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The Role of the Vascular Lab and Imaging in Chronic Venous Insufficiency

Clinical Review

The Role of the Vascular Lab and Imaging in Chronic Venous Insufficiency

Author Information:
Ali F. AbuRahma, MD

Introduction

Seven million of the 25 million Americans with venous insufficiency exhibit serious symptoms such as edema, skin changes and venous ulcers.1 One million of these patients seek medical advice annually. Overall, 80% of patients with venous insufficiency are managed conservatively, e.g., leg elevation and support stockings, and 20% are treated with vein stripping or endovenous ablation.

Etiology

The underlying cause of chronic venous insufficiency (CVI) is venous hypertension, where primary valve incompetence is the causative factor in 70–80% of cases.2 The other 20–25% of cases are caused by secondary valve incompetence as a result of deep vein thrombosis (DVT) or trauma. Congenital anomalies are responsible for 2 Generally, a combination of reflux and obstruction is more common than either abnormality.

Diagnostic Testing for CVI

The ideal test for CVI should provide anatomic and hemodynamic data. Over the past few decades, the standard tests used for the diagnosis of CVI have included descending/ascending phlebography and ambulatory venous pressures, however, both tests are invasive and have some limitations. Competent proximal valves may prevent assessment of distal reflux, whereas a hypertonic contrast medium may stream past normal valves in elevated legs. Evaluation of the great and small saphenous veins is also limited when using these techniques.3 Measurement of the ambulatory venous pressure reflects the global hemodynamics within the extremity and has a linear relationship with the presence of ulceration.4 Ambulatory venous pressure, however, cannot localize hemodynamic abnormalities, and is influenced by reflux and obstruction. Because of these limitations, the modern diagnosis of CVI relies on the use of noninvasive testing.

Noninvasive Testing for CVI

Indirect physiological methods include strain-gauge plethysmography (SPG) and impedance plethysmography (IPG), both of which are outdated; and photoplethysmography (PPG) and air plethysmography (APG), both of which have limited use in some vascular laboratories, therefore we will only discuss these tests briefly.

Photoplethysmography (PPG)

PPG is an indirect method of measuring volume change occurring in the cutaneous capillary network using a light (photo) source. PPG is mainly used to detect the presence of venous reflux (venous valvular incompetence). The test is performed by placing an infrared light source on the leg with an adjacent photoreceptor (sensor) to receive the backscattered light. This allows for the continuous recording on a strip chart of the signal intensity reflected from the cutaneous capillary network. The patient is seated and legs are allowed to hang freely. (Figure 1). A baseline recording is obtained, then the patient performs five successive plantar flexion/extension maneuvers. The venous refill time with PPG measures the time it takes capillaries to empty and is dependent on the arterial inflow and efficiency of the venous outflow (Figure 2).5,6 When reflux is identified by PPG, the placement of a tourniquet (or narrow occluding cuff inflated to 50 mmHg) alternately above and below the knee may help the investigator in localizing the site of reflux (Figure 3).6 There may be considerable variability in the measurements obtained from the same patient. Transducer position may also cause variations in measurements. Color-flow scanning can identify the sites of reflux more precisely and is currently the preferred method to evaluate patients with valvular incompetence and CVI.7

Air Plethysmography (APG)

APG is more accurate than impedance plethysmography, strain-gauge plethysmography or photo plethysmography in measuring true volume and is easier to use. Essentially, it has three major components: a transducer, which is a form of closed air bladder used to surround the limb segment, a pressure sensor that measures the pressure in the air bladder as a function of time and an electrical circuit that controls the pressure sensor and displays measured results (Figure 4). Since the air bladder surrounds the limb, any change in volume will cause pressure within the bladder to change. If limb volume increases, bladder volume will decrease, causing bladder pressure to increase. The test will detect changes in venous limb volume, secondary to patient maneuvers.

Parameters/Maneuvers Used for the Diagnosis of CVI Using APG

The patient is placed in supine position. This will lower venous pressure in the lower extremities to a value only slightly above the right atrial pressure (~0 mmHg). A baseline volume in the segment of interest is then recorded. When the patient is placed in the erect position, lower-extremity venous pressure increases due to the hydrostatic column of blood extending from the right atrium to the segment of interest. This volume increase is displayed on a graph as seen in Figure 5. The Y-axis is volume and the X-axis is time, since all measurements are either times or ratios. The measurement between the baseline supine volume and the erect volume plateau is known as the venous volume (VV). The operator can also determine the venous refilling time (VRT), which is the time measured from when the baseline volume begins to increase to its plateau. While the patient is in the erect position, the operator instructs the patient to perform a single brisk ankle flexion. This will produce a momentary reduction in Y-axis volume. This change in volume is the ejection volume (EV). To calculate the ejection fraction (EF), the operator divides EV by VV. The patient is then instructed to perform ten brisk ankle flexions that will produce a reduction in Y-axis volume, which should be larger than the volume reduction experienced with one flexion. This allows measurement of the residual volume (RV), which is defined as the difference between the volume after ten flexions and the baseline volume. The operator can also calculate the residual volume fraction (RVF) by dividing RV by VV.6,7 Table 1 summarizes a simplified diagnostic criteria for venous insufficiency.

Limitations of PPG and APG

Both of these tests are limited in patients with the ability to stand or perform vigorous tip-toe maneuvers, and in patients with Class 5 and 6 CVI who have limited ankle joint range of motion. The APG is also limited in obese patients because of the maximum cuff size at the ankle.

Laser Doppler Flowmetry

This uncommonly used noninvasive testing utilizes a narrow monochromatic incident light source (laser) to interrogate blood particles, mainly red blood cells (RBCs) moving in the dermal microcirculation. The recorded reflected light and the Doppler-shifted signal corresponds to the average velocity of the RBC particles. These velocities are affected by several factors including the significant scattering effect on both the incident and reflected light beams, epidermal thickness and/or pigmentation and the number of RBCs in the sample volume. The term RBC flux has been used to describe the measurement. This signal is a product of the number of moving RBCs in the sample volume and their mean velocity (Flux = Mean Velocity x RBC Volume Fraction). This noninvasive test is easy to operate and provides continuous readout, however, it cannot be calibrated and reproducibility may be difficult. Laser Doppler flowmetry has been used to detect microangiopathy and to predict certain clinical outcomes. The sympathetic axonal reflex of vasoconstriction and the loss of venoarteriolar response when the foot is lowered below the level of the heart occur in the presence of advanced peripheral neuropathy in diabetic patients and predicts wound-healing difficulties. Additional findings of microangiopathy in diabetic patients with compromised wound healing can also be secondary to loss of reactive hyperemia response following temporary arterial occlusion and failure to increase RBC flux with skin heating using this instrumentation.

Direct Methods: Duplex Ultrasound

Duplex ultrasound is used in patients with CVI to verify anatomic obstruction and/or valve incompetence of the deep veins, superficial veins and perforating veins.

Equipment

Dedicated high-resolution vascular scanners with color/ power Doppler functions and pulsed-wave Doppler are usually used. Smaller miniaturized devices with a single probe to image across a greater range of depth (5–10 MHz) can also be used. These venous exams utilize linear transducers with a range of 4–7 MHz. Examinations of the inferior vena cava, pelvic, and deep veins may need three MHz probes

Normal Valve Closure

Lower-extremity valve cups remain open while the patient is resting in the supine position. Valve closure is initiated by reversal of resting antegrade transvalvular pressure gradient. As the pressure gradient is reversed, there is a short period of retrograde flow or reflux until the gradient becomes sufficient to cause valve closure. At low velocities, reverse flow may persist, even with competent valves (Figure 6). Since clinically relevant reflux occurs during calf muscle contraction and relaxation in the erect position, maneuvers to elicit reflux should be done in the erect position.

Venous Duplex Ultrasound

Examination The patient stands in an upright position and the veins are scanned along their course. Transverse and longitudinal scans are performed to assess vein patency by compression. Venous reflux is detected on release of compression. Elements of venous duplex exams for the diagnosis of CVI should include the following: venous reflux, sapheno-femoral junction, great saphenous vein, small saphenous vein, deep veins and perforating veins.

Venous Reflux

Reflux is the most important pathology in patients with CVI. Several maneuvers can be used to elicit venous reflux: release phase of flow augmentation maneuvers, proximal compression and during the closed epiglottis apneic phase of the Valsalva maneuver. It should be noted that retrograde backflow is present in normal vein valves immediately before closure, but the period is short with a cut-off value of 500 ms defining pathologic reflux in superficial veins, profunda femoris and deep calf veins. The value of 350 ms is used in perforator veins and 1,000 ms for femoral, superficial and popliteal veins (Figure 7).7,8

Standardized Standing Cuff

Deflation for Reflux The patient stands supported by a frame with the leg slightly flexed and the weight borne by the contralateral leg (Figure 8). Pneumatic cuffs are placed distal to the segment of interest. The inflation pressure is varied according to the hydrostatic pressure at that level. The common femoral, proximal femoral, profunda femoris and proximal greater saphenous veins are evaluated with a 24-cm thigh cuff (Hokanson, Bellevue, Washingon) inflated to 80 mmHg; the distal femoral and popliteal veins, with a 12-cm calf cuff inflated to 100 mmHg; and the tibial veins, using a 7-cm foot cuff inflated to 120 mmHg. A rapid cuff inflator (Hokanson) is used to provide inflation over 3 seconds and deflation within 0.3 seconds. The Doppler spectral display is adjusted to show antegrade flow below the baseline and reverse flow (reflux) above the baseline. Each segment is sequentially imaged in a long plane at a distance of 9,10

Sapheno-Femoral Junction

The sapheno-femoral junction is examined while standing. The sapheno-femoral junction, the common femoral vein, the femoral vein and the profunda femoris veins are identified (Figure 9). The diameter of the sapheno-femoral junction is then recorded. Valsalva and thigh/calf compression-release maneuvers for reflux are also done.

The Great and Small Saphenous Veins

The great saphenous veins are scanned from the groin distally. The anterior and posterior accessory veins are often seen during the duplex exam. The diameters of the great saphenous veins are recorded at several levels. The anterior and posterior arch veins can be seen in the lower leg. The small saphenous vein is identified at the popliteal fossa (saphenous-popliteal junction). This vein can also be examined for reflux.

Perforating Veins

The perforator veins penetrate anatomic (fascial) layers. Communicating veins, such as intersaphenous veins, connect veins within the same anatomic layer. One of the innovations of the new terminology of the venous system of lower limbs is the complete elimination of eponyms such as the Boyd, Cockett and Sherman perforators. Descriptive terms designating vein location have been adopted.11 A classification of these veins is shown in Table 2. Perforating veins are evaluated in the upright position by scanning along the course of the femoral vein in the mid-thigh and posterior tibial and posterior arch veins in the calf. One to five perforating veins are usually traceable as they penetrate the fascia between superficial and deep veins. Perforating veins may occur anywhere along the medial calf, most commonly just below malleolus and 15–20 cm and 30–35 cm proximally. The flow in normal perforating veins is unidirectional, i.e., occurs only during distal compression of the foot or calf. In patients with incompetent perforating veins, the flow is bidirectional with reverse flow during relaxation after compression.

Deep Veins

The femoral and popliteal veins are usually studied in the supine position. Their patency is assessed by distal compression. Irregularities of the vein wall should be noted. Other deep veins, e.g., sural, tibial,and peroneal veins are imaged in the sitting position.

Noninvasive Venous Evaluation Based on CEAP Clinical Severity Criteria

Table 3 illustrates the clinical, etiology, anatomy and pathophysiology (CEAP) classifications of CVI. CEAP Classes 0 (Normal) and 1: These patients have no evidence of leg swelling or limb changes and generally require no further testing prior to treatment of their veins, which may include sclerotherapy. CEAP Class 2: These patients require further evaluation only if sclerotherapy or surgical varicose vein removal is considered. Duplex reflux examination will assist in determining the contribution of great or small saphenous reflux or other abnormal venous contributions to the development of the varicosities, allowing treatment of these abnormalities when present. CEAP Classes 3 and 4: In these patients, supine and reflux duplex exams are recommended to determine the sites of reflux, evaluate the deep and perforator systems for obstruction or reflux and guide the selection of ablative or surgical treatment. PPG or APG can provide evidence of global venous dysfunction, separating Class 2 patients with a primarily cosmetic problem from Class 3 and 4 patients with more significant venous dysfunction. APG is recommended, particularly to document the severity of CVI in patients considering intervention and to document improvement and predict long-term outcome after treatment. CEAP Classes 5 and 6: These patients should undergo a duplex exam as outlined for Class 3 and 4 patients to determine whether they are candidates for corrective venous surgery to aid in ulcer healing. Patients with superficial and/or perforator incompetence who do not have deep venous obstruction are good candidates for surgical treatment. Patients with deep venous abnormalities may benefit from surgery if they have severe recurrent ulceration. Most should undergo venography prior to surgical reconstruction as outlined by Raju.13 APG measurements are helpful in predicting patients at high risk for recurrent ulceration and should be performed for patients undergoing venous intervention.

Conclusions

The diagnosis of CVI is usually made by a history and physical, supplemented with a noninvasive venous exam, which will help in optimal management. The primary diagnostic test is a duplex ultrasound exam. PPG and APG may have a limited role in these patients.

References

1. Barron HC, Ross BA. Varicose veins: A guide to prevention and treatment. Facts on File, Inc. New York, New York (An Infobase Holdings Company). 1995, p. vii. 2. Labropoulos N, Leon LR Jr. Duplex évaluation of venous insufficiency. Semin Vasc Surg 2005;18:5–9. 3. Baker SR, Burnand KG, Sommerville KM, et al. Comparison of venous reflux assessed by duplex scanning and descending phlebography in chronic venous disease. Lancet 1993;341:400. 4. Nicolaides AN, Hussein MK, Szendro G, et al. The relationship of venous ulceration with ambulatory venous pressure measurements. J Vasc Surg 1993;17:414. 5. Criado E. Laboratory evaluation of the patient with chronic venous insufficiency. In: Rutherford RB (ed). Vascular Surgery. Philadelphia: W. B. Saunders Company, 1995, pp. 1771–1785. 6. Mansour MA, Sumner DS. Overview: Plethysmographic techniques in the diagnosis of venous disease, In: AbuRahma AF, Bergan JJ (eds). Noninvasive Vascular Diagnosis: A Practical Guide to Therapy, 2nd Edition. Springer-Verlag: London. 2007, pp. 375–384. 7. Labropoulos N, Giannoukas AD, Delis K, et al. Where does venous reflux start? J Vasc Surg 1997;26:736–742. 8. Needham T. Assessment of lower extremity venous valvular insufficiency examinations. J Vasc Ultrasound 2005;29:123–129. 9. Labropoulos N, Tiongson J, Pryor L, et al. Definition of venous reflux in lower extremity veins. J Vasc Surg 2003;38:793–798. 10. Araki CT, Back TL, Padberg FT, et al. Refinements in the ultrasonic detection of popliteal vein reflux. J Vasc Surg 1993;18:742. 11. Caggiati A, Bergan JJ, Gloviczki P, et al. Nomenclature of the veins of the lower limbs: An international interdisciplinary consensus statement. J Vasc Surg 2002;36:416–422. 12. Kistner RL, Eklof B, Masuda EM. Diagnosis of chronic venous disease of the lower extremities: The “CEAP” classification. May Clin Proc 1996;71:338–345. 13. Raju S. Surgical treatment of deep venous valvular incompetence. In: Rutherford RB (ed.). Vascular Surgery, Vol 2, 5th ed. Philadelphia: WB Saunders. 2000, pp. 2037–2049.

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From the Robert C. Byrd Health Sciences Center, West Virginia University, Charleston Area Medical Center, Charleston, West Virginia. The author reports no conflicts of interest regarding the content herein. Manuscript submitted December 17, 2007, provisional acceptance given April 5, 2010, and final version accepted May 14, 2010. Address for correspondence: Ali F. AbuRahma, MD, Department of Surgery, Robert C. Byrd Health Sciences Center, West Virginia University, Charleston Area Medical Center, 3110 MacCorkle Ave., S.E., Charleston, WV 25304. E-mail: ali.aburahma@camc.org>
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