20 - Risk Factors and the Role of Ultrasound in the ... · tions in venous hemodynamics....

442

RISK FACTORS AND THE ROLE OF ULTRASOUND IN THE MANAGEMENT OF EXTREMITY VENOUS DISEASE

Joseph F. Polak MD, MPH, and John S. Pellerito MD, FACR, FSRU, FAIUM

20 Introduction

Duplex sonography can effectively diagnose the presence of acute and chronic venous thrombosis in the extremity veins. Most commonly, duplex sonography is used when acute deep vein throm-bosis is suspected, but it is also a reliable means for determining the extent of chronic venous disease and the accompanying physiologic altera-tions in venous hemodynamics. Performance of the diagnostic venous ultrasound examination is also tailored to current approaches in patient management and the availability of various treat-ments. Both these aspects will be covered in the following pages.

Acute Deep Vein Thrombosis Etiology and Risk Factors

Venous thromboembolic (VTE) disease includes both deep vein thrombosis (DVT) and pulmonary embolism (PE) because they represent different aspects of the same disease process. Suspected VTE is the most common indication for the clinical evaluation of the extremity veins. Although a com-prehensive review of VTE is beyond the scope of this chapter, a brief review of risk factors and condi-tions fostering the development of VTE is given. The annual incidence of VTE in the United States is estimated at over 2.5 million cases.1 Roughly 25% of untreated patients with DVT will sustain a nonfatal PE. Moreover, without treatment, PE is associated with mortality of approximately 30%.2 A myriad of clinical conditions increases the risk of incident venous thrombosis. This susceptibility to develop venous thrombosis was first described in 1865 as Virchow’s triad: (1) venous stasis, (2) endothelial damage, and (3) hypercoagulability.

Venous stasis can occur in any situation of prolonged immobility. It may also be promoted by any situation where venous return to the heart is obstructed by compression of the vein lumen as can be seen in cases of pelvic tumors.

Endothelial damage includes direct trauma to the vein through puncture of the lumen. It can also occur in cases of trauma when shearing forces are applied to the vein wall and the endothelial layer is disrupted. This exposes the underlying collagen-rich tissues to blood.

Thrombus formation occurs through the activa-tion of enzymatic reactions in the intrinsic and tissue factor coagulation pathways (Fig. 20.1). This leads to thrombin formation via the prothrombin enzyme complex. The thrombomodulin-protein C system primarily limits coagulation, while the fibrinolytic system further limits fibrin deposi-tion. This homeostatic system is continuously active and balances activation and inhibition of coagulation and fibrinolysis. The predisposition to thrombus formation results either from nonrevers-ible (genetic factors, age) or reversible (acquired) prothrombotic conditions (Table 20.1).

Inherited prothrombotic disease states have been described with increasing frequency over the past 30 years. This category of venous thrombosis is considered nonreversible and, as such, the patient keeps his/her increased risk of developing venous thromboembolic disease throughout life.

Antithrombin III deficiency was the first reported congenital thrombotic condition.3 It is transmitted as an autosomal dominant pattern with a preva-lence of 1 : 5000. Isolated spontaneous thrombosis has been described with this condition. This defi-ciency lowers the threshold for the development of DVT in the presence of precipitating circumstances, such as trauma, pregnancy, and surgical procedures.

Protein C and protein S are vitamin K–dependent cofactors that facilitate degradation of activated factor V. Deficiencies therefore predispose to thrombosis. Congenital deficiencies of these factors are well described.4 Because these proteins are synthesized in the liver, acquired deficiencies may also occur from variations in liver function as well as with dietary changes. Protein C or S deficiency confers a roughly sevenfold increased risk of developing venous thrombosis. Resistance

44320 RISK FACTORS AND THE ROLE OF ULTRASOUND IN THE MANAGEMENT OF EXTREMITY VENOUS DISEASE

spontaneous VTE,5 making it the most common inherited hypercoagulable condition.

Factor II (prothrombin) G20210A is a mutation seen in 2% to 3% of individuals, predominantly those of European descent. It can increase the risk of VTE by as much as 2.8 times compared with individuals without this mutation.6

Primary hyperhomocysteinemia increases risk for VTE, along with the development of premature atherosclerosis. Serum elevation of coagulation factors VIII, IX, and XI have been shown to confer elevated risk for venous thrombosis in the Leiden thrombophilia study.7 Factor IX and XI levels greater than the 90th percentile, respectively, confer a 2.5-fold and 2.2-fold increased risk of VTE. Dysfibrogenemias and hypofibrinolysis impair the steps involved in the generation, cross-linkage, and breakdown of fibrin. Bleeding diathesis, as well as VTE, has been described with this condition.

Acquired prothrombotic states are more numer-ous than inherited states. Clinical conditions that predispose to VTE are listed in Table 20.1. Several of these conditions are briefly considered. Pregnancy and the postpartum period increase VTE risk compared with the nonpregnant state.8 PE is a leading cause of maternal death after childbirth, with one fatal PE per 100,000 births.9,10 Oral contraceptives and hormone replacement therapy can increase the risk of VTE in premenopausal and postmenopausal women. Lidegaard and colleagues

(Prothrombin) (Thrombin)

(thrombus)

FIG. 20.1 This diagram summarizes the coagulation cascade. The major coagulation factors are listed. On the left is the extrinsic pathway. On the right, the intrinsic pathway is responsible for the response to a direct injury to the blood vessel and the tissue factor (TF). The new direct oral anticoagulants are listed on the right. Low molecular weight heparin (LMWH) has its principle effect at the level of factor Xa. Not listed is fondaparinux, which also acts at the level of factor Xa.

TABLE 20.1 Risk Factors for Venous Thromboembolic Disease.Genetic Risk Factors Acquired Risk Factors Environmental

Elevated factor VIII, IX, or XI Age Immobilization including travel

Factor V Leiden Prior venous thrombosis or pulmonary embolism

Major surgery within 3 months

Primary hyperhomocysteinemia Oral contraception and hormone replacement therapy

Oral contraception and hormone replacement therapy

Protein S deficiency Malignancy Central venous catheters

Antithrombin III deficiency Obesity (BMI ≥30 kg/m2) Pregnancy and postpartum state

Protein C deficiency Cigarette smoking Trauma

Non-O ABO blood group Hypertension Chemotherapy

Dysfibrinogenemia Secondary hyperhomocysteinemia

Acquired antiphospholipid syndrome

Congestive heart failure

Myeloproliferative disorders

Nephrotic syndrome

Inflammatory bowel disease

Sickle cell anemia

Marked leukocytosis in acute leukemia

Infectious (e.g., sepsis, HIV)

to activated protein C is also known as factor V Leiden. This disorder results from a point mutation in the factor V gene, rendering activated factor V resistant to degradation by activated protein C. It is present in 12% to 33% of patients with

444 SECTION 4 EXTREMITY VEINS

The D-dimer test is often combined with the Wells score to help triage patients requiring compression ultrasound. For example, venous imaging may not be performed if a patient has both a low Wells score and a negative D-dimer test.19 This situation can occur in up to 40% of the outpatient population.19

Anticoagulation and Thrombolysis in the Management of Venous Thrombosis

OverviewThe management of patients with suspected DVT may affect the protocol implemented during ultrasound

reported a prevalence of VTE in women receiv-ing oral contraceptives of one to three in 10,000. Women receiving hormone replacement therapy have a twofold increased risk of VTE with rates depending on the type of contraceptive and a greater risk at the onset of therapy.11 Antiphospho-lipid antibody syndrome is an acquired condition due to the presence of either the lupus anticoagulant antibody or anticardiolipin antibodies. Overall, the syndrome can be identified in 1% to 5% of the population. Among those with positive titers for the lupus anticoagulant, the risk of developing VTE is 6% to 8%. Patients with anticardiolipin antibody titers greater than the 95th percentile have a 5.3-fold increased risk of developing VTE.12

Other risk factors for VTE that are often ignored include age and elevated body mass index (BMI). VTE is uncommon in children but increases progressively with age after adolescence.13,14 Obesity, defined as an increased BMI ≥30 kg/m2 is associated with a 2 to 3 times increased risk of DVT.15 Trauma16 and concurrent malignancy17 remain two major sources of provoked episodes of deep vein thrombosis.

Wells score and D-dimer levelsAn important consideration for the triage of patients is the application of the Wells score (Table 20.2). This clinical prediction rule is a useful guide for determining the need to perform a diagnostic imaging test, most often venous ultrasound, given an a priori likelihood that the patient has deep vein thrombosis.18 Once calculated, the Wells score can be used to estimate the likelihood of DVT: a low risk is a score of 0 or less, an intermediate probability is a score of 1 or 2, and a high prob-ability is a score of 3 or more.19

The D-dimer test detects the presence of breakdown products of linked fibrin, the main constituent of thrombus, due to in vivo throm-bolysis. Although the test is very sensitive for the presence of thrombus, it is not specific. False positives can be due to trauma, malignancy, recent surgery, pregnancy, liver disease, or renal disease. In addition, the sensitivity of the test depends on the method used. The most sensitive is the ELISA (enzyme-linked immunosorbent assay) method, a test that is time-consuming, has an overall sensitivity of 95%, and is considered abnormal at a level above 500 µg/L.20 Other, more rapidly processed D-dimer tests show some heterogeneity in sensitivity and cut points.21

TABLE 20.2 The Wells Score for Deep Vein Thrombosis.Clinical Characteristics Points

Active cancer (patient receiving treatment for cancer within the previous 6 months or currently receiving palliative treatment)

+1

Paralysis, paresis, or recent plaster immobilization of the lower extremities

+1

Recently bedridden for 3 days or more or major surgery within the previous 12 weeks requiring general or regional anesthesia

+1

Localized tenderness along the distribution of the deep venous system

+1

Entire leg is swollen +1

Calf swelling at least 3 cm larger than that on the asymptomatic side (measured 10 cm below tibial tuberosity)

+1

Pitting edema confined to the symptomatic leg

+1

Collateral superficial veins (nonvaricose) +1

Previously documented DVT +1

Alternative diagnosis at least as likely as DVT

–2

The points obtained are summed.There are two ways to use the score. The first is as a two-level indicator of DVT93: if the total is <2, then the probability of DVT is low at 5.5% (95% confidence intervals: 3.8% to 7.6%). If the score is ≥2, then the likelihood of DVT is relatively high at 27.9% (95% confidence interval: 23.9% to 31.8%). The second approach is to use a three level score19: if the total is 0 or less, then the probability of DVT is low at 5.0% (95% confidence intervals: 4% to 8%); if the total is between 1 and 2, then the probability of DVT is intermediate at 17.0% (95% confidence intervals: 13% to 23%). If the score is >2, then the likelihood of DVT is high at 53% (95% confidence interval: 44% to 61%).DVT, Deep vein thrombosis.


institution of warfarin therapy (with an INR target of 2 to 3) usually result from inhibition of factor VII because of its short half-life. Effective anticoagulation depends on the depletion of factor II (thrombin) and typically requires about 3 to 4 days of warfarin therapy25 to achieve a stable INR. This leads to a transition period of approximately 5 days.24 Therapy with oral warfarin in the absence of heparin anticoagulation should be avoided, as days will pass before anticoagulation is adequate, leaving the patient unprotected against PE; moreover, warfarin therapy in the absence of heparin anticoagulation may paradoxically intensify hypercoagulability and predispose to recurrent DVT.

The duration of anticoagulation varies with the clinical scenario. In general, for initial cases of

imaging of the extremity veins. Anticoagulation with an agent that offers a lower risk of bleeding than unfractionated heparin can justify postponing a venous ultrasound examination requested in the middle of the night to the next morning.22 The availability of new oral agents that permit effective treatment of calf vein DVT without excess risk of bleeding may help justify imaging of the calf veins.23 Low-risk anticoagulation being performed in the outpatient setting may necessitate a more quantita-tive evaluation of thrombus burden in order to help triage patients to outpatient or inpatient treatment.

HeparinAnticoagulation with intravenous (unfractionated) heparin has been the gold standard for the initial management of DVT for decades (see Fig. 20.1). Heparin has an antifactor Xa effect. Heparin potentiates the action of antithrombin III, thereby preventing additional thrombus formation and permitting endogenous fibrinolysis. It also has an effect on inflammation (the “itis” in thrombophle-bitis). Use of low molecular weight (fractionated) heparin compounds (enoxaparin [Lovenox] or dalteparin [Fragmin]) has decreased the risk of bleeding while keeping most of the benefits of unfractionated heparin. Low molecular weight heparins can be administered subcutaneously once or twice a day and do not require monitoring of the aPTT (activated partial thromboplastin time). They have permitted the empirical treatment of patients with suspected DVT22 while waiting for definite diagnostic testing (Fig. 20.2).

In the absence of a contraindication to anti-coagulation, prompt institution of heparin therapy is indicated for patients with either confirmed DVT (through imaging techniques) or for patients in whom a moderate or high clinical suspicion of DVT exists (see Fig. 20.2). Low molecular weight heparin is preferred if confirmatory venous ultra-sound is not immediately available.

Vitamin K antagonistsOral warfarin therapy is started while therapeutic heparin anticoagulation is being administered, usually over 5 days.24 Warfarin dosing is guided by measuring the International Normalized Ratio (INR), a reflection of the inhibition of vitamin K–dependent cofactors (see Fig. 20.1). Although the target INR will vary depending on the clinical circumstance, it is important to understand that early elevations in the INR (1 to 3 days after

Suspected DVTNo Imaging Available

High Probabilityof

DVT?

Yes

YesIntermediateProbability

ofDVT?

AnticoagulateUntil

Imaging Available

No

AnticoagulateIf

Imaging Delayed

No

YesDo Not Anticoagulate

IfImaging Done

Low Probabilityof

DVT?

>–4 Hours

<–24 Hours

FIG. 20.2 This algorithm is modified from the American College of Chest Physicians (ACCP) guidelines (9th and 10th editions). The availability of an imaging test affects the decision to anticoagulate as a function of the prob-ability of deep vein thrombosis (DVT) (see Table 20.2 for calculation of probability).


example, the American College of Chest Physicians (ACCP) generates guidelines based on the review of the current literature. The last set of complete guidelines, the 9th set, was published in 2012.39 Some of the topics were reviewed in 2016 and published as the 10th set.26 Ultrasound imaging strategies for the diagnosis and management of DVT will be discussed in the next few sections. Whenever possible, reference will be made to these guidelines.

uncomplicated DVT, 3 months of anticoagulation is recommended. Inherited and acquired proco-agulant states, and cases of recurrent DVT may require longer anticoagulation therapy, typically 6 months. In some cases of recurrent VTE and irreversible risk factors, lifelong anticoagulation may be recommended.

New therapeutic agentsOral agents not based on suppression of vitamin K–dependent coagulation factors are increasingly used to treat DVT. They are referred to as the direct oral anticoagulants (DOACs). There are currently two classes of these medications available: direct factor Xa inhibitors and direct factor IIa inhibi-tors. Both are considered acceptable substitutes to vitamin K–inhibitors for the treatment of deep vein thrombosis.26,27 Overall, these agents have a lower risk of bleeding than warfarin. The factor IIa (direct thrombin) inhibitors require coverage with heparin for the first 5 days in the same way as warfarin. The Xa inhibitors rivaroxaban and apixaban can be administered on the day of diagnosis without the need for 5 days of heparin treatment.24 Edoxaban has only been administered after heparin coverage in the Hokusai trial.28

ThrombolysisThrombolysis is not commonly used to treat patients with DVT, but there are situations in which it should be considered. Thrombolysis may be used to treat patients with extensive iliofemoral venous thrombosis and severe symptoms,29–33 where the risk of development of the postthrombotic syndrome is high.34,35 The prevalence and severity of the postthrombotic syndrome is believed to be decreased if rapid thrombolysis is achieved.35,36 However, the substantial proportion of patients with contraindications to thrombolysis and the associated increase in major bleeding episodes severely limit the use of thrombolytic therapy in more peripherally located DVT.

Thrombolysis is a therapeutic consideration in patients with upper extremity effort associated venous thrombosis, especially if correction of the underlying abnormality is to be attempted.31,37,38

Guidelines for the management of acute deep vein thrombosisPatients may be selected for ultrasound imaging of suspected DVT based on published guidelines. For

PRACTICAL TIPS

• Well-recognizedriskfactorsforDVTinclude stasis, endothelial damage, and hypercoagulopathy (Virchow’s triad).

• Hypercoagulopathymaybeassociatedwith reversible risk factors such as pregnancy or be caused by genetic factors.

• TheWellsscoreassignsaleveloflikelihood for the presence of DVT by considering predetermined risk factors.

• TheD-dimertestisaverysensitivebutnonspecific method for determining the likelihood of DVT.

• TheD-dimertestandtheWellsscorecanbe combined to triage patients for further ultrasound imaging.

• Availableanticoagulantswithlowerriskofbleeding than heparin or warfarin may impact the imaging protocol by:• inclusionofthecalfveinsinthe

imaging protocol• permittingovernightanticoagulationof

patients when ultrasound imaging is not available

• facilitatingoutpatientmanagementofpatients with DVT

• Althoughthrombolysiscandissolvethrombus quickly and decrease the incidence of chronic venous disease, it is preferably used in cases of iliofemoral DVT because of the risk of bleeding.

• Useofguidelines,suchasthosegeneratedbytheAmericanCollegeofChestPhysicians, may affect patient selection for ultrasound imaging and may modify the imaging protocol.


calf DVT propagation varies markedly. In postop-erative patients, the reported rate of propagation varies from 6% to 34%.47–49 Although it is not possible to identify thrombi that are likely to propagate and distinguish them from those that do not, there are certain markers that suggest a higher risk of propagation: (1) length of thrombus 5 cm or more, (2) diameter of the involved vein of 7 mm or more, and (3) involvement of multiple veins.22

Some authors argue that few, if any, significant pulmonary emboli arise from isolated calf DVT50–52 and therefore anticoagulation is unnecessary in the absence of demonstrable propagation. Other investigators have reported that the prevalence of PE in patients with calf-only thrombi is about 6.9%53 and that distal vein thrombi, especially in the soleal veins, are the most common finding in patients dying of acute pulmonary embolism.54 These studies are limited by the fact that they are not prospective. Meta-analysis of the importance of calf vein thrombosis have provided indetermi-nate results.55

Studies have tended to show an advantage in treating distal vein DVT.44,56–58 However, recent controlled trials have shown a trade-off between a minimal decrease in DVT extension and PE versus an increased risk of bleeding while undergoing therapy.59,60

Although there is no strong consensus over the prevalence of isolated calf DVT, current clinical practice guidelines give consideration to treating calf vein DVT because of its propensity to progress, the underlying risk of PE, and the likelihood of the postthrombotic syndrome.44,61

Recent ACCP guidelines provide a somewhat complex strategy for dealing with suspected distal DVT.22,26,39 The primary recommendation is not to look at the calf veins during the lower-extremity ultrasound examination if the D-dimer levels are not elevated (Fig. 20.3). Depending on the clinical assessment, repeat above-the-knee ultrasound is considered in a subset of the population.25 The argument in favor of this strategy is a risk-benefit analysis taking into consideration the cost of treat-ment, the risk of bleeding when on treatment, and the low likelihood of calf-vein extension in most patients.25 A repeat above-the-knee (popliteal and common femoral veins) ultrasound performed at 7 days following a first negative above-the-knee venous ultrasound also has a false negative rate of

Acute Deep Vein Thrombosis of Specific Extremity Veins

Isolated calf vein/distal deep vein thrombosisAlthough the term calf vein thrombosis is com-monly used, another way of classifying the location of the veins is to refer to isolated distal deep vein thrombosis (IDDVT). This allows for the fact that the below-the-knee popliteal vein is a proximal vein. In this case, extension of thrombus from the muscular (gastrocnemius) or the axial (tibial and peroneal) veins to the popliteal vein is an indication for anticoagulation. Most lower extrem-ity DVTs originate in the deep veins of the calf,40,41 although acute thrombus can form anywhere in the venous system. The soleal sinuses of the calf are thought to be the most common site of origin of DVT42 and are the most common site of residual thrombus in patients dying of pulmonary embo-lism.43 Untreated calf vein thrombus can progress into the popliteal and femoral veins in up to 30% of cases,44 whereas this risk is drastically reduced by anticoagulation.45 Once the thrombus propa-gates into the popliteal or femoral vein, therapeutic anticoagulation is needed to decrease the likeli-hood of pulmonary embolism. However, the clinical importance of isolated distal DVT remains uncertain. Abundant literature has been published, but much of it is contradictory.

The prevalence of isolated distal DVT in specific patient groups is difficult to establish because many studies include mixed patient populations and a variety of diagnostic techniques. For example, a study by Atri and colleagues46 attempted to separate patient populations by examining an asymptomatic postoperative high-risk group and a symptomatic ambulatory group. In the asymptomatic postopera-tive group, 20% of patients were found to have isolated calf DVT; in the symptomatic ambulatory group, the prevalence was 30%. This and similar studies indicate that although it is difficult to establish the incidence precisely, isolated calf DVT is not uncommon.

Once started, calf DVT can propagate to the popliteal vein and more proximal veins. There are two important questions that need addressing: (1) what is the likelihood that a distal DVT will propagate, and (2) are there indicators of possible thrombus propagation? The reported frequency of


(1) thrombus length of 5 cm or more, (2) diameter of the involved vein of 7 mm or greater, and (3) involvement of multiple veins. The currently recommended duration of anticoagulation for calf-vein DVT is 3 months, although prior guidelines had recommended 6 weeks.61

0.6% to 0.9%.62,63 The guidelines also recognize that the false-negative rate, in essence the 3 months recurrence rate of VTE after a negative complete lower extremity venous ultrasound, is very low and estimated within the range of 0.1% to 1.25%.62,64 However, if a complete lower extremity venous ultrasound identifies a calf-vein DVT, there are two strategies (Fig. 20.4): (1) treat for 3 months, and (2) repeat the venous ultrasound for evidence of extension at 5 to 7 days.22,26 In addition to a positive D-dimer, the following imaging criteria are believed to indicate a higher likelihood of IDDVT extension and can justify anticoagulation:

Calf Veins Not Imaged

Low ProbabilityDVT

NegativeD-dimer

Repeat Imagingat

Common Femoraland

Popliteal Veins

No Follow-up Needed

No Follow-up NeededPositive

forDVT

Yes

No

No

Yes

3 Months of Treatment

FIG. 20.3 This algorithm is modified from the American College of Chest Physicians (ACCP) guidelines (9th and 10th editions). Because of the risk-benefit analysis of anticoagulation for calf-vein deep vein thrombosis (DVT), the recommendation is not to look at the calf veins. However, given that thrombus propagation can occur, repeat imaging at 7 days should capture all significant cases of isolated distal DVT that have propagated.

PRACTICAL TIPS

• Calf-veinDVTis,inessence,distalDVT,taking into consideration that a portion of the popliteal vein is below the knee. Popliteal vein involvement by DVT is evidence of proximal DVT.

• Thespreadofthrombusfromthecalfveins to the popliteal vein is an indication for full anticoagulation.

• Thelikelihoodofcalf-veinthrombusextension to the proximal veins varies between6%and34%.Aplausiblesetofindicators for the spread of calf vein DVT include:• lengthofthrombus5cmormore• diameteroftheinvolvedveinof7mm

or more• involvementofmultipleveins

• Argumentshavebeenmadenottoimagethe calf veins in cases with a clinically low risk for DVT.

• Localizedpainisanindicationfordirectimaging of the calf veins with the location identified by the patient.

• Guidelinessuggestthatifthecalfveinsare not imaged, repeat common femoral and popliteal vein ultrasound at 7 days can exclude the spread of thrombus.

• Ifthrombusisidentifiedinthecalfveins,monitoring for possible progression by 5 to 7 days while withholding anticoagulation is a possible strategy.

Femoropopliteal vein thrombosisAbove-the-knee or proximal deep vein thrombosis is a more serious clinical problem than isolated calf (distal) DVT. The risk of PE is greater, thus absolutely requiring therapeutic anticoagulation. For patients in whom anticoagulation is contra-indicated, vena cava filter placement is a therapeutic alternative. The clinical presentation of DVT may change appreciably as thrombus propagates more proximally. The calf is usually painful when the


of proximal vein partially occlusive thrombi is thought by some to indicate an increased risk of embolization, although there are no extensive studies confirming this concern.

Duplex sonography is not very reliable for distinguishing acute from subacute thrombus. However, chronic wall changes seen months or years after an episode of DVT are unlikely to be mistaken for an acute DVT. Repeat ultrasound examination following therapy may be useful in establishing a baseline given the possibility of DVT recurrence. It has been estimated that this rate can reach 5% per patient-year in the first 3 years following a first proximal DVT.65

lower femoral vein or upper popliteal vein are involved. Swelling and warmth are typically evident on physical examination. With thrombus extension into the common femoral or iliac vein, the leg becomes painful and the patient will complain that it feels tight. Swelling may extend to the inguinal ligament, and the patient may be tender over the course of the veins, particularly in the inguinal region.

Duplex sonography is accepted as the definitive diagnostic test in patients suspected of having femoropopliteal DVT (see Chapter 19). Duplex sonography easily permits visualization of occlusive as well as partially occlusive thrombi. The presence

Calf Veins Imaged

Positive DVT?No

No

Yes

Yes

Yes

Repeat Imaging

NoClot Spread?

Anticoagulate?

No Follow-up Needed

No Follow-up Needed3 Months of Treatment

3 Months of Treatment

FIG. 20.4 This algorithm, modified from the American College of Chest Physicians (ACCP) guidelines (9th and 10th editions), addresses the issue of finding isolated distal deep vein thrombosis (IDDVT). Serial monitoring to identify significant cases that show evidence of propagation, even if the thrombus stays in the calf, should be treated.


vein Doppler signals can be normal in the presence of partially occlusive thrombi. Partially occlusive common or external iliac vein thrombi, or thrombi isolated to the internal iliac vein, are likely to be missed by duplex sonography. Therefore, when needed, further evaluation of the deep venous system is usually obtained with either magnetic resonance venography or computed tomographic venography.

Iliofemoral vein thrombosis is considered a risk factor for long-term venous insufficiency and thrombus recurrence.35,69 It is also an entity that may benefit from thrombolytic therapy.24

PRACTICAL TIPS

• FemoropoplitealveinDVTrequiresprompttreatment.

• Ithasahighriskofsubsequentpulmonaryembolism.

• PartiallyobstructingDVT(thrombustail)may be a risk factor for pulmonary embolization,butthishasnotbeenproven by any extensive study.

• RecurrenceratesoffemoropoplitealDVTcan be quite high and may be an indication for establishing a posttreatment baseline.

PRACTICAL TIPS

• IliofemoralveinDVTcanpresentintwoways:• extensionfromthecalfveinsintothe

popliteal and femoral veins and then into the iliac vein

• downwardextensionfromtheiliacvein• Duringpregnancy,thereisapredilection

for left-sided, primary iliac vein DVT because of uterine compression of the left iliac vein, presence of a web-like lesion, May-Thurner syndrome, or multiple factors.

• Iliofemoralveinthrombosisisconsideredarisk factor for long-term venous insufficiency and thrombus recurrence.

• Severesymptomsinapatientwithiliofemoral DVT may warrant thrombolytic treatment after weighing the risks/benefits.

Iliac vein thrombosisThe clinical presentation and therapeutic implica-tions of iliac vein thrombosis are generally similar to those of femoropopliteal vein thrombosis. There are two variants of iliac vein thrombosis: (1) thrombus extension from the femoral system, and (2) primary involvement of the iliac vein.66 For example, both scenarios can be seen during preg-nancy (prepartum) and in the postpartum period. Calf, thigh, and pelvic extension of thrombus is seen in the postpartum period. During pregnancy, primary iliac vein thrombosis is typically more common. The diagnostic approach is slightly different. In the first scenario, the diagnosis is easily made but the full extent of involvement may not be readily ascertained. In the second scenario, the thrombus is located in the pelvis and may be difficult to visualize directly with ultrasound.

In primary iliac vein thrombosis, the only evidence of proximal DVT may come from Doppler waveform alterations in the common femoral vein. Indirect Doppler evidence for proximal venous thrombosis includes (1) the loss of respiratory phasicity on the common femoral vein Doppler waveforms, and (2) the inability to augment the Doppler signal with calf or distal thigh compres-sion. A coexistent entity that must be considered is the May-Thurner syndrome, thrombosis associ-ated with a left common femoral vein obstruction, either mechanical by compression of the vein by the right common iliac artery, or intrinsic because of a web. This might help explain the predilection for left-side DVT seen during pregnancy.67,68 It is important to recognize that the common femoral

Lower Extremity Duplex Scanning in Suspected Pulmonary Embolism

Because duplex ultrasound has become the diagnostic test of choice in the evaluation of patients with suspected DVT, and because the majority of pulmonary emboli originate in the lower extremity veins, some clinicians now utilize lower extremity duplex ultrasound as the first diagnostic study in evaluating possible pulmo-nary embolism. This approach is based on the noninvasive nature of the study, the portability of the machine, and the rapidity with which results may be obtained in institutions where technical


deciding whether or not a patient with a subseg-mental defect on CTPA should be anticoagulated (Fig. 20.5).26,76

In summary, it appears that the lower extremity venous duplex examination may be useful in the patient with a high clinical suspicion of pulmonary embolism. However, CTPA is the first test of choice; V/Q scans can be used as a substitute when the patient cannot tolerate a CTPA. A negative venous

support is readily available. The merit of this approach is supported when the diagnosis of extremity DVT is confirmed, as the diagnosis of PE may then be safely assumed in the appropriate clinical setting and therapy begun. However, the chance of obtaining a positive venous ultrasound in patients with positive D-dimer and PE is only 39%.70

The two major limitations are: (1) the yield of positive lower extremity duplex sonography is low, and (2) a negative venous ultrasound test does not exclude pulmonary embolism.

Beecham and colleagues71 reviewed 225 patients who underwent both ventilation perfusion (V/Q) scans and lower extremity duplex sonography in evaluating suspected PE. Of 56 patients with high-probability V/Q scans, only 36% demon-strated duplex evidence of DVT. Furthermore, of the 22 patients without evidence of DVT by duplex scanning, 25% were found to have suf-fered PE detected by angiography. Killewich and coworkers72 similarly documented the absence of duplex-diagnosed DVT in 60% of patients with PE confirmed by pulmonary angiography. Eze and associates73 demonstrated the usefulness of stratifying patients with suspected PE based on unilateral leg symptoms. In their series of 336 patients with clinically suspected PE, 7% dem-onstrated proximal DVT by duplex sonography. However, in the 25 patients with unilateral leg swelling, 40% were found to have DVT by duplex scanning, whereas DVT was evident in only 5% of patients in the absence of leg swelling. This group further confirmed that most patients with high-probability V/Q scans had no DVT visualized by duplex sonography. Other studies have reaffirmed the overall low yield of venous duplex examination in the evaluation of PE and confirmed that the majority of patients with PE do not demonstrate DVT74,75 although the yield is higher if the patient has a swollen leg.

Computed tomographic pulmonary angiogra-phy (CTPA) has essentially replaced V/Q scans and catheter based pulmonary angiography for the diagnosis of pulmonary embolism. Coexistent PE and DVT is more likely with larger pulmo-nary emboli.70 For example, lobar, segmental, and multiple subsegmental PE are respectively associated with a 57%, 15%, and 7% probability of having a positive compression ultrasound examination.70 This is part of the justification for using compression ultrasound as a means of

Subsegmental Defecton

Computed TomographicPulmonary Angiography

Ultrasound Imagingof the

Above the KneeVeins

3 Monthsof

Anticoagulation

ClinicalSurveillance

Low Riskof

Recurrent VTE

3 Monthsof

Anticoagulation

YesAbove the Knee

Thrombus?

No

Yes

No

FIG. 20.5 This algorithm is modified from the American College of Chest Physicians (ACCP) guidelines (9th and 10th editions). It addresses the finding of small subsegmental defects on computed tomographic pulmonary angiography. In the absence of deep vein thrombosis, these lesions have low probability of significant morbidity over 3 months of follow-up. VTE, Venous thromboembolism.


thrombus and treating with a prophylactic dose of low molecular weight heparin or fondaparinux for 45 days39 if thrombus extends over more than a 5 cm long segment.

Duplex evaluation of superficial venous throm-bosis, especially occurring in the great saphenous vein, is important for two reasons. Although the clinical examination is useful in establishing the diagnosis, it is not reliable in identifying the extent of the thrombus. Thrombus often extends beyond the apparent area of involvement particularly into the common femoral vein.79 Duplex sonography documents the proximal extent and can be used to monitor progression. Although data are limited, after excluding patients with thrombus within 3 cm of the saphenous-femoral junction, a small proportion (approximately 7%) of patients with isolated superficial venous thrombosis of the great saphenous vein can progress to DVT if untreated.80,81 Most clinicians will institute systemic anticoagula-tion if proximal great saphenous vein thrombosis progresses to within 3 cm of the saphenous-femoral junction.81 A similar recommendation is made when small saphenous vein thrombus extends into the popliteal vein. Occasionally, a suspected superficial phlebitis turns out to be a soft tissue infection or hematoma. These conditions can easily be distinguished from superficial venous thrombosis with duplex scanning but are more difficult to differentiate clinically.

ultrasound in a patient with suspected PE must be followed by CTPA (or V/Q scans) because more than half of the patients who have suffered a PE do not have evidence of DVT by ultrasound.

PRACTICAL TIPS

• Lowerextremityvenousultrasounddetectsthe presence of DVT in less than 50% of patient with pulmonary embolism.

• ADVTseenonlowerextremityvenousultrasound can abrogate the need for aCTPA.

• ThelikelihoodofaDVTseenbyultrasounddecreaseswiththesizeofthepulmonaryembolusonCTPA.

• Sub-segmentaldefectsonCTPAareamanagementissue.Anegativelowerextremity venous ultrasound in these patients may help in deciding that anticoagulation is not needed.

PRACTICAL TIPS

• Superficialthrombophlebitisisnotabenign entity because it is associated with the presence of PE and DVT.

• Agreatsaphenousveinthrombuswithin3 cm of the saphenous-femoral junction (SFJ)isconsidered,inmanyinstances,anindication for anticoagulation.

• ThelikelihoodofDVTspreadintothedeep system in an untreated patient with superficial venous thrombosis located more than 3 cm from the common femoral vein junction is likely around 7%.

• Asuperficialveinthrombosisofmorethan5 cm is considered an indication for treatment (duration 45 days).

Lower Extremity Superficial Thrombophlebitis

Superficial venous thrombosis has traditionally been considered a relatively benign disease. It is now recognized as an important marker of coex-istent DVT and hypercoagulability.77,78

The diagnosis of superficial venous thrombosis has typically been made clinically. Physical findings include a painful superficial cord with surrounding erythema in the course of the vein. Treatment of patients with superficial venous thrombosis used to be symptomatic and included ambulation, heat application, compression, and nonsteroidal anti-inflammatory drug therapy. Duplex sonography of the extremity with superficial venous thrombosis can identify concomitant but clinically silent involvement of the deep system. According to Decousus et al., unsuspected DVT or PE can be seen in 24.9% of patients presenting with super-ficial venous thrombosis.78 Of these, most DVTs were located distally (54%), and PE was seen at presentation in 3.7% of patients.

The new treatment guidelines based on the results of the Comparison of Arixtra in lower Limb Superficial vein Thrombosis with Placebo (CALISTO), recommend assessing the length of


workup, including antithrombin III, Factor V Leiden, antiphospholipid antibodies, and protein C and S levels, should be performed. Prompt heparin anticoagulation is undertaken to protect from PE, reported to occur in up to 36% of patients.82,83 For thromboses associated with an indwelling catheter, anticoagulation can be admin-istered without removing the catheter unless it is no longer needed, is associated with infection, or is malfunctioning.26,39 However, anticoagula-tion alone among young, healthy patients who have compression syndrome may lead to an unacceptably high rate of postthrombotic dis-ability, caused by incomplete recanalization of the axillary-subclavian system. Venous claudication, a bursting sensation in the arm, may develop, leading to significant disability. Local thrombolysis is reserved for low-risk patients who are very symptomatic.26

The most common extrinsic cause of axillary-subclavian thrombosis is compression of the vein between the clavicle and the first rib. Addi-tional causes of extrinsic compression include hypertrophic scalene or subclavius muscles, the costoclavicular ligament, or the head of the clavicle. Congenital or acquired intrinsic venous lesions may also cause venous stenosis, leading to thrombosis. Extrinsic causes are usually treated by thoracic inlet decompression, typi-cally including first rib resection and resection of the anterior scalene muscle. A combination of thrombolysis, surgical decompression, and endovascular intervention is often used to treat these patients.31,37,86 The order of the interventions varies with local practice patterns.38 After thoracic inlet decompression, intrinsic venous lesions can be treated, either concurrently, with open surgical reconstruction, or through endovascular techniques performed 1 to 2 days postoperatively. The timing of decompression after thrombolysis varies with the surgeon’s preference. Some prefer to wait 1 to 3 months after lysis while anticoagulating the patient to reduce recurrent thrombosis and letting the exposed endothelium recover. Others advocate decompression 1 to 2 days after lysis to minimize the probability of recurrent thrombosis.37 Neverthe-less, utilizing this general approach, Machleder86 reported reducing upper extremity disability from 60% to 12%, when compared with anticoagulation alone. Subsequent reports have shown variable results.87–89

Upper Extremity Venous Thrombosis

Upper extremity deep vein thrombosis (UEDVT) can be divided into four categories: superior vena cava (SVC) syndrome, idiopathic, catheter associ-ated, and thoracic outlet/effort thrombosis. The increased incidence of axillary-subclavian DVT over the last two decades parallels the increased use of central venous catheters.82,83 In the absence of central catheters, central (SVC syndrome) and axillary-subclavian DVT may be seen among patients affected by certain cancers (especially mediastinal lymphomas), trauma, surgery, and radiation therapy. However, spontaneous effort thrombosis, also known as the Paget-Schroetter syndrome, is the most common presentation of axillary-subclavian DVT in the ambulatory cancer-free population.84 This condition may be associated with demonstrable anatomic abnormalities of the thoracic inlet (e.g., cervical rib). Men are affected more often than women, and the incidence is higher in the veins of the dominant arm. The clinical presentation of an upper extremity DVT can be dramatic. The acute onset of marked arm swelling and prominent superficial veins leaves little doubt of the clinical diagnosis and the role of duplex sonography is a confirma-tory one. Sometimes the presentation is subtle. The patient may complain of vague discomfort, with minimal swelling; in these cases, duplex sonography is an effective way of evaluating the status of the deep venous system. The proximal upper extremities are drained by a rich collateral venous network around the neck and shoulder. Visualization of all major veins and collateral channels with duplex ultrasound is, however, limited by the bony structures in the neck and shoulder, impeding imaging of the medial portion of the subclavian vein. Blood flow characteristics of the proximal subclavian and brachiocephalic veins may offer indirect evidence of central vein patency by showing preservation of cardiac phasicity.85

Initial treatment of axillary-subclavian throm-bosis follows standard guidelines for lower extremity deep vein thrombosis. It is not clear whether superficial vein (basilic/cephalic) vein thrombosis or brachial vein thrombosis require the same anticoagulation regimen. If there is no obvious underlying cause for DVT, a thrombophilia


to interstitial edema. The term venous hyperten-sion is a misnomer because calf-venous pressures depend only on patient height and are equivalent to the hydrostatic pressure. The lack of an efficient cyclical pressure reduction because of venous reflux exposes the soft tissues to a constantly elevated mean venous pressure (see Fig. 20.7). Because venous reflux renders the calf pump ineffective, venous pressures remain elevated, cause dilation of the vein segments, and lead to incompetence of the valves of the perforating veins thereby promoting varicose vein formation (Fig. 20.8). Red blood cells are deposited in the subcutaneous tissue surrounding the perforators. Melanin deposition is responsible for the characteristic brown skin pigmentation seen in the postphlebitic syndrome and the breakdown of the hemoglobin with soft tissue hemosiderin deposition is seen in the later stages of lipodermatosclerosis and ulceration.91,92 Ulceration can develop either spontaneously or as the result of minor trauma. Although the patho-physiology of the ulceration is not clear, it appears to be related to an inflammatory reaction in the tissue, fibrin cuffing, and lipodermatosclerosis. Whatever the cause, ulceration is undoubtedly

Sequelae of Deep Vein Thrombosis

Pathophysiology of chronic venous diseaseThe sequelae of DVT result from proximal chronic venous obstruction, acquired incompetence of the valves of the deep venous system follow-ing recanalization, or both. In most patients who have suffered from DVT, the thrombosed vein shows partial recanalization over a period of months, allowing adequate venous return. Despite recanalization, the vein wall and valves are permanently damaged in at least 60% of cases36,90 leaving the valve leaflets immobile and fixed to the vein wall. Failure of the venous valve mechanism causes venous reflux and prolonged residence time of de-oxygenated blood in the lower extremity especially in the standing position. In some individuals, the thrombosed veins do not recanalize, resulting in chronic obstruction to venous return. Venous obstruction, venous reflux, or both manifest clinically as chronic leg swelling, ankle pigmentation, and, ultimately, ulceration in the gaiter zone just above the ankle (Fig. 20.6). These changes define the postthrombotic syndrome.

The underlying pathophysiology is complex. Increased venous pressures because of venous reflux elevates the mean hydrostatic pressure in the deep venous system (Fig. 20.7), causes extravasation of protein-rich tissue fluid, and leads

PRACTICAL TIPS

• UEDVTmaybe:• duetocentralveinobstruction(SVC

syndrome)• catheterrelated• idiopathic• thoracicoutletsyndromeandeffort

induced(Paget-Schroetter)• UEDVTistreatedthesamewayaslower

extremity DVT.• Treatmentisnormallyinstitutedfor

axillary-subclavian involvement.• Anindwellingcatheterwillnormallybe

kept in place during anticoagulation unless there is a contraindication.

• Thrombolysisandadditionalinterventionsare normally done in cases of thoracic outlet syndrome. FIG. 20.6 The gaiter zone is located in the lower calf

and ankle. In this region, the ambulatory superficial venous pressures are the highest, leading to edema, pigmentation, and ultimately, ulceration. The skin, after years of edema, is difficult to examine for incompetent perforators (both clinically and with duplex sonography) because of extensive fibrosis.


widely incompetent, valve repair or transplantation may be required. However, if the deep venous system is competent, perforator interruption or superficial venous system intervention may suffice (see Chapter 21).

related to persistent chronic elevations in venous pressures.

Duplex ultrasound assessment of the post-thrombotic extremity is useful for both diagnosis and therapy. First, indirect confirmation of the diagnosis of chronic elevations in venous pres-sures due to reflux can be made with duplex ultrasound by direct observation of deep vein valve incompetence or documentation of chronic deep vein obstruction. The perforating veins and the superficial venous system can be similarly assessed. This information assists in planning therapy; for example, if the deep venous system is

Hydrostatic pressure

Mea

npr

ess

ure

Mea

npr

ess

ure

Normal response

Abnormal response

Hydrostatic pressure

FIG. 20.7 This diagram shows the response following exercise and activation of the calf pump. (A) A normal response. After exercise, the calf pump empties a portion of blood from the calf, in effect decreasing venous pressure below hydrostatic pressure. Slow return of blood into the veins from arterial inflow in the presence of competent venous valves keeps the venous pressure low for a significant time interval. (B) The response with venous incompetence. Exercise also decreases venous pressure. However, because of rapid refill and incompetent valves, venous pressure returns to hydrostatic pressure more rapidly than in (A). Overall, mean venous pressures in scenario (B) are higher than in (A).

A B CFIG. 20.8 With incompetent deep veins and perforating veins, elevated venous pressure below the fascia of the leg is transmitted to the superficial system. (A) Normal. (B) Great saphenous vein incompetence. (C) Deep and perforator vein incompetence.

PRACTICAL TIPS

• Venousvalveincompetenceissecondaryto scarring following venous thrombosis.

• Venousvalveincompetencecauses:• venousreflux• secondarychronicvenouspressure

elevations• Chronicvenousdiseaseprogressesto:

• chronicskinchanges(darkening)• lipodermatosclerosiswithhemosiderin

deposition in the skin and subcutaneous tissues

• ulceration

Primary Varicose Veins

Primary varicose veins are abnormally dilated and tortuous superficial vein segments developing in the absence of coexisting deep venous disease. Varicose veins are classified as secondary when they are associated with obstruction or incompetence of the deep venous system and recurrent if they reap-pear after ablation. For most patients, the medical


to a few centimeters below the saphenous-femoral junction.

Perforator incompetence may also cause or accompany varicose veins in the absence of deep venous incompetence. Occasionally, an incom-petent perforator causes primary varicose veins, even though the deep venous system is intact. Ligation of the incompetent perforator and, if needed, ablation of the varicosities are the key to successful management of the problem. Incom-petent perforator veins are easily localized with duplex sonography.

Recurrence of primary varicose veins is caused either by inadequate initial treatment or by development of new primary varicose veins. Initial treatment unwittingly directed at second-ary varicose veins uniformly results in recurrence. The most easily identified and managed cause of recurrent primary varicose veins is inadequate high ligation of the great saphenous vein at the saphenous-femoral junction with persistence of an incompetent valve (see Fig. 20.9) or recanalization of a vein treated with laser or radiofrequency abla-tion. Failure to ligate the great saphenous vein flush with the common femoral vein preserves the incompetent valve, allowing reflux into the subcutaneous branches at the saphenous bulb (Fig. 20.10). This condition may be identified, either by physical examination or by duplex scanning, as a cluster of veins in the inguinal region. When incompetence and reflux are identified in these veins, flush ligation is curative.

history and physical examination provide sufficient information to distinguish between primary and secondary varicose veins.

In the patient with primary varicose veins, a history of DVT is uncommon. Physical signs of the postthrombotic syndrome, such as brown skin discoloration in the lower ankle (gaiter zone) and venous stasis ulcers, are uncommon. However, in the occasional patient, it can be difficult to rule out involvement of the deep venous system by the medical history and physical examination. In this instance, duplex sonography can be especially helpful. Exclusion of pathology of the deep venous system confirms the diagnosis of primary varicose veins and predicts a high likelihood of cure with complete excision of the varicosities or endovas-cular ablation of the superficial veins.

A careful assessment of the great saphenous vein is critical before considering treatment of varicose veins. If the great saphenous vein is competent (no venous reflux), treatment can be confined to the clinically evident varicosities. Conversely, if the great saphenous is incompetent (venous reflux), the vein should be ablated to reduce the probability of recurrence, even if it is not clinically apparent that it is varicose. A careful evaluation of the saphenous-femoral junction is needed. Valve incompetence at the saphenous-femoral junction occurs in most cases of primary varicose veins. Nevertheless, the varicosities may be clinically apparent in only the calf or distal thigh (Fig. 20.9). If the saphenous-femoral valve is incompetent, the saphenous vein must be either ligated at the saphenous-femoral junction and stripped, or endovascular ablation must extend

A B CFIG. 20.9 Varicose veins in the calf may be isolated to the superficial calf veins, or they may be associated with incompetence of the entire saphenous vein (A). Physical examination (B) and (C) and duplex sonography can determine the extent of superficial venous involvement.

GSV

FIG. 20.10 The great saphenous vein (GSV) enters the femoral vein through the fossa ovalis. There are several large superficial branches that enter the saphenous vein at the saphenofemoral junction. These veins, as well as the great saphenous vein, must be ligated to prevent recurrence of varicose veins.


great and small saphenous, cephalic, and basilic veins are all potentially useful as bypass conduits and are easily evaluated and mapped with duplex sonography.

The evaluation of a patient prior to venous ablation should include not only the status of the refluxing conduit vein, its depth, and its diameter, but also the level and extent of reflux. The status of the deep system should be reported.

Preprocedure evaluation of the superficial arm veins before fistula creation for dialysis access requires careful attention to not only the size of the vein but also its depth because it will have to be easily accessed during dialysis. The presence of major venous branches should be reported because they may lead to failure of dialysis access matura-tion. Finally, because the patient has probably had prior dialysis catheter placements, the status of the outflow axillary, subclavian, and brachiocephalic veins should be evaluated.

PRACTICAL TIPS

• Varicoseveinscandevelopbecauseof:• primaryvalvefailureofsuperficialveins• perforatorveinincompetence

• Recurrenceofvaricoseveinsmaybecaused by:• primaryfailureofsurgicalremoval/

ablation• openingofparallelvenouschannels• newvenousrefluxinpreviouslynormal

vein segments

PRACTICAL TIPS

• Mappingofthesuperficialveinscanbedone for:• potentialcoronaryarterybypassgraft• possiblelowerextremitybypassgraft• preprocedureveinablation• beforedialysisaccesscreation

• Additionalevaluationofthestatusofthedeep veins may be needed.

• Evaluationofsuperficialveindepthfromthe skin is typically needed before:• venousablation• fistulacreationfordialysisaccess

A variety of other causes of recurrent primary varicosities are known, including incomplete ligation of incompetent perforators, a duplicated saphenous system, and failure to differentiate great from small saphenous vein incompetence. As usual, careful physical examination, complemented with duplex sonography, determines the cause of recurrent varicosities. The importance of evaluat-ing the deep venous system cannot be overstated because secondary varicose veins resulting from deep venous incompetence are a common cause of recurrence.

Preprocedure Venous Mapping

The presence, location, and adequacy of a proposed venous bypass conduit are typically evaluated prior to harvest for coronary artery and lower extremity bypass surgery. The depth of the superficial veins is also evaluated prior to venous ablation and the creation of a dialysis access fistula. This is especially useful in individuals with a history of thrombo-phlebitis, prior superficial vein harvest or prior dialysis access. This is accurately done with duplex sonography. In obese patients, for example, the course of the vein may be hidden by subcutaneous tissue. Duplex scanning can confirm the patency and location of the veins, avoiding the undesirable consequence of raising large skin flaps.

In the patient who had prior saphenous vein thrombosis, duplex scanning can identify chronic occlusion or scarring, conditions that obviate vein use as a bypass graft. In those patients who have undergone venous surgery or prior vein harvesting, the great saphenous vein may be absent. A diligent search using the duplex scanner can facilitate identification of alternative bypass conduits for the planned procedure. In our experience, the

Summary

Duplex ultrasound is the primary modality used for the evaluation of suspected deep vein thrombosis in the extremities. While it can be performed in all comers as a rule-out examination, it yields higher benefits when combined with a clinical decision algorithm. The diagnosis of deep vein thrombosis is not only important because of the direct link between deep vein thrombosis and pulmonary embolism, but its timely diagnosis permits early anticoagulation and therefore helps to prevent chronic venous disease. The technique is used to diagnose not only acute deep and superficial vein


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