Deep Vein Thrombosis

Deep Venous Thrombosis

1. Lower Extremity Venous Anatomy and Physiology
1. Anatomy
1. Superficial Veins
• composed of the greater and lesser saphenous veins
• large, relatively thick-walled structures lying above the deep fascia
• lesser saphenous vein ascends posterior to the lateral malleolus and terminates in the popliteal vein
• greater saphenous vein ascends medially and empties into the common femoral vein



2. Deep Veins
• primarily responsible for venous return
• follow the course of the major arteries
• in the lower leg the veins are paired and join at the knee to form the popliteal vein



3. Perforating Veins
• connect the superficial and deep systems
• contain valves that direct flow from the superficial to the deep veins



4. Valves
• bicuspid valves are located within a dilated sinus of the lower extremity veins
• valves direct blood flow centrally and prevent reflux of venous blood, especially during standing and ambulation
• more valves are located distally than proximally
• common iliac vein and vena cava do not have valves


2. Physiology
1. Venous Return
1. Supine Position
• lower extremity venous return depends primarily on the respiratory cycle
• during inspiration, intraabdominal pressure increases and decreases venous return
• valve closure prevents reflux of blood
• during expiration, venous return is increased as a result of the decreased intraabdominal pressure


2. Upright Position
• as a result of hydrostatic forces, the standing venous pressure in the foot veins is 80 to 90 mm Hg
• calf muscle pump is necessary to overcome these hydrostatic forces
• when the soleus and gastrocnemius muscles contract, blood in the deep veins is propelled centrally
• valves in the perforating veins prevent flow of blood from the deep to the superficial veins


2. Etiology
• Virchow’s triad: venous stasis, endothelial damage, and hypercoagulability


1. Stasis
• most important factor for surgical patients
• general anesthesia causes a significant reduction in flow in the lower extremities
• prolonged bedrest also increases the incidence of DVT
• stasis alone is not sufficient to cause DVT: aging, obesity, malignancy, trauma, shock, congestive heart failure, and infection are contributory factors


2. Endothelial Damage
• can occur in collapsed vessels when the intimal walls are in contact
• also may occur from central venous catheters or hip arthroplasty
• in most cases of DVT, the role of endothelial injury is questionable because the DVT often occurs in veins remote from the site of operation


3. Hypercoagulability
• in experimental systems, stasis and endothelial injury alone are not sufficient to cause thrombosis in the absence of activated clotting factors
• hereditary hypercoagulable conditions include antithrombin III deficiency, Protein C and S deficiency
• acquired hypercoagulable conditions include malnutrition, nephrotic syndrome, malignancy, pregnancy, use of oral contraceptives
• surgery reduces antithrombin III, suppresses plasma fibrinolytic activity, and releases large amounts of prothrombotic tissue factor into the circulation


3. Pathophysiology
• in most cases, spontaneous clot lysis occurs, and the vessel lumen is recanalized
• damage to the venous valves results in chronic venous insufficiency in 50% of patients with DVT
• most feared complication of DVT is pulmonary embolism, which accounts for over 100,000 deaths per year in the U.S.


4. Clinical Manifestations
• only 40% of patients have clinical signs of DVT
• first manifestation of a DVT may be a pulmonary embolus
• calf tenderness may be elicited by Homan’s test (dorsiflexing the foot) but the false-positive rate is high (30%)
• swelling is often not present in calf vein thrombosis because the veins are paired, and the obstruction is usually not complete
• iliofemoral thrombosis may present with massive swelling of the entire leg – phlegmasia alba dolens
• phlegmasia cerulea dolens occurs when venous thrombosis impedes most of the venous return from the leg, ultimately causing cessation of arterial flow



5. Diagnosis
1. Venous Duplex Ultrasonography
• 90% accurate in diagnosing DVT
• may be performed at the bedside
• 3 elements to the venous duplex scan: 1) thrombus visualization, 2) vein compressibility, 3) venous flow analysis
• thrombus may be difficult to visualize in its acute form
• veins filled with thrombus do not compress



2. Venography
• most accurate test, but it is invasive and requires the use of contrast
• main indication is when clinical suspicion is high, and the duplex scan is not definitive


3. MRI
• useful for imaging the iliac veins and IVC, which are not well-visualized by duplex ultrasound


6. Prophylaxis
1. Risk Factors for DVT
1. Medical
• previous DVT or PE
• age > 40
• pregnancy
• malignancy
• hormonal therapy
• obesity
• hypercoagulable state


2. Surgical
• general anesthesia
• laparoscopic procedures
• major abdominal or pelvic surgery
• hip or knee replacement
• closed head injury, spinal cord injury, paralysis
• pelvic fractures, extremity fractures
• prolonged immobilization


2. Mechanical Prophylaxis
1. Ambulation
• activates the calf pump mechanism
• when sitting, the legs should be elevated to avoid venous pooling


2. Sequential Compression Devices (SCDs)
• sleeves intermittently inflate with a gradient pressure from the ankle to the thigh
• replicates the calf pump mechanism
• some studies suggest that they also increase fibrinolytic activity
• compliance is an issue because many patients complain that they are uncomfortable
• often combined with graded compression stockings
• high risk patients will also receive pharmacologic prophylaxis


3. Pharmacologic Prophylaxis
1. Low-Dose Heparin
• 5000 U preop and then bid or tid
• prevents ~ 50% of all PE’s and 66% of all DVTs
• enhances antithrombin III activity, which inhibits factor Xa
• does not increase the rate of major hemorrhage, but wound hematomas occur in ~ 2% of patients
• another complication is heparin-induced thrombocytopenia (HIT)
• has largely been replaced by Lovenox


2. Enoxaparin (Lovenox)
• low molecular weight heparin polymer (LMWH)
• has increased bioavailability, longer half-life, increased antithrombotic activity when compared to standard heparin
• incidence of thrombocytopenia is lower than in those receiving standard heparin
• in trauma patients, it is superior to low-dose heparin in preventing DVT
• also superior to mechanical prophylaxis in preventing DVT


3. Fondaparinux (Arixtra)
• factor Xa inhibitor
• often used in patients with a history of HIT


7. Treatment
1. Medical Treatment
• goals are to minimize the risk of PE, limit further thrombosis, and facilitate resolution of existing thrombi to avoid chronic venous insufficiency


1. Anticoagulation
• historical treatment has been IV heparin (4 – 5 days) followed by long-term Coumadin (3 months)
• heparin is initially given as a bolus injection and the therapeutic level is maintained by a continuous infusion
• adequate anticoagulation is necessary in the first 24 – 48 hours of treatment in order to prevent a high incidence of recurrent disease
• to minimize bleeding complications, the dose of heparin should be adjusted to keep the PTT between 1.5 – 2.0 times control
• the dose of Coumadin should be adjusted to keep the INR between 2.5 – 3.0
• use of low-molecular-weight heparins appears to be as effective as standard heparin and can be done on an outpatient basis with no need for laboratory monitoring
• other effective treatment options include subcutaneous Lovenox, subcutaneous fondaparinux, or oral factor Xa inhibitors for a period of 3 – 6 months


2. Thrombolysis
• reserved for patients with phlegmasia cerulea dolens
• goal is to completely eliminate the thrombus and maintain valvular function
• systemic thrombolysis has a high rate of incomplete thrombolysis and bleeding complications
• catheter-directed thrombolysis is associated with better results and less bleeding complications
• catheter-directed thrombolysis also has had good results in subclavian vein thrombosis


2. Surgical Therapy
1. Thrombectomy
• reserved for limb salvage in the presence of phlegmasia cerulea dolens
• the use of a small arteriovenous fistula after iliofemoral thrombectomy may reduce the incidence of early rethrombosis


2. Vena Caval Filters
• indicated when there is a failure of or contraindication to anticoagulation (recent surgery, hemorrhagic stroke, GI bleeding)
• goal is to provide filtration of clot without occlusion of the infrarenal IVC
• percutaneous transvenous approach (Greenfield filter) is the technique of choice
• retrievable filters now exist for patients who only require short-term caval protection