eMedicine Specialties > Radiology > Vascular/Interventional

Deep Venous Thrombosis, Lower Extremity

Author: Eric K Hoffer, MD, Director, Vascular and Interventional Radiology, Associate Professor of Radiology, Section of Angiography and Interventional Radiology, Dartmouth-Hitchcock Medical Center
Coauthor(s): John J Borsa, MD, Consulting Staff, Department of Radiology, St Joseph Medical Center
Contributor Information and Disclosures

Updated: Apr 10, 2009

Introduction

Background

Deep venous thrombosis (DVT) is the presence of coagulated blood, a thrombus, in one of the deep venous conduits that return blood to the heart. The clinical conundrum is that symptoms (pain and swelling) are often nonspecific or absent. However, if left untreated, the thrombus may become fragmented or dislodged and migrate to obstruct the arterial supply to the lung, causing a potentially life-threatening pulmonary embolus (PE).

DVT and PE are the manifestations of a single disease entity, namely, venous thromboembolism (VTE). In terms of incidence, lower-extremity DVT is the most common venous thrombosis, with a prevalence of 1 case per 1000 population. In addition, it is the underlying source of 90% of acute PEs, which cause 25,000 deaths per year in the United States (National Center for Health Statistics [NCHS], 2006). Other than the immediate threat of PE, the risk of long-term major disability from postthrombotic syndrome (PTS) is high.1,2,3,4,5

Pathophysiology

In 1856, Virchow described the classic triad of predisposing factors for DVT, namely, venous stasis, injury of the vascular wall, and a hypercoagulable state.6 Events or conditions that alter the equilibrium of one or more of these factors may produce DVT.

Thrombosis is the homeostatic mechanism whereby blood coagulates or clots, a process crucial to the establishment of hemostasis after a wound. Several pathways initiate thrombosis and usually consisting of cascading activation of enzymes that magnify the effect of an initial trigger event. A similar complex of events results in fibrinolysis, or the dissolution of thrombi. The balance of trigger factors and enzymes is complex. Microscopic thrombus formation and thrombolysis (dissolution) are continuous events, but with increased stasis, procoagulant factors, or endothelial injury, the coagulation-fibrinolysis balance may favor the pathologic formation of an obstructive thrombus. Clinically relevant DVT is the persistent formation of macroscopic thrombus in the deep proximal veins.

In the absence of rhythmic contraction of the leg muscles, as in walking or moving, blood flow in the veins slows and even stops in some areas, predisposing patients to thrombosis.7

Thrombus usually forms behind valve cusps or at venous branch points, the majority of which begin in the calf. Venodilation may disrupt the endothelial cell barrier and expose the subendothelium. Platelets adhere to the subendothelial surface by means of von Willebrand factor or fibrinogen in the vessel wall. Neutrophils and platelets are activated, releasing procoagulant and inflammatory mediators. Neutrophils also adhere to the basement membrane and migrate into the subendothelium. Complexes form of the surface of platelets and increase the rate of thrombin generation and fibrin formation. Stimulated leukocytes irreversibly bind to endothelial receptors and extravasate into the vein wall by means of mural chemotaxis. Because mature thrombus composed of platelets, leukocytes and fibrin develops, and an active thrombotic and inflammatory process occurs at the inner surface of the vein, and an active inflammatory response occurs in the wall of the vein.8,9

In the postoperative patient, up to one half of all isolated calf vein thrombi resolve spontaneously within a few hours, whereas approximately 15% extend to involve the femoral vein. A many as one third of untreated symptomatic calf vein DVTs extend to the proximal veins.10 At 1-month follow-up of untreated proximal DVT, 20% regress and 25% propagate. Although calf vein thrombi are rare sources of clinically significant PE, the incidence of PE with untreated proximal thrombi is 29-50%.11,10 Most PEs are first diagnosed at autopsy.12,13

Over a few months, most acute DVTs evolve to complete or partial recanalization, and collaterals develop (see Images below and Multimedia Images 2-3).14,15,16,17,18,19 Although blood flow may be restored, residual evidence of thrombus or stenosis is observed in one half of patients after 1 year. Furthermore, the damage to the underlying valves and those compromised by peripheral dilation and insufficiency usually persists and may progress. Venous stasis, venous reflux, and chronic edema are common in patients who have had a large DVT.20

Lower-extremity venogram shows outlining of an ac...

Lower-extremity venogram shows outlining of an acute deep venous thrombosis in the popliteal vein with contrast enhancement.

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Lower-extremity venogram shows outlining of an ac...

Lower-extremity venogram shows outlining of an acute deep venous thrombosis in the popliteal vein with contrast enhancement.


Lower-extremity venogram shows a nonocclusive chr...

Lower-extremity venogram shows a nonocclusive chronic thrombus. The superficial femoral vein (lateral vein) has the appearance of 2 parallel veins, when in fact, it is 1 lumen containing a chronic linear thrombus. Although the chronic clot is not obstructive after it recanalizes, it effectively causes the venous valves to adhere in an open position, predisposing the patient to reflux in the involved segment.

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Lower-extremity venogram shows a nonocclusive chr...

Lower-extremity venogram shows a nonocclusive chronic thrombus. The superficial femoral vein (lateral vein) has the appearance of 2 parallel veins, when in fact, it is 1 lumen containing a chronic linear thrombus. Although the chronic clot is not obstructive after it recanalizes, it effectively causes the venous valves to adhere in an open position, predisposing the patient to reflux in the involved segment.


The acute effect of an occluded outflow vein may be minimal if adequate collateral pathways exist. As an alternative, it may produce marked pain and swelling if flow is forced retrograde. In the presence of deep vein outflow obstruction, contraction of the calf muscle produces dilation of the feeding perforating veins, it renders the valves nonfunctional (because the leaflets no longer coapt), and it forces the blood retrograde through the perforator branches and into the superficial system. This high-pressure flow may cause dilation of the superficial (usually low-pressure) system and produce superficial venous incompetence. In clinical terms, the increased incidence of reflux in the ipsilateral greater saphenous vein increases 8.7-fold on follow-up of DVT.14 This chain of events, ie, obstruction to antegrade flow producing dilation, stasis, further valve dysfunction, with upstream increased pressure, dilation, and other processes, may produce hemodynamic findings of venous insufficiency.

Another mechanism that contributes to venous incompetence is the natural healing process of the thrombotic vein. The thrombotic mass is broken down over weeks to months by inflammatory reaction and fibrinolysis, and the valves and venous wall are altered by organization and ingrowth of smooth muscle cells and production of neointima. This process leaves damaged, incompetent, underlying valves, predisposing them to venous reflux. The mural inflammatory reaction breaks down collagen and elastin, leaving a noncompliant venous wall.9,14,15,16,17,18,19

Persistent obstructive thrombus, coupled with valvular damage, ensures continuation of this cycle. Over time, the venous damage may become irreversible. Hemodynamic venous insufficiency is the underlying pathology of PTS. If numerous valves are affected, flow does not occur centrally unless the leg is elevated. Inadequate expulsion of venous blood results in stasis and a persistently elevated venous pressure or venous hypertension. As fibrin extravasates and inflammation occurs, the superficial tissues become edematous and hyperpigmented. With progression, fibrosis compromises tissue oxygenation, and ulceration may result. After venous insufficiency occurs, no treatment is ideal; elevation and use of compression stockings may compensate, or surgical thrombectomy or venous bypass may be attempted.21,22,23,24

With anticoagulation alone, as many as 75% of patients with symptomatic DVT present with PTS at 5-10 years.24,25 However, the incidence of venous ulceration is far less, at 5%. Of the half million patients with venous ulcers in the United States, 17-45% report having a history of DVT.26

Mortality/Morbidity

The sequelae and treatment complications tend to be more problematic in chronic disease than the acute disease.

  • DVT: DVT classically produces pain and limb edema. The classic finding of pain on dorsiflexion of the calf (Homans sign) is specific but insensitive and present in one half of patients with DVT.27 Symptoms often resolve with symptomatic treatment because collateral flow develops; symptoms may be most persistent with iliac involvement. In relatively rare instances, acute extensive (lower leg–to-iliac) occlusion of venous outflow may create a blanched appearance of the leg because of edema. The clinical triad of pain, edema, and blanched appearance is termed phlegmasia alba dolens. This is also known as milk-leg syndrome when it is associated with compression of the iliac vein by the gravid uterus. If the collateral outflow veins are thrombosed, the appearance is dusky discoloration or cyanosis, which is phlegmasia cerulea dolens. As many as one half of patients with this condition have capillary involvement, which poses a risk of irreversible venous gangrene with massive fluid sequestration. In severely affected patients, immediate therapy is necessary to prevent limb loss.
  • PE: As many as 40% of patients have silent PE when symptomatic DVT is diagnosed.28 Approximately 4% of individuals treated for DVT develop symptomatic PE. Almost 1% of postoperative hospitalized patients develop PE (National Healthcare Quality Report [NHQR], 2003). The 10-12% mortality rate for PE in hospitalized patients underscores the need for prevention of this complication. Treatment options include anticoagulation therapy and placement of an IVC filter. If evidence of right-heart failure is present or if adequate oxygenation cannot be maintained, the thrombus may be removed with pharmacomechanical thrombolytic intervention.
  • Paradoxic emboli: Although rare, paradoxic emboli can occur in patients with cardiac defects (usually atrial septal defect), who are at risk for the passage of emboli to the arterial circulation and resultant stroke or embolization of a peripheral artery. Patients can present after cardiac failure occurs late in life, with resultant bedrest that increases the risk for DVT.
  • Recurrent DVT: Without treatment, one half of patients have a recurrent, symptomatic VTE event within 3 months. After anticoagulation for an unprovoked VTE event is discontinued, the incidence is 5-15% per year. Presentations are similar, with pain and edema. However, the diagnosis may be difficult (ie, differentiating acute from chronic thrombus). (See Nuclear Medicine below.) Recurrence increases the risk of PTS.
  • Hemorrhage: Anticoagulation therapy for 3-6 months results in major bleeding complications in 3-10% of patients a.29 High-risk populations (>65 y with a history of stroke, GI bleed, renal insufficiency, or diabetes) have a 5-23% risk of having major hemorrhage at 90 days. Patients who require year-long or indefinite anticoagulation (because of chronic risk factors) have double the risk of hemorrhage.
  • PTS: PTS is a chronic complication of DVT that manifests months to many years after the initial event. Symptoms range from mild erythema and localized induration to massive extremity swelling and ulceration, usually exacerbated by standing and relieved by elevation of the extremity. Evaluations of the incidence or of improvements with therapy have been problematic because reporting is not standardized. Furthermore, correlation between objectively measured hemodynamic changes and the severity of PTS is poor.30 After symptomatic DVT is treated with anticoagulation, the incidence of PTS at 2 years is 25-50% despite long-term anticoagulation for iliofemoral DVT, and after 7-10 years, the incidence is 70-90%.31,32 The only current treatment is use of a compression hose and elevation. In many patients, this is only partly effective in relieving swelling, pain, and venous ulcers. In the United States, the annual direct cost of post-DVT PTS-related venous ulcers is estimated to be $45 million per year, and 300,000 work days are lost.{Ref177}}

Anatomy

Deep venous thrombosis (DVT) is often divided into proximal and distal thromboses. The proximal veins are the popliteal, femoral (also known as superficial femoral), deep femoral, common femoral, and iliac veins and the inferior vena cava (IVC). Calf-vein DVT involves at least 1 of the paired deep calf veins: anterior tibial, posterior tibial, peroneal, or deep muscular veins. Calf-vein DVT is rarely a cause of symptomatic PE (Buller, 2004). Proximal DVT is reported to produce relatively severe symptoms and consequences related both to the congestion of collateral veins and to the risk of PE.30

Presentation

Risk factors

Numerous factors, often in combination, contribute to DVT. These may be categorized as acquired (eg, medication, illness) or congenital (eg, anatomic variant, enzyme deficiency, mutation). A useful categorization may be an acute provoking condition versus a chronic condition, as this distinction affects the length of anticoagulant therapy.

The most common risk factors are obesity, previous VTE, malignancy, surgery, and immobility. Each is found in 20-30% of patients. Hospitalized and nursing home patients often have several risk factors and account for one half of all DVTs (with an incidence of 1 case per 100 population).12,33

Venous stasis

The frequent causes of DVT are due to augmentation of venous stasis due to immobilization or central venous obstruction. Immobility can be as transient as that occurring during a transcontinental airplane flight or that during an operation under general anesthesia. It can also be extended, as during hospitalization for pelvic, hip, or spinal surgery, or due to stroke or paraplegia. Individuals in these circumstances warrant surveillance, prophylaxis, and treatment if they develop DVT.34,35

Increased blood viscosity may decrease venous blood flow. This change may be due to an increase in the cellular component of the blood in polycythemia rubra vera or thrombocytosis or a decrease in the fluid component due to dehydration.

Increased central venous pressure, either mechanical or functional, may reduce the flow in the veins of the leg. Mass effect on the iliac veins or IVC from neoplasm, pregnancy, stenosis, or congenital anomaly increases outflow resistance.

Anatomic variants that result in diminution or absence of the IVC or iliac veins may contribute to venous stasis. In iliocaval thromboses, an underlying anatomic contributor is identified in 60-80% of patients. The best-known anomaly is compression of left common iliac vein at the anatomic crossing of the right common iliac artery. The vein normally passes under the right common iliac artery during its normal course (see Image 1).

In some individuals, this anatomy results in compression of the left iliac vein and can lead to band or web formation, subsequent stasis, and left leg DVT. The reasons are poorly understood. Compression of the iliac vein is also called May-Thurner syndrome or Cockett syndrome.

IVC variants are uncommon. Anomalous development is most commonly detected and diagnosed on cross-sectional imaging or venography. The embryologic evolution of the IVC is from an enlargement or atrophy of paired supracardinal and subcardinal veins. Anomalous embryologic development may result in absence of the normal cava. These variations may increase the risk of symptoms because small-caliber vessels may be most subject to obstruction. In patients younger than 50 years who have DVT, the incidence of a caval anomaly is as high as 5%.36

A double or duplicated IVC results from lack of atrophy in part of the left supracardinal vein, resulting in a duplicate structure to the left of the aorta. The common form is a partial paired IVC that connects the left common iliac and left renal veins. When caval interruption, such as placement of a filter, is planned, these alternate pathways must be considered. As an alternative, the IVC may not develop. The most common alternate route for blood flow is through the azygous vein, which enlarges to compensate. If a venous stenosis is present at the communication of iliac veins and azygous vein, back pressure can result in insufficiency, stasis, or thrombosis.37

In rare cases, neither the IVC nor the azygous vein develops, and the iliac veins drain through internal iliac collaterals to the hemorrhoidal veins and superior mesenteric vein to the portal system of the liver. Hepatic venous drainage to the atrium is patent. Because this pathway involves small hemorrhoidal vessels, thrombosis of these veins can cause severe acute swelling of the legs.

Thrombosis of the IVC is a rare occurrence and is an unusual result of leg DVT unless an IVC filter is present and stops a large embolus in the cava, resulting in obstruction and extension of thrombosis. Common causes of caval thrombosis include tumors involving the kidney or liver, tumors invading the IVC, compression of the IVC by extrinsic mass, and retroperitoneal fibrosis.38,39

Hypercoagulability

Researchers have identified inherited hypercoagulable states as contributing risk factors in many cases of DVT, particularly recurrent DVT. Genetic thrombophilia is identified in 30% of patients with idiopathic venous thrombosis. Altered procoagulant enzyme proteins include factor V, factor VIII, factor IX, factor XI, and prothrombin. Altered or diminished anticoagulants include protein C and protein S.40,41

Factor V Leiden is a mutation that results in a form of factor Va resists degradation by activated protein C, leading to a hypercoagulable state. Its importance lies in the 5% prevalence in the American population and its association with a 3- to 6-fold increased risk for VTE . Antiphospholipid syndrome is considered a disorder of the immune system, where antiphospholipid antibodies (cardiolipin or lupus anticoagulant antibodies) are associated with a syndrome of hypercoagulability. Although not a normal blood component, the antiphospholipid antibody may be asymptomatic. It is present in 2% of the population, and it may be detected in association with infections or the administration of certain drugs, including antibiotics, cocaine, hydralazine, procainamide, and quinine.41

Tests for these genetic defects are often not performed in patients with recurrent venous thrombosis because therapy remains symptomatic. In most patients with these genetic defects, lifetime anticoagulation therapy with warfarin (Coumadin) or low molecular weight heparin (LMWH) is recommended after recurrent DVT without an alternative identifiable etiology is documented. The risk of recurrent DVT is multiplied 1.4-2 times, with the most common genetic polymorphisms predisposing individuals to DVT. However, the low incidence of factor V Leiden and prothrombin G20210A may not warrant aggressive prophylaxis. Therefore, genetic testing might not be warranted until a second event occurs.42

Other diseases and states can induce hypercoagulability in patients without other underlying risks for DVT. They can predispose patients to DVT, though their ability to cause DVT without intrinsic hypercoagulability is in question. The conditions include malignancy, dehydration, and use of medications (eg, estrogens). Acute hypercoagulable states also occur, as in disseminated intravascular coagulopathy (DIC) resulting from infection or heparin-induced thrombocytopenia.43

Injury to the vessel wall

Injury may be obvious, such as those due to trauma, surgical intervention, or iatrogenic injury, but they may also be obscure, such as those due to remote DVT (perhaps asymptomatic) or minor (forgotten) trauma. Previous DVT is a major risk factor for further DVT. The increased incidence of DVT in the setting of acute urinary tract or respiratory infection may be due to an inflammation-induced alteration in endothelial function.

The presence of risk factors plays a prominent role in the assessing the pretest probability of DVT. Furthermore, transient risk factors permit successful short-term anticoagulation, whereas idiopathic DVT or chronic or persistent risk factors warrant long-term therapy.

Clinical evaluation

DVT and thromboembolism remain a common cause of morbidity and mortality in bedridden or hospitalized patients, as well as generally healthy individuals. The annual incidence of DVT in the United States is estimated to be 250,000, or 48 cases per 100,000 population. In the elderly, the incidence is increased 4-fold. The reported incidence of PE with or without DVT is 23-69 cases per 100,000 population, and 25,000 per year die from PE. The in-hospital case-fatality rate for VTE is 12%, rising to 21% in the elderly.

VTE remains an underdiagnosed disease, and most PEs are diagnosed at autopsy. Diagnosis depends on a high level of clinical suspicion and the presence of risk factors that prompt diagnostic study. Because the presentation is nonspecific and because the consequence of missing the diagnosis is serious, it must be excluded whenever it is a feasible differential diagnosis. Because the prevalence of the disease is 15-30% in the population at clinical risk, a widely applicable (inexpensive and simple) screening test is required.

Conclusive diagnosis historically required invasive and expensive venography, which is still considered the criterion standard. Since 1990, the diagnosis has been obtained noninvasively by means of (still expensive) sonographic exam (see Ultrasound). The recent validation of the simpler and cheaper D-dimer test as an initial screening test permits a rapid, widely applicable screening that may reduce the rate of missed diagnoses. Algorithms are based on pretest probabilities and D-dimer results. As many of 40% of patients with a low clinical suspicion and a negative D-dimer result require no further evaluation.44,45

Treatment

Traditional therapy entails anticoagulation with intravenous (IV) unfractionated heparin (UFH) and conversion to oral warfarin to prevent further clot formation. Treatment guidelines from the American College of Chest Physicians (ACCP) recommend LMWH or UFH for 5 days in conjunction with a vitamin K antagonist (eg, warfarin) until an international normalized ratio (INR) of greater than 2 is stable. At that time, heparin can be discontinued.

Acute DVT may be treated in an outpatient setting with LMWH. Anticoagulant therapy is recommended for 3-12 months depending on site of thrombosis and on the ongoing presence of risk factors. If DVT recurs, if a chronic hypercoagulability is identified, or if a PE is life threatening, lifetime anticoagulation therapy may be recommended. This treatment protocol has a cumulative risk of bleeding complications of less than 12%.

Anticoagulant therapy remains the mainstay of medical therapy for DVT because it is noninvasive, it treats most patients (¡Ý90%) with no immediate demonstrable physical sequelae of DVT, it has a low risk of complications, and its outcome data demonstrate an improvement in morbidity and mortality. Meta-analyses of randomized trials of UFH and LMWH showed that they were similar, with risk of recurrent DVT of 4%, a risk of PE of 2%, and a risk of major bleeding of 3%.46,47

Anticoagulation does have problems. Although it inhibits propagation, it does not remove the thrombus, and a variable risk of clinically significant bleeding is observed. In 2-4% of patients, DVT progresses to symptomatic PE despite anticoagulation. In the setting of a PE, 8% of patients have recurrences despite anticoagulation, 30-45% of which are fatal. Although anticoagulation markedly reducing the risk of PE and extension of the DVT, it does not reduce the incidence of PTS, which requires expedited removal of the existing thrombus without damaging the underlying venous valves.

Systemic IV thrombolysis once improved the rate of thrombosed vein recanalization; however, it is no longer recommended because of an elevated incidence of bleeding complications, slightly increased risk of death, and insignificant improvement in PTS. The lack of a significantly reduced incidence of PTS after systemic thrombolysis (40-60%) likely reflects the inadequacy of the relatively low threshold volume of thrombus removal that was considered successful.

Percutaneous transcatheter therapy of DVT is aimed at removing the thrombus and/or preventing PE. PE prevention is achieved by mean of caval interruption with an IVC filter. Pharmacologic thrombolysis entails the administration of enzymes to reduce the hypercoagulable component of the triad and to shift the balance to thrombus removal. Direct administration of a thrombolytic into the thrombus during percutaneous catheter-directed thrombolysis (CDT) is most effective approach. Significant lysis is achieved in 12% of patients with anticoagulation, in 30% receiving a systemic administration of a thrombolytic, and in 80% with CDT. Furthermore, the transvenous approach allows for treatment of an underlying venous stenosis by means angioplasty (balloon dilation) or stent placement. The cost of rapid, more complete lysis is reflected in the major risk of bleeding, which is increased to 8-11% with CDT.

As discussed, the immediate symptoms of DVT often resolve with anticoagulation alone, and the rationale for intervention is often reduction of the 75% long-term risk of PTS. Patients' negative assessments of the trade-off between an increased risk of major bleeding in exchange for a potentially decreased risk of PTS has reduced the use of systemic thrombolysis. The bleeding risk is similar to that of CDT, and the risk of PTS may further decrease risk. However, whether CDT is preferred to anticoagulation has not been examined. The addition of percutaneous mechanical thrombectomy to the interventional options may facilitate decision-making, because recanalization may be achieved faster than before and with a decreased dose of lytic; therefore, the bleeding risk may be decreased.

Differential diagnoses

Of patients evaluated for DVT of the lower extremity, only a quarter of them have the disease. DVT is characterized by pain and swelling of the limb, which are not specific. Numerous patients with DVT are asymptomatic.

Differential diagnoses to be considered include the following:

  • Musculoskeletal conditions - Achilles tendonitis, arthritis, rupture of a Baker cyst, cellulitis
  • Trauma - Muscle strain or tear, hematoma, soft-tissue injury, stress fracture
  • Neurogenic conditions - Pain, swelling in a paralyzed limb
  • Vascular conditions - Arterial insufficiency, peripheral occlusive disease, thromboembolism, superficial thrombophlebitis, postphlebitic syndrome, varicose veins, central venous occlusion (Budd-Chiari syndrome), dependent edema, congestive heart failure (CHF), hepatic disease, renal failure, nephritic syndrome, lymphedema

Differential Diagnoses

Baker Cyst
Budd-Chiari Syndrome
Congestive Heart Failure

Other Problems to Be Considered

Achilles tendonitis
Arthritis
Cellulitis
Muscle strain or tear
Hematoma
Soft-tissue injury
Stress fracture
Pain
Swelling in a paralyzed limb
Arterial insufficiency
Peripheral occlusive disease
Thromboembolism
Superficial thrombophlebitis
Postphlebitic syndrome
Varicose veins
Dependent edema
Hepatic disease
Renal failure
Nephritic syndrome
Lymphedema

More on Deep Venous Thrombosis, Lower Extremity

Overview: Deep Venous Thrombosis, Lower Extremity
Imaging: Deep Venous Thrombosis, Lower Extremity
Follow-up: Deep Venous Thrombosis, Lower Extremity
Multimedia: Deep Venous Thrombosis, Lower Extremity
References
Further Reading
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References

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[ CLOSE WINDOW ]

Keywords

deep vein thrombosis, venous thrombosis, thrombophlebitis, May-Thurner syndrome, Cockett syndrome, iliofemoral thrombosis, DVT, lower extremity thrombosis, lower-extremity thrombosis, leg thrombosis, lower extremity deep venous thrombosis, occlusions of the deep veins, below-knee thrombosis, venous thromboembolism, VTE, pulmonary embolus, pulmonary embolism, PE, post-thrombotic syndrome, postthrombotic syndrome, PTE

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Eric K Hoffer, MD, Director, Vascular and Interventional Radiology, Associate Professor of Radiology, Section of Angiography and Interventional Radiology, Dartmouth-Hitchcock Medical Center
Eric K Hoffer, MD is a member of the following medical societies: American Heart Association, Radiological Society of North America, Society for Cardiac Angiography and Interventions, and Society of Interventional Radiology
Disclosure: Nothing to disclose.

Coauthor(s)

John J Borsa, MD, Consulting Staff, Department of Radiology, St Joseph Medical Center
John J Borsa, MD is a member of the following medical societies: American College of Radiology, American Society of Neuroradiology, Cardiovascular and Interventional Radiological Society of Europe, Radiological Society of North America, Royal College of Physicians and Surgeons of Canada, and Society of Interventional Radiology
Disclosure: Nothing to disclose.

Medical Editor

Anthony Watkinson, MD, Professor of Interventional Radiology, The Peninsula Medical School; Consultant and Senior Lecturer, Department of Radiology, The Royal Devon and Exeter Hospital, UK
Anthony Watkinson, MD is a member of the following medical societies: Radiological Society of North America, Royal College of Radiologists, and Royal College of Surgeons of England
Disclosure: Nothing to disclose.

Pharmacy Editor

Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand
Disclosure: Nothing to disclose.

Managing Editor

Douglas M Coldwell, MD, PhD,, Principal, Coldwell Associates. Interventional Radiologist, Jane Phillips Medical Center, Bartlesville, OK
Douglas M Coldwell, MD, PhD, is a member of the following medical societies: American Association for Cancer Research, American College of Radiology, American Heart Association, American Physical Society, American Roentgen Ray Society, Society of Cardiovascular and Interventional Radiology, Southwest Oncology Group, and Special Operations Medical Association
Disclosure: Sirtex, Inc. Consulting fee Speaking and teaching

CME Editor

Robert M Krasny, MD, Consulting Staff, Department of Radiology, Resolution Imaging Medical Corporation
Robert M Krasny, MD is a member of the following medical societies: American Roentgen Ray Society and Radiological Society of North America
Disclosure: Nothing to disclose.

Chief Editor

Kyung J Cho, MD, FACR, William Martel Professor of Radiology, Interventional Radiology Fellowship Director, University of Michigan Health System
Kyung J Cho, MD, FACR is a member of the following medical societies: American College of Radiology, American Heart Association, American Medical Association, American Roentgen Ray Society, Association of University Radiologists, and Radiological Society of North America
Disclosure: Nothing to disclose.

 
 
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