized controlled comparison of baseline imaging for diagnosis of suspected recur­rence. J Thromb Haemost 2011;9:2406–10.
13
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Duplex ultrasound scanning for chronic venous obstruction and valvular incompetence
RAFAEL D. MALGOR AND NICOS LABROPOULOS
13.1 Introduction 151
13.2 Duplex ultrasound 151
13.3 Obstruction 152
13.4 Reflux 153
13.5 Technique 155
13.6 Role of DUS in understanding the pathophysiology of CVD 157
13.1 INTRODUCTION
Venous obstruction and reux are the two pathologies that lead to venous hypertension, which causes the sequelae of chronic venous disease (CVD). Despite the high prevalence of CVD and the number of studies that have been performed in this area, the etiology of CVD is poorly understood. e challenge to the clinician is to nd a method of reliably evaluating a patient for CVD. e physical examination is useful. Many of the signs and symptoms of CVD can be detected by physical examination, but physical examination alone is inadequate.
Phlebography, plethysmography, and duplex ultra­sound (DUS) are the main methods for the evaluation of the venous system. Computed tomography and magnetic resonance imaging have also been utilized lately in CVD workups, especially in cases where iliocaval obstruction is suspected.1 Plethysmography is used in the assessment of the amount of reux, the eciency of the calf muscle pump, and obstruction. Phlebography is used when there is a need for endovenous therapy and deep vein reconstruction. Plethysmography is also recommended in patients with advanced CVD if duplex scanning does not provide deni­tive information on pathophysiology.1 DUS has become the test of choice for the evaluation of CVD in most patients as it is safe, noninvasive, cost-eective, and reliable. Although the evaluation of acute venous pathology has been discussed in Chapter 18, it must be mentioned that such pathology can
recur in new or previously aected vein segments and can worsen the clinical severity of CVD.
13.7 Progression of CVD 159
13.8 Recurrent varicose veins 160
13.9 Use of DUS before, during, and after treatment 160 References 162
e CEAP classication was developed by the American Venous Forum in 1994 and revised in 2004 to delineate the severity of CVD, improve standards of reporting, and develop treatment plans for the various stages of the dis­ease.2 It relies on the four components of clinical signs (C), etiology (E), anatomy (A), and pathophysiology (P). Recently, a more detailed venous score system, the Venous Clinical Severity Score (VCSS), has been utilized to grade the severity of CVD. e VCSS is composed of 10 categories which mainly consider the degree of pain, amount of vari­cose veins, skin damage, and the use of compression stock­ings. Both the physical examination and diagnostic tests are employed in order to report the patient’s condition before and aer treatment.
13.2 DUPLEX ULTRASOUND
e choice of the ultrasound probe is important. e pulse­wave Doppler of a 4–7-MHz linear array transducer is ideal for the examination of most veins. Other multi-frequency arrays can be used as well. e more supercial veins can be evaluated using higher-frequency probes that give better resolution. e deep veins and veins in obese patients are evaluated using a 3-MHz curvilinear probe that provides better depth of penetration. Lower-frequency probes are also used to evaluate the venous system in the pelvis and abdomen. Curvilinear lower-frequency transducers should also be utilized whenever the depth of imaging is >6 cm (large l imbs).
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152 Duplex ultrasound scanning for chronic venous obstruction and valvular incompetence
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During imaging, low ow settings are most commonly used. e pulse repetition frequency (PRF) is set at 1500 Hz or lower. In cases of vein stenosis or arteriovenous stula, the PRF is set higher, since the ow velocity is signicantly elevated in such situations. e focus is set with the poste­rior wall (far wall in relation to the skin) to enable better lateral resolution in the eld of imaging. e vein lumen should be set to appear dark in the absence of stasis and thrombosis. e time gain compensation is set according to the echogenicity and depth of the relevant tissues in order to perfect the imaging of the pertinent pathology. When obtaining velocity waveforms, the gain is set to have a dark background in order to avoid overestimation. If the signal is weak because of depth, the gain is increased accordingly. e angle of insonation in the venous system is oen set at 0°. However, because most veins run parallel to the skin, if a precise velocity is needed, then the angle has to be corrected to be parallel to the ow channel.
e examination room conditions should also be condu­cive to obtaining optimal results. e room should be warm and comfortable and a warm gel must be utilized on the skin in order to ensure that there is no spasm of veins at the time of examination and that the veins are at their natural size.
13.3 OBSTRUCTION
Obstruction in the venous system can occur due to extrinsic and intrinsic pathologies. Tumors, hematomas, cysts, aneu­rysms, and musculoskeletal structures can cause extrinsic vein compression. However, the most common cause of obstruction is venous thrombosis. Its diagnosis is critical, as deep vein thrombosis (DVT) is obviously a signicant cause of long-term morbidity and premature mortality in those aicted with the disease.
e long-term consequences of DVT are devastating in terms of numbers and cost of care. Post-thrombotic syn­drome (PTS) is a term that is used to describe the sequelae of CVD. e typical ndings are pain, a burning sensation, itching, varicose veins, chronic limb swelling, skin dis­coloration, and ulceration. Aer a single episode of DVT, the incidence of PTS has been reported to range from 23% to 79%. A large prospective study showed an incidence of about 25% at 5 years. shown to increase the odds for developing PTS by six times.3 e sensitivity and specicity of DUS for identifying throm­bosis is >95% proximal to the knee, whereas the accuracy may decrease in the below-knee segment.4 e evaluation of functional obstruction cannot be achieved with DUS, as it assesses a single vein segment at a time. Unfortunately, it is dicult to measure functional obstruction, since there are no validated tests to quantify functional obstruction.
Duplex techniques for the evaluation of CVD are similar to those used in the evaluation of acute venous thrombosis. In chronic disease states, the major veins might be chroni­cally obstructed. Collateralization and recanalization may also occur. e major veins are seen in immediate proxim­ity to the corresponding artery. If a vein is seen more than
3
Ipsilateral recurrent DVT has been
1 cm away from the artery, one must consider the possibility of a dilated collateral vein. Normal venous Doppler signals are obtained in cases where full recanalization has occurred or in the presence of duplicated veins that were unaected by the thrombotic process. e popliteal vein is duplicated in 35%–40% of people and occasionally is triplicated. e femoral vein in the thigh is duplicated in about 25%–30% of people, and this duplication may have dierent patterns along the course of the vein. e veins in the calf are oen paired around the corresponding artery. A single calf vein or a triplication may also be found. Aplasia of the posterior tibial veins has also been reported. In cases of venous dupli­cation or aplasia, direct visualization, attention to detail, and experience with the ultrasound techniques are invalu­able for reducing erroneous results. In patients with previ­ous DVT, the technician has to be vigilant when scanning the previously aected and the contralateral limb for recur­rence of DVT. Risk factors for recurrent DVT are previous ipsilateral DVT, age >65 years, residual thrombus, or previ-
3,5
ous iliofemoral involvement.
Knowing these risk factors aids the operator when carefully seeking signs of recurrent DVT, such as thrombus found in a new location, thrombus extending >9 cm further in the vein, a previously recana­lized segment that is not compressible, and thrombus thick­ness ≥2 mm for calf veins and ≥4 mm for proximal veins.
6
Venous ultrasound studies are reasonably well stan­dardized. In brief, the patient is placed on the examina­tion table in the reverse Trendelenburg position. e knee is bent and externally rotated. e examination is started below the inguinal ligament at the common femoral vein and saphenofemoral junction (SFJ). e probe is placed in transverse direction to the vein and compression is applied. e probe is then turned longitudinally to evaluate ow and augmentation. e veins are examined in 3–5-cm inter­vals. In a similar manner, all of the deep veins of the leg, including the femoral, deep femoral, popliteal, peroneal, soleal, gastrocnemial, and posterior tibial veins, are exam­ined for obstruction. An examination of the anterior tibial veins is not routinely performed due to their low incidence of thrombosis, unless local symptoms or trauma to the anterior leg compartment area are present. e supercial veins, including the great saphenous vein (GSV) and small saphenous vein (SSV), are then evaluated. Finally, in cases of obstruction, it is important to check the iliac veins and the inferior vena cava (IVC). In abdominal and pelvic veins, mainly ow is evaluated, since compression can be di­cult and uncomfortable for the patient. A normal venous ow is phasic with respiration and is augmented with dis­tal compression or is stopped with the Valsalva maneuver. Asymmetry in ow velocity and waveform patterns at rest and during ow augmentation in the common femoral veins indicate proximal obstruction. However, the absence of such asymmetry does not exclude obstruction. erefore, when iliocaval obstruction is suspected, the full extent of these veins must be imaged.
e presence of stenosis, usually from extrinsic compres­sion, is recognized by a mosaic color pattern that denotes
13.4 Reflux 153
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post-stenotic turbulence, abnormal Doppler waveform at the area of stenosis, slow ow, spontaneous contrast, and vein dilatation prior to the stenosis.7 e vein diameter reduction can be measured by planimetry, comparing the smallest lumen to the normal lumen. Peak vein velocity ratios comparing intra-stenotic to pre-stenotic peak veloci­ties or comparing post-stenotic to pre-stenotic peak veloci­ties can be calculated. In patients with a pressure gradient across the stenosis 3 mmHg, the peak systolic velocity (PSV) ratio has been shown to be >2.5. is is particularly useful when investigating central vein stenosis.
7
e four components that should be examined in all venous duplex examinations are visualization, compress­ibility, ow, and augmentation. ere are ways to potentially distinguish acute obstruction from chronic obstruction (Table 13.1). e veins with acute thrombosis are echolu- cent, distended, and have smooth walls. In chronic throm­bosis, the veins are echogenic, contracted, and have thick, irregular walls (Figure 13.1). Acute thrombus is “spongy” on compression examination, but will still keep the walls of the vein from coapting with probe compression. On the color ow examination, acute thrombus will have conu­ent ow channels. Chronic thrombus will either have mul­tiple channels or collateralization. Intraluminal webs and wall thickening, with or without reux, indicate a previous thrombosis in the absence of visible thrombus. e presence of dilated collateral veins indicates the presence of obstruc­tion, but unfortunately, their absence cannot exclude it. It is also possible for the veins to be fully recanalized without any evidence of anatomic obstruction. However, the thick­ening and increased stiness of the vein wall can still result in functional obstruction.
Signs and symptoms in both lower extremities are pres­ent when there is bilateral iliac vein obstruction or when the IVC is involved. e iliac veins and IVC may have extrinsic
compression from masses (Figure 13.2). e extrinsic com- pression can lead to signs and symptoms of CVD. In such patients, thrombosis of the compressed vein is a common event.
13.4 REFLUX
Venous reux is the reversal of ow in the veins of the lower extremity. e reversal of ow in the vein can be subdivided into physiologic and pathologic. Physiologic reversal of ow accounts for the fraction of the second it takes for the valve leaets to appose. A prospective study has demonstrated that the acceptable physiologic reversal of ow is dierent for various venous systems in the lower limb.6 e cut-o value for reux, in the authors’ experience, in the common femoral, femoral, and popliteal veins is >1000 ms. For the supercial, deep femoral, deep calf axial, and muscular veins, the value is 500 ms, and in the perforating veins (PVs) it is 350 ms. It is postulated that in the larger veins with fewer valves, the time it takes for the valve leaets to come together is longer in comparison to smaller, shorter veins. A recent multicenter prospective study has determined that a reux of 0.5 seconds is accepted as abnormal.8 Dierent patterns of reux are displayed in Figure 13.3.
It is important to dierentiate between primary, second­ary, and congenital reux. is classication is based on the pathophysiology of the reux. Congenital reux exists at birth, but is rarely recognized early, since there is a lag in the presenting signs and symptoms. Secondary reux is most oen the result of thrombosis. e most common type of reux is primary, where the cause has not been determined. A study that has used the CEAP classication to investigate the causes of CVD showed that congenital reux accounts for 1%–3% of CVD, secondary reux accounts for 18%–28% of CVD, and primary reux accounts for 64%–79% of CVD.
9
Table 13.1 Duplex ultrasound criteria used to differentiate acute versus chronic obstruction
Criterion
Size Distended No longer distended
Echogenicity Echolucent: acute
Lumen characteristics The lumen is not
Wall characteristics Thin and smooth Thickened Thickening with luminal reduction due to
Flow characteristics Absence of flow/
Thrombus
characteristic
Collateral veins Absent May be present Often found around the obstructed segments
Acute (days to
weeks)
thrombi
present or only partially present
fillings defects
Presence of tail Decreased linear extension of thrombus
Subacute (weeks to
months) Chronic (months to years)
Reduced; sometimes unable to be traced
due to lysis
Moderate
echogenecity
Recanalization with
adherence
Partial recanalization Partial recanalization with reflux. Enhanced flow
byduplex ultrasound
Echogenic: as the clot ages, dense material,
increased cellular components, fibroblasts, and collagen deposits form.
Partial recanalization with compressible filling,
often has residual thrombus or vein wall defects, and reflux may have a spongy feel on compression
inflammatory response to the thrombus
in dilated collateral veins
154 Duplex ultrasound scanning for chronic venous obstruction and valvular incompetence
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(a) (b)
(c) (d)
W : 4.0 MHz
Right + 38.4
(e) (f)
– 38.4
cm/s
(g)
θ = 54°
(h)
Figure 13.1 (a) Acute thrombosis in the common femoral vein. There is absence of color, the vein is dilated (twice the
sizeof the adjacent common femoral artery in red) with a homogeneous echolucent texture. (b) Acute on chronic thrombosis in the soleal vein in a patient with recent calf pain. The vein is dilated and has echogenic material (old thrombus), and echolucent material (fresh thrombus). (c) Chronic thrombus with partial recanalization in the great saphenous vein. Flow channels with reflux are seen over the old thrombus that appears as an echogenic band in the lumen.
(d) Complete recanalization with prolonged reflux in the popliteal vein. Thickening is seen in the far wall.
(e)Chronic iliofemoral occlusion with collaterals from the inferior epigastric and internal iliac veins. (f) Chronic IVC
obstruction with partial recanalization. The lumen of the IVC is smaller than the adjacent aorta. The azygos vein is dilated and larger than the aorta. (g) Nonphasic flow in a groin collateral in a patient with iliofemoral occlusion. (h) Chronic occlusion of the external iliac vein in a female patient who underwent stenting for previous thrombosis. Flow is seen in the adjacent artery. The vein has a small diameter and echogenic material in the lumen. The stent is seen in both the near and the far wall as an echogenic rim between the wall and the thrombus.
(a)
(b)
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2
2
1
1
0.4
Figure 13.2 (a) Bilateral swelling in a patient with inferior
vena cava (IVC) compression. Notice the pitting edema in both limbs after digital compression over the tibia.
(b)Compression of the IVC by a tumor at the level of the
liver. The lumen of the IVC at the site of compression measured 0.4 mm whereas the normal distal segment measured 1.4 mm. The color changes from blue in the normal portion of the IVC to white at the area of compression indicating significant vein stenosis.
1.4
13.5 TECHNIQUE
Reux can be elicited in two ways. During the Valsalva maneuver, the intra-abdominal pressure is increased, and this can lead to reversal of ow if there is valvular incom­petence. is technique is mainly useful in the evaluation of valves in the groin, as competent valves proximally will limit its usefulness.
Compression and release distal to the point of examina­tion on the limb is a reliable method of evaluating reux, and is referred to as augmentation. With compression there is an initial increased ow in the vein as the blood is pushed in the normal direction of ow from distal to proximal. Once the pressure is released, the blood ow reverses momentarily. If there are competent valves, there is minimal to no back
13.5 Technique 155
ow. However, with incompetent valves, the blood contin­ues to ow in the reverse direction. For the purposes of more precise measurement and standardization, the use of auto­mated pneumatic cus with rapid ination and deation is essential. e cu is placed around the leg 5 cm below the probe site. A 24-cm cu is used around the thigh, a 12-cm cu around the calf, and a 7-cm cu around the foot. e ination lasts for 3 seconds followed by rapid deation in
0.3 seconds. To ensure complete venous emptying and to overcome the hydrostatic pressures from above, thigh cus are inated to 80 mmHg, those on the calf to 100 mmHg, and 120 mmHg is required for foot cus. Occasionally in patients with signicant edema, the above techniques are inadequate and dorsiexion/plantar exion is also used.
To obtain the best results, the examination should start with the patient in the standing position, with the weight of the patient on the contralateral limb. e limb of interest should be slightly exed and externally rotated. If a patient is unable to stand for the time required, the veins from the mid-thigh and below can be assessed in the sitting posi­tion. If the test is performed on a bed, the torso should be elevated to >45°. A tilt-table with a leg rest to keep weight on the contralateral limb and reected backwards into a 60° position is another technique that can be used for reux measurements.
e routine examination of the veins of the lower extremity starts at the common femoral vein above the junction of the femoral and deep femoral veins. e SFJ at the terminal and pre-terminal valve and the associated tributaries are examined next. is is followed by the pop­liteal and the deep calf veins. e GSV, SSV, their tribu­taries, and non-saphenous veins are examined in detail, as these are the most common sites of reux. Reux in veins that are not part of the GSV or SSV system are found in about 10% of the patients. Veins of interest involved in non­saphenous vein reux are the gluteal vein, postero-lateral thigh PV, vulvar vein, lower posterior thigh vein, popliteal fossa vein, knee perforator vein, and sciatic nerve vein.
10
e GSV can be identied and dierentiated from other supercial veins because it is surrounded by two layers of fascia in the saphenous eye.
11
e SSV is found in the tri­angular fascia and is surrounded by the crural fascia and the medial and lateral heads of the gastrocnemius muscle.12 e tributaries of the supercial veins that are oen incom­petent in the thigh are the anterior and medial accessory veins, and in the calf they are the posterior and anterior arch veins. ese veins should be examined along their full length if they are incompetent.
Duplication of the saphenous veins is rare, reecting
<3% of patients with CVD.12 e most common anatomic variations of the saphenous veins are segmental hypoplasia and aplasia.13 Accessory veins ensuring good venous drain­age are frequently found close to such segments.
13
PVs are the last to be examined. ey can be distin­guished from the supercial and deep veins since they course perpendicular to these veins and pierce the deep fascia. e deep fascia is dense and echogenic and can
156 Duplex ultrasound scanning for chronic venous obstruction and valvular incompetence
Loyola University Med L7–4 38 mm PVasc/ven
2 : 32 : 50 pm F# 15 4.1 cm
(a)
Loyola Medical Center
L7–4 38 mm PVasc/ven
F# 48 3.1 cm
(b)
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Map 8 DynRg 50 dB Persist med Fr rate med
Col 68% Map 5 WF low PRF 2000 Hz Flow Opt : Med V
(c)
(e)
R T
+19.2
–19.2 cm/s
SV angle 60°
Dep 1.1 cm
Size 2.0 mm Freq 4.0 MHz WF low Dop 59% Map 2 PRF 1515 Hz
cm/s
–10
–20
20
10
Map 8 DynRg 50 dB Persist med Fr rate med
Col 74% Map 5 WF low PRF 2000 Hz
Flow Opt : Med V
(d)
(f)
10 : 59 : 05
R T
+19.2
–19.2 cm/s
SV angle –60°
Dep 1.9 cm Size 2.0 mm
Freq 4.0 MHz
WF low Dop 55% Map 2 PRF 2500 Hz
–40
–20
cm/s
20
40
(g)
Figure 13.3 (a) Normal saphenofemoral junction. During distal augmentation there is flow towards the heart (negative
deflection as blood traveling away from the transducer). After release of the compression there is a short duration of ret­rograde flow until the valve is closed. (b) Prolonged reflux in the great saphenous vein (GSV) below the knee. The vein has a normal diameter indicating that a vein does not have to be dilated when it is incompetent. This patient had asymptom­atic CEAP class 2 disease. (c) Reflux in the popliteal, medial gastrocnemial, and small saphenous vein (SSV). This patient had a chronic thrombosis that was fully recanalized. He presented with CEAP class 4 and had pain and itching. (d) Reflux in a lower calf medial perforator in a patient with a healed ulcer (C5). The vein was dilated (>6 mm) and had prolonged outward flow. (e) Cross-sectional view of a focal dilation in the lower thigh GSV with a frozen valve seen at the 4 o’clock position. (f) Dilation of the SSV in the upper calf with wall thickening in a patient with skin changes, edema, and varicose veins in the posterior calf. The diameter of the SSV measured 8 mm and the reflux duration was longer than 5 seconds. (g) Prolonged reflux from the medial gastrocnemius vein (GV) to the SSV. The SSV was incompetent from its junction with the gastrocnemial vein at mid-calf to the lateral malleolus. The proximal SSV was normal.
be easily visualized on an ultrasound scan. ere are approximately 150 PVs in the lower extremity, of which only 20 are of clinical signicance in terms of reux pos­sibly leading to clinical pathology. e normal direction
of ow is from the supercial to the deep veins through the PVs. ese veins are examined using transverse and oblique scanning, since their long axes are seen in these planes. ey are found by following the course of the GSV,
13.6 Role of DUS in understanding the pathophysiology of CVD 157
N
N
LT par
C1–3A EP AS+P PR C1–4S EP AS+P+D PR+O
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the SSV, and the tributaries. Outward ow in these veins is seen only in the presence of supercial and deep vein reux. Based on the current Society for Vascular Surgery and American Venous Forum guidelines for the care of patients with CVD, duplex scanning of the PVs should be performed selectively.1 PVs are deemed to be “pathologic” when an outward ow of duration of 500 ms, a diameter of 3.5 mm, and a location beneath healed or open venous ulcers (CEAP class C5–C6) are present.1 ese guidelines aid physicians in making their decisions on whether or not PVs need to be treated.
1
e results of an ultrasound examination in patients with CVD are oen depicted in drawings. An example of this is given in Figure 13.4. e le and right lower extrem­ities have been drawn to scale and have skin, muscular, and bony landmarks such as the popliteal skin crease, sar­torious muscle, knee, and medial malleolus. Such draw­ings enable better understanding and interpretation of the ndings and therefore facilitate the planning of treatment in each limb.
Right
13.6 ROLE OF DUS IN UNDERSTANDING THE PATHOPHYSIOLOGY OF CVD
e majority (70%–80%) of patients presenting wit h CVD are symptomatic. ese symptoms include itching, ache, restless limb, heaviness, burning, and ulceration. Varicose veins and telangiectasias are present in 80% of patients. Skin changes of some sort are seen in 20%–25%, and active or healed ulcerations in 12%–14% of patients with CVD (Figure13.5). Patients with C1 and C2 disease have reux conned to the supercial system. As the clinical severity worsens (C3–C6), the prevalence of incompetence in the perforator and deep veins increases. In limbs with CVD, reux alone exists in 80% of patients, reux and obstruction are present in 17% of patients, and only 2% of patients have obstruction alone.9 In addition, the combination of reux and obstruction has a worse prognosis for the development of skin lesions.
e most common location of reux in patients with CVD is the saphenous vein trunks and their tributaries, irrespective of clinical class. ese veins are aected in 90%
Left
3
R
R
R
N
R
R
: POPV + MGV
tial recanalization with reux
R
R
R
R
R
R
R
R
Figure 13.4 Report of a duplex ultrasound examination in a patient with bilateral chronic venous disease (CVD). She was
a 53-year-old female with two pregnancies and a positive family history of CVD in both parents. She noticed signs and symptoms of CVD after her second pregnancy, first in the left lower extremity and 2 years later in the right lower extrem­ity. She had also developed thrombosis in the left lower extremity 7 years previously. LT, left; MGV, medial gastrocnemius veins; N, no reflux; POPV, popliteal vein; and R, reflux.
158 Duplex ultrasound scanning for chronic venous obstruction and valvular incompetence
Class 0
1.3
Percentage (%)
0
Primary + secondary
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Figure 13.5 Presentation of 1000 consecutive limbs with chronic venous disease according to the CEAP classification.
of patients. Of the supercial veins, the GSV is involved in 70%–80% of cases, the SSV is involved in 15%–20%, and non-saphenous veins are involved in about 10%. e deep system is only aected in 30% of patients with CVD, and the PVs in 20%.9 Complex patterns of reux are present in patients with skin damage.14 Several studies have demon­strated that reux in the supercial system alone is the cause of 17%–54% of venous ulcerations. Of all limbs with venous ulceration, 74%–93% have reux in the supercial sys­tem. is present in more than 50% of patients with ulceration. is subclass of patients will benet from intervention directed towards the supercial venous system.18 Isolated deep vein reux occurs in <10% of patients. popliteal vein reux has the strongest association with the severity of CVD. Two vein systems are involved in ulcer­ated limbs in 52%–70% of patients, and all three systems are involved in 16%–50% of patients. the ulcer bed or within 2 cm of the ulcer have reux in 86% of cases. However, perforator vein reux is found only in a third of cases in this area.17 Saphenous reux can occur with­out SFJ and saphenopopliteal junction (SPJ) incompetence; therefore, ligation of these junctions may not be appropriate in such patients. obstruction is found in any of the systems. In these patients, other causes of ulceration should be evaluated.
in varicose limbs more frequently than in healthy ones (P < 0.001). It greatly inuences the path of the reux and the anatomy of the varicose veins. GSV segmental hypopla­sia can be detected pre-operatively by duplex ultrasonog­raphy. Its occurrence may inuence surgical management for two main reasons: in about 68% of varicose limbs with segmental hypoplasia, the distal GSV is competent; if the distal GSV is incompetent, its size and ow direction are normalized by treating the accessory vein that bypasses the hypoplastic segment.
worthy of discussion, as treatment of the saphenous trunks
Class 1 Class 2 Class 3 Class 4 Class 5 Class 6
Primary
Secondary
Congenital
Superficial
Perforating
Deep
Reflux
Obstruction
Reflux + obstruction
15–17
Supercial reux, with or without perforator reux,
17–19
Among the deep veins,
17–19
e veins that are in
20, 21
In 2.6%–4.0% of patients, no reux or
5.9
20.4
4.3
8.2
6.1
0.9
1.8
010203040
22
21.6
24.7
24.2
16.7
It has been shown that saphenous hypoplasia occurs
13
Several patterns of reux in the supercial veins are
38.3
68.3
90.7
28.8
81.6
50 60 70 80 90 10
may be avoided. In fact, there are occasions where both the GSV and SSV should be spared. An incompetent anterior accessory vein with or without involvement of the SFJ in the absence of GSV reux is found in 9% of patients. Aer treating the anterior accessory vein, at 1-year follow-up, no patients had reux in the GSV and 95% were satised with the treatment. In a large series of patients with reux in the SSV system, 3.1% had incompetence in the thigh extension of the SSV only.12 In another series where the thigh exten­sion was studied, in the GSV and SSV system, reux was found in 4.7%.23 Reux in the tributaries alone was detected in 9.7% of limbs with CVD. e most common site was the posterior arch vein.
24
Reux in non-saphenous veins, such as those of the vulvar, gluteal, posterolateral thigh, and other locations, is found in 10% of limbs with CVD.10 ese are mostly mul­tiparous female patients with a mean of three pregnancies. On all of these occasions, treatment can be targeted by ultrasound and the saphenous veins spared. Reux in non­saphenous veins is seen in Figure 13.6.
It has been suggested that in patients with primary reux in the supercial and deep system, deep venous reux may be directly linked to supercial reux. e reux circuit theory of venous overload states that reux in the super­cial system at the level of the perforators and major supercial to deep vein junctions will ow into the deep system and overload the deep system. is leads to dilata­tion and the development of reux in the deep system. It has been demonstrated that, by surgically correcting the reux in the supercial system, the deep system reux is also eliminated in more than 90% of patients.25 In a pro­spective study, deep reux in patients with primary CVD was shown to occur near the SFJ, SPJ, and gastropopliteal junction.26 It was more likely to occur when the reux at these junctions had high peak velocity and long duration. e reux in the deep veins was usually segmental and of shorter duration than post-thrombotic reux. A recent study of 30 limbs has demonstrated that signicant hemo­dynamic compromise is present when deep vein reux is
(a) (b)
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(c) (d)
13.7 Progression of CVD 159
Figure 13.6 Examples of reflux in nonsaphenous veins. (a) Varicose tributaries are seen in the right popliteal fossa of a male
patient who presented with pain and itching. The varicosities disappear above the popliteal skin crease as they dive deeper to join the popliteal vein. (b) Significant reflux in the vein of the popliteal fossa of the same patient. The vein is dilated and varicose and pierces the deep fascia just above the popliteal skin crease. It unites with the lateral aspect of the popliteal vein above the saphenopopliteal junction. (c) Reflux in the dilated and tortuous veins of vastus medialis muscle. These veins were connected with a perforating vein at the lower thigh that was in continuity with posteromedial varicose tributaries. ovarian vein reflux in a 24-year-old woman with three pregnancies. She presented with left vulvar veins that were extending from the groin medial to the GSV to the posterolateral calf. The ovarian vein measured 8.8 mm in diameter.
caused by supercial vein reux only when the popliteal vein valves are incompetent.
27
Most PVs have at least one subfascial bicuspid valve that prevents reux from the deep system to the supercial sys­tem. e role of PV incompetence in the development of the signs and symptoms of CVD remains unclear. However, there is evidence to suggest that the number of incompe­tent PVs and the sizes of competent and incompetent PVs increase with worsening CVD.
28,29
It has also been reported that patients with increasing numbers of incompetent PVs have a higher venous lling index. e venous lling index is known to correlate well with the severity of CVD. incompetence occurs more in the calf than in the thigh.
29
PV
16,28,29
ere are more incompetent PVs found in the lower and
e correction of reux in the supercial system has been shown to eliminate reux in the PV. is is not the case when the deep system is incompetent.31 In a prospec­tive study where PVs were treated with surgical ligation using DUS guidance, it was shown that recurrence of PVs at 3 years was very common (76%).32 e recurrent PVs were due to neovascularization or the development of incompe­tence in new sites, and not because of poor surgery.
DUS can also identify other uncommon pathologies in the veins, such as aneurysms, tumors, and phlebosclerosis (Figure 13.7). ese pathologies are not usually associated with the signs and symptoms of CVD unless there is con­comitant reux or obstruction. However, their diagnosis is important, and can alter management.
(d) Left
middle thirds of the medial calf. Most PVs that are >3.5 mm in diameter will be incompetent.28 However, the sensitivity
13.7 PROGRESSION OF CVD
of size alone determining incompetence is low, as about a third of the reuxing PVs have a diameter of <3.5 mm. e duration of outward ow and local hemodynamics worsen in PVs when both the supercial and deep veins connected to those PVs are incompetent.
28,30
e development of new PV reux is closely related to reux in the supercial sys­tem. In primary CVD, reux in PVs develops in an ascend­ing manner through the adjoining incompetent supercial vein, in a descending manner from the re-entry ow of a reuxing supercial vein, and in new locations where the supercial veins are also involved.
It was previously hypothesized that because of hydrostatic pressure, reux must start at the level of the iliac or common femoral valves and develop in a retrograde manner. However, studies on the morphology, biochemistry, and function of the venous wall have demonstrated that changes can occur in any vein segment, irrespective of the site and function of the valves. With the use of DUS, it has been clearly shown that in the early stages of CVD, reux develops in most people in the lower thigh, knee, and calf, without having a
26
connection to the groin area.
Reux, therefore, may have