Deep Vein Thrombosis

Deep vein thrombosis (DVT) usually occurs in the deep veins of the lower extremities. The
affected veins include the femoral, popliteal, iliofemoral, and pelvic veins. Proximal DVT is
more likely to cause a pulmonary embolism (PE) and is generally considered more serious.
Ultrasound can visualize the thrombus and anticoagulation is the primary mode of treatment; the
main objective is the prevention of development of a PE.

Last update:

 August 31, 2020

  8:06 am

Table of Contents
 Epidemiology and Risk Factors
 Pathophysiology
 Clinical Manifestations
 Diagnosis
 Treatment
 Differential Diagnosis

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Epidemiology and Risk Factors

Epidemiology

 More common in Caucasians

 Incidence is slightly higher in males and increases with age.
 Proximal deep vein thrombosis (DVTs) are more likely to cause pulmonary embolism
(PE).
o 10% of proximal leg vein DVTs will lead to PE.
o 50% of untreated proximal DVTs will lead to PE within 3 months.
o > 90% of PEs are due to lower leg DVTs.

Risk Factors

Resulting in endothelial damage:

 Smoking: Oxidant gases and other chemicals in cigarette smoke produce free radicals that
lead to platelet aggregation and an increase in the production of procoagulant molecules.
 Hypertension: Increased shear stress leads to damage of the endothelium.
 Surgery
 Vascular catheter placement (hemodialysis catheters, peripherally inserted central
catheters [PICC] lines): most common cause of upper extremity DVT
 Trauma, especially involving the vasculature
 Nephrotic syndrome
o Leads to loss of anticoagulant proteins (antithrombin III, protein C and S) via the
urine due to damaged glomerular membranes
o Leads to an increase in the production of fibrinogen and other procoagulant
proteins in the liver due to protein loss and hypoalbuminemia
 Antiphospholipid syndrome

Resulting in venous stasis:

 Immobilization (long air travel, after orthopedic surgery): 20 times increased risk of
developing a DVT
 Age > 60
 Polycythemia

Resulting in hypercoagulability:

 Hereditary thrombophilia
o Factor V Leiden
o Protein C or S deficiency
o Elevated levels of homocysteine
 Pregnancy/oral contraceptive pill (OCP) use: Estrogen increases the production of
clotting factors in the liver.
 Obesity
  Cancer: gastric, pancreatic, pulmonary, gynecologic, and urologic tumors particularly
associated with increased risk of DVT (produce proteins and cytokines with
thrombophilic effect)
 Chemotherapy: affects vascular endothelium, coagulation cascades, and tumor cell lysis
 Heparin-induced thrombocytopenia

Other risk factors:

 Prior DVT/pulmonary embolism: 30 times increased risk of recurrent DVT/PE

 Family history

Mnemonic

To remember DVT risk factors, think THROMBOSIS.

 Travel
 Hypercoagulable/Hormone replacement therapy (HRT)
 Recreational drugs
 Old (age > 60)
 Malignancy
 Blood disorders
 Obesity/Obstetrics
 Surgery/Smoking
 Immobilization
 Sickness (congestive heart failure [CHF]/myocardial infarction [MI], inflammatory
bowel disease [IBD], nephrotic syndrome, vasculitis)

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Deep Vein Thrombosis: Definition

1:33
Deep Vein Thrombosis: Epidemiology

4:02
Deep Vein Thrombosis: Etiology

2:45
Deep Vein Thrombosis: Risk Factors
Pathophysiology
Site of origin

 Deep vein thrombosis commonly beings to form in the venous valves; the nature of the
blood flow causes this area to be hypoxic.
 Veins affected the most:
o Femoral, popliteal, and iliofemoral veins
o During pregnancy: pelvis veins

Composition of thrombus

 Red blood cells

 Platelets
 Fibrin

Three pathophysiologic mechanisms (Virchow’s triad)

1. Blood hypercoagulability: increased clotting factor synthesis (e.g., hypoxia-inducible

factor-1) and increased platelet adhesion
2. Endothelial damage: inflammation/trauma → exposure of tissue factor → conversion of
prothrombin to thrombin → conversion of fibrinogen into fibrin and clot formation
3. Abnormal flow/stasis: immobilization, venous valve incompetence → stasis of blood →
clot formation
The main pathophysiologic mechanisms leading to deep vein thrombosis: endothelial damage,
blood hypercoagulability, and blood stasis.

Image by Lecturio.

Complications of DVT

 Pulmonary embolism:
o Potentially fatal
o Occurs as a result of mechanical obstruction of the pulmonary artery or its
branches by a variety of materials (e.g., thrombus, air, or fat) 
o Has both cardiovascular and respiratory effects (hypotension and hypoxia)
 Chronic venous insufficiency: 
o Due to wear and tear, congenital causes, or presence of thrombus 
o Most superficial venous insufficiency is attributed to valvular conditions of the
greater saphenous vein.
 Post-thrombotic syndrome (most common complication of proximal DVT)
o Symptoms include pain and swelling.
o Ulcers develop in the long term on lower extremities.
o Mobility can be reduced.
o Some patients experience paresthesias.
o Occurs in 25%–50% of all patients with DVT

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3:28
Deep Vein Thrombosis: Pathogenesis

Clinical Manifestations
 Symptoms/manifestations are usually unilateral.
o Pain
o Warmth
o Edema
o Intact distal pulses
o Fever (due to cytokine release)
o Homan sign: calf pain on dorsiflexion of the foot (neither sensitive nor specific)
o The first manifestation can be pulmonary embolism (e.g., chest pain, dyspnea)
o Chronic DVT can be asymptomatic and cause chronic venous insufficiency.
 Phlegmasia cerulea dolens: obstruction of all veins of 1 extremity → limited arterial
flow → manifestations:
o Edema
 o Pulselessness
o Pain
o Cyanosis
 Phlegmasia alba dolens: total occlusion of deep iliofemoral venous system →
significant fluid sequestration, edema, and white coloring
o Presents with edema, pain, and blanching without cyanosis
o Edema precipitates phlegmasia cerulea dolens and compartment syndrome →
arterial occlusion and impending limb ischemia
o First described in pregnant and postpartum women

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6:24
Deep Vein Thrombosis: Symptoms

Diagnosis
First test, depending on degree of suspicion

 If the suspicion of DVT is high (Wells score > 2), the test of choice is ultrasonography
with Doppler. Diagnostic imaging findings include:
o Lumen is noncompressible
o Hyperechoic mass
o Decreased/absent flow
 If the suspicion of DVT is low (Wells score < 2), the first test should be D-dimer.
o Highly sensitive test
o Negative test rules out DVT
o Positive test warrants ultrasonography for confirmation

Table: Wells criteria for DVT

Tenderness along with deep venous system +1
Unilateral pitting edema +1
Swelling of the entire leg +1
Calf swelling ≥ 3 cm (compared to asymptomatic calf) +1
Collateral superficial non-varicose veins +1
Active cancer +1
Previous DVT +1
Paralysis or cast immobilization +1
Bedridden ≥ 3 days or major surgery within past 12 weeks +1
Alternative diagnosis as likely/more likely than DVT -2

Diagnostic algorithm for DVT: If the Wells score is < 2, the first test is D-dimer. If the Wells
score is > 2, the first test is ultrasound.

Image by Lecturio.

Further tests

 Age-appropriate screening (e.g., digital rectal exam [DRE], mammography, colonoscopy)

 Coagulation studies are indicated in patients with:
o Positive family history
o Young age
o Unusual localization of thrombus
o Recurrence 
 Hemodynamic stable with a DVT and signs of pulmonary embolism (e.g., chest pain,
dyspnea): contrast-enhanced computed tomography (CT) scan of the chest 
 Hemodynamically unstable with DVT and signs of pulmonary embolism:
echocardiogram to visualize right ventricular dilation
  Venography
o A most accurate test for DVT 
o Invasive and only done in patients with equivocal findings on non-invasive tests,
or in those with severe obesity/edema (limits the usefulness of ultrasound)

Treatment
 Initial treatment
o Heparin bolus (80 units/kg) + heparin infusion (18 units/kg/hr) for 4–5 days
o Alternative to heparin: fondaparinux (indirect factor Xa inhibitor)
o In patients with renal failure, unfractionated heparin is preferred over
fondaparinux and low-molecular-weight heparin (LMWH)
 Secondary prevention of DVT
o Initiate warfarin once activated partial thromboplastin time (aPTT) is 1.5–2.5x
normal (continue only heparin if the patient has increased risk of bleeding/peptic
ulcer disease)
o Alternative to warfarin for secondary prophylaxis:
 Direct oral factor Xa inhibitor (e.g., rivaroxaban, apixaban)
 Does not require regular monitoring of international normalized ratio
(INR), but is more expensive
 Other preventive measures
o Early mobilization after surgery 
o Postoperative anticoagulation
o Exercise
o Weight loss
o Stopping smoking
o Control of hypertension
o Avoidance of OCPs
o Compression stockings
 Indications for thrombolysis (tPA, urokinase, streptokinase)
o Large proximal DVT
o Pulmonary embolism with hemodynamic instability (systolic blood pressure < 90)
o Refractory to anticoagulation
 Indications for thrombectomy (removal of thrombus by a catheter)
o Phlegmasia cerulea dolens
o Large thrombus refractory to fibrinolysis
o Large thrombus + contraindications to anticoagulation/thrombolytics
 Indications for an inferior vena cava (IVC) filter
o Contraindications to anticoagulation/thrombolytics/thrombectomy (e.g., major
bleeding)
o Patients who have DVT or PE while on appropriate anticoagulation
 Treatment of phlegmasia alba dolens
o Initiation of adequate anticoagulation
o IV fluid resuscitation
  Treatment of phlegmasia cerulea dolens
o Initiation of adequate anticoagulation
o Thrombectomy
o Fasciotomy if compartment syndrome present
o Fibrinolysis if thrombectomy fails
o Amputation: if both thrombectomy and fibrinolysis fail, leading to critical limb
ischemia and limb loss
 Treatment of upper extremity DVT
o Anticoagulation (LMWH/unfractionated heparin [UFH]/fondaparinux)
o Fibrinolysis if refractory/large thrombus

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4:07
Deep Vein Thrombosis: Therapy

Differential Diagnosis
The following condtions are differential diagnoses of DVT:

 Peripheral vascular disease: a chronic disease involving arteries in the extremities, and
the main cause of intermittent claudication. The chronic atherosclerotic process leads to
arterial stenosis and, at a later stage, to the complete occlusion of the arteries (either from
embolism or thrombosis).
 Baker cyst: Baker cyst is a swelling in the popliteal space (space behind the knee). The
pain worsens if the patient fully flexes or extends the knee. Baker cysts are commonly
associated with rheumatoid arthritis. A ruptured Baker cyst can mimic an acute DVT.
 Lymphedema: localized fluid retention and tissue swelling caused by a compromised
lymphatic system. Lymphedema can be caused by surgery, parasitic infections, or
hereditary conditions. The condition is often bilateral, unlike a DVT, which is unilateral.
 Cellulitis: a condition that presents with localized swelling, warmth, redness, and pain in
an area. Cellulitis is an infection of the dermis and subcutaneous fat and may form
abscesses.