Deep vein thrombosis

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"DVT" redirects here. For other uses, see DVT (disambiguation).
Deep vein thrombosis
Classification and external resources

A deep vein thrombosis in the right leg. Note the swelling and redness.
ICD-10 I80.2
ICD-9 453.40
DiseasesDB 3498
MedlinePlus 000156
eMedicine med/2785
MeSH D020246

Deep vein thrombosis (DVT) is the formation of a blood clot ("thrombus") in a deep vein. Deep vein thrombosis commonly affects the leg veins (such as the femoral vein or the popliteal vein) or the deep veins of the pelvis. Occasionally the veins of the arm are affected (such as in Paget-Schrötter disease). A DVT can occur without symptoms, but in many cases the affected extremity will be painful, swollen, red, and warm, and the superficial veins may be engorged. The most serious complication of a DVT is that the clot could dislodge and travel to the lungs, which is called a pulmonary embolism (PE). DVT is a medical emergency, so, all limb swellings, however trivial, should be regarded as a DVT until proven otherwise. Untreated lower extremity DVT has a 3% PE-related mortality rate. Deaths associated with upper extremity DVT are extremely rare.[1] A late complication of DVT is the post-thrombotic syndrome, which can manifest itself as edema, pain or discomfort and skin problems.

According to Virchow's triad, venous thrombosis occurs due to three factors: decreased flow rate of the blood (venous stasis), damage or activation of the blood vessel wall and an increased tendency of the blood to clot (hypercoagulability). Several medical conditions can lead to DVT, such as compression of the veins, physical trauma, cancer, infections, certain inflammatory diseases and specific conditions such as stroke, heart failure or nephrotic syndrome. There are several factors which can increase a person's risk for DVT, including older age (the strongest risk factor), surgery, hospitalization, immobilization (such as when orthopedic casts are used or during long-haul flights), heavy smoking, obesity, certain drugs (such as estrogen or erythropoietin) and inborn tendencies to form clots known as thrombophilia (for example, in carriers of factor V Leiden). Women have an increased risk during pregnancy and in the postnatal period, due to increased estrogen levels.

The most commonly used tests for the diagnosis of DVT are a blood test called D-dimers and doppler ultrasound of the affected veins. Sometimes, further testing is required to find the cause of the DVT. In specific cases, an attempt can be made to break down the clot (using thrombolytic agents). To prevent further accrual and formation of new clots with a risk of pulmonary embolism, anticoagulation (blood thinners) is advised (if not possible, an inferior vena cava filter may be used). Prevention of DVT is advised in many medical and surgical inpatients using anticoagulants, graduated compression stockings (also known as thromboembolic deterrent stockings) or intermittent pneumatic compression (IPC) devices.

Contents

[edit] Classification

DVTs can be lower extremity (from the lower limbs) or upper extremity in origin. DVTs in the legs are proximal (or iliofemoral)[2] when above the knee and distal when below the knee.[3] DVTs below the popliteal vein, a proximal vein behind the knee, are in distal calf veins.[4] An incident DVT is an initial episode and any subsequent DVTs are termed recurrent.[5] DVTs that have no symptoms, but are found only by screening, are termed asymptomatic.[6] Pain and swelling are symptoms of acute DVT.[7] Acute DVTs are usually occlusive,[4] meaning they obstruct blood flow, whereas nonocclusive DVTs are more asymptomatic.[8] The label of chronic has been applied to symptomatic DVTs which persist longer than 10 or 14 days.[9] A severe and uncommon form of DVT is phlegmasia cerulea dolens, which often develops on top of a life-threatening illness.[8][10] DVTs that develop in association with surgery are perioperative and can form during surgery (intraoperative) or afterwards (postoperative).[11]

As a type of blood clot in a vein (venous thrombosis), DVTs are considered, along with pulmonary embolisms (PEs), as a venous thromboembolism.[12]

[edit] Signs and symptoms

There may be no symptoms referable to the location of the DVT, but the classical symptoms of DVT include pain, swelling and redness of the leg and dilation of the surface veins. In up to 25% of all hospitalized patients, there may be some form of DVT, which often remains clinically inapparent (unless pulmonary embolism develops).

There are several techniques during physical examination to increase the detection of DVT, such as measuring the circumference of the affected and the contralateral limb at a fixed point (to objectivate edema), and palpating the venous tract, which is often tender. Physical examination is unreliable for excluding the diagnosis of deep vein thrombosis.

In phlegmasia alba dolens, the leg is pale and cool with a diminished arterial pulse caused by spasm. It usually results from acute occlusion of the iliac and femoral veins because of DVT.

In phlegmasia cerulea dolens, there is an acute and nearly total venous occlusion of the entire extremity outflow, including the iliac and femoral veins. The leg is usually painful, cyanosed (blue from lack of oxygen) and edematous (filled with fluid). Venous gangrene may develop as a result.

It is vital that the possibility of pulmonary embolism be included in the history, as this may warrant further investigation.

A careful history has to be taken considering risk factors (see below), including the use of estrogen-containing methods of hormonal contraception, recent long-haul flying, intravenous drug use and a history of miscarriage (which is a feature of several disorders that can also cause thrombosis). In the case of long-haul flying, recent studies have shown that risk of DVT is higher in travellers who smoke, are obese, or are currently taking contraceptive pills.[13] A family history can reveal a hereditary factor in the development of DVT. Approximately 35 percent of DVT patients have at least one hereditary thrombophilia, including deficiencies in the anticoagulation factors protein C, protein S, antithrombin, or mutations in the factor V and prothrombin genes.[14]

[edit] Causes

Venous thrombi are recognized to be caused mainly by a combination of venous stasis and hypercoagulability—but to a lesser extent endothelial damage and activation.[15] The three factors of stasis, hypercoaguability, and alterations in the blood vessel wall represent Virchow's triad, and changes to the vessel wall are the least understood.[16] Various risk factors increase the likelhood of any one individual developing a thrombosis. Older age is the strongest risk factor;[16] after aging, blood composition favors clotting.[15]

[edit] Risk factors

[edit] Pathophysiology

DVTs usually develops first in the calf veins, "growing" in the direction of flow of the vein (proximally).[19] Very extensive DVTs can extend into the iliac veins or the inferior vena cava. The risk of pulmonary embolism is higher in the presence of more extensive clots.

In contrast to the understanding for how arterial thromboses occur, as with heart attacks, venous thrombosis formation is not well understood.[20] With arterial thrombosis, blood vessel wall damage is required for thrombosis formation, as it initiates coagulation,[20] but the majority of venous thrombi form without any injured epithelium.[15]

Red blood cells and fibrin are the main components of venous thrombi,[15] and the thrombi appear to attach to the blood vessel wall endothelium, normally a non-thrombogenic surface, with fibrin.[20] Platelets in venous thorombi attach to downstream fibrin, while in arterial thrombi, they compose the core.[20] As a whole, platelets constitute less of venous thrombi when compared to arterial ones.[15] The beginning of the process is thought to be initiated by tissue factor effected thrombin production, which leads to fibrin deposition.[16]

The valves of veins are a recognized site of VT initiation. Due to the blood flow pattern, the base of the valve sinus is particularly deprived of oxygen (hypoxic). Stasis excacerbates hypoxia, and this state is linked to the activation of white blood cells (leukocytes) and the endothelium. Specifically, the two pathways of hypoxia-inducible factor-1 (HIF-1) and early growth response 1 (EGR-1) are activated by hypoxia, and they contribute to monocyte and endothelial activation. Hypoxia also causes reactive oxygen species (ROS) production that can activate HIF-1, EGR-1, and nuclear factor-κB (NF-κB), which regulates HIF-1 transcription.[16]

HIF-1 and EGR-1 pathways lead to monocyte association with endothelial proteins, such as P-selectin, prompting monocytes to release tissue factor filled microvesicles, which presumably initiate fibrin deposition (via thrombin) after binding the endothelial surface.[16]

[edit] Diagnosis

Abdominal computed tomographic scan showing a common iliac vein thrombosis. The arrow indicates the filling defect in the vein visualised using radiocontrast.

The gold standard is intravenous venography, which involves injecting a peripheral vein of the affected limb with a contrast agent and taking X-rays, to reveal whether the venous supply has been obstructed. Because of its invasiveness, this test is rarely performed.

[edit] Physical examination

Homans sign: Dorsiflexion of foot elicits pain in posterior calf. Pratt's sign: Squeezing of posterior calf elicits pain. However, these medical signs do not perform well and are not included in clinical prediction rules that combine best findings in order to diagnose DVT.[21]

[edit] Probability scoring

In 2006, Scarvelis and Wells overviewed a set of clinical prediction rules for DVT,[4] on the heels of a widely adopted set of clinical criteria for pulmonary embolism.[22][23]

Wells score or criteria: (Possible score -2 to 9)

  1. Active cancer (treatment within last 6 months or palliative) +1 point
  2. Calf swelling >3 cm compared to other calf (measured 10 cm below tibial tuberosity) +1 point
  3. Collateral superficial veins (non-varicose) +1 point
  4. Pitting edema (confined to symptomatic leg) +1 point
  5. Previous documented DVT +1 point.
  6. Swelling of entire leg +1 point
  7. Localized pain along distribution of deep venous system +1 point
  8. Paralysis, paresis, or recent cast immobilization of lower extremities +1 point
  9. Recently bedridden > 3 days, or major surgery requiring regional or general anesthetic in past 4 weeks +1 point
  10. Alternative diagnosis at least as likely -2 points

Interpretation:

Score of 2 or higher — deep vein thrombosis is likely. Consider imaging the leg veins.
Score of less than 2 — deep vein thrombosis is unlikely. Consider blood test such as d-dimer test to further rule out deep vein thrombosis.

[edit] Blood tests

[edit] D-dimer

In a low-probability situation, current practice is to commence investigations by testing for D-dimer levels. This cross-linked fibrin degradation product is an indication that thrombosis is occurring, and that the blood clot is being dissolved by plasmin. A low D-dimer level should prompt other possible diagnoses (such as a ruptured Baker's cyst, if the patient is at sufficiently low clinical probability of DVT).[24][25]

[edit] Other blood tests

Other blood tests usually performed at this point are[citation needed]:

[edit] Imaging

An ultrasound image demonstrating a blood clot in the left common femoral vein.

Impedance plethysmography, Doppler ultrasonography, compression ultrasound scanning of the leg veins, combined with duplex measurements (to determine blood flow), can reveal a blood clot and its extent (i.e. whether it is below or above the knee). Duplex ultrasonography, due to its high sensitivity, specificity and reproducibility, has replaced venography as the most widely used test in the evaluation of the disease. This test involves both a B mode image and Doppler flow analysis. It is most sensitive and specific for detecting proximal thrombi (in the popliteal and femoral veins), but substantially less so for distal thrombi (in the calf veins).[26]

[edit] Prevention

[edit] Medical inpatients

Walking is an effective preventative measure.[27] Clinical practice guidelines state:

  • American College of Physicians (ACP) in 2011:[28][29]
    • "ACP recommends assessment of the risk for thromboembolism and bleeding in medical (including stroke) patients prior to initiation of prophylaxis of venous thromboembolism (Grade: strong recommendation, moderate-quality evidence)."
    • "ACP recommends pharmacologic prophylaxis with heparin or a related drug for venous thromboembolism in medical (including stroke) patients unless the assessed risk for bleeding outweighs the likely benefits (Grade: strong recommendation, moderate-quality evidence)."
    • "ACP recommends against the use of mechanical prophylaxis with graduated compression stockings for prevention of venous thromboembolism (Grade: strong recommendation, moderate-quality evidence)."
    • "ACP does not support the application of performance measures in medical (including stroke) patients that promotes universal venous thromboembolism prophylaxis regardless of risk."
  • American College of Chest Physicians (ACCP) in 2012:[30]
    • "For acutely ill hospitalized medical patients at increased risk of thrombosis, we recommend anticoagulant thromboprophylaxis with low-molecular-weight heparin (LMWH), low-dose unfractionated heparin (LDUH) bid, LDUH tid, or fondaparinux (Grade 1B) and suggest against extending the duration of thromboprophylaxis beyond the period of patient immobilization or acute hospital stay (Grade 2B). For acutely ill hospitalized medical patients at low risk of thrombosis, we recommend against the use of pharmacologic prophylaxis or mechanical prophylaxis (Grade 1B). For acutely ill hospitalized medical patients at increased risk of thrombosis who are bleeding or are at high risk for major bleeding, we suggest mechanical thromboprophylaxis with graduated compression stockings (GCS) (Grade 2C) or intermittent pneumatic compression (IPC) (Grade 2C). For critically ill patients, we suggest using LMWH or LDUH thromboprophylaxis (Grade 2C). For critically ill patients who are bleeding or are at high risk for major bleeding, we suggest mechanical thromboprophylaxis with GCS and/or IPC at least until the bleeding risk decreases (Grade 2C). In outpatients with cancer who have no additional risk factors for VTE we suggest against routine prophylaxis with LMWH or LDUH (Grade 2B) and recommend against the prophylactic use of vitamin K antagonists (Grade 1B)."

Enoxaparin or unfractionated heparin may be used.[31] LMWH may be more effective than unfractionated heparin (UFH). If UFH is used, 5000 U 3 times daily may be more effective.[32]

[edit] Surgery patients

In patients who have undergone surgery, low molecular weight heparins (LMWH) are routinely administered to prevent thrombosis. LMWH can only currently be administered subcutaneously by injection. Prophylaxis for pregnant women who have a history of thrombosis may be limited to LMWH injections or may not be necessary if their risk factors are mainly temporary.

Early and regular ambulation (walking) is a treatment that predates anticoagulants and is still recognized and used today. Walking activates the body's muscle pumps, increasing venous velocity and preventing stasis. IPC devices have proven protective in bed- or chair-ridden patients at very high risk or with contraindications to heparins. IPC machines use air bladders that are wrapped around the thigh and/or calf. The bladders alternately inflate and deflate, squeezing the muscles and increasing blood velocity by as much as 500%. IPC machines have been proven effective on knee and hip surgery patients (a population with a risk as high as 80% with no prophylactic treatment) of developing DVT and PE.

[edit] Pregnancy

See also: Hypercoagulability in pregnancy

The risk of deep vein thrombosis is increased in pregnancy because of a physiologically adaptive mechanism of increased hypercoagulability to prevent postpartum hemorrhage.[33] In addition to this increased risk, pregnant women with genetic suceptibility to blood coagulation are subject to an additional a 3- to 30-fold increased risk for VTE, depending upon the risk factor(s).[34]

While the general consensus among physicians is that the safety of the mother supersedes the safety of the developing fetus, changes in the anticoagulation regimen during pregnancy can be performed to minimize the risks to the developing fetus while maintaining therapeutic levels of anticoagulation in the mother.

The main issue with anticoagulation in pregnancy is that warfarin, the most commonly used anticoagulant in chronic administration, is known to have teratogenic effects on the fetus if administered in early pregnancy.[35][36]

[edit] Travellers

In the 2012 ACCP clinical guidelines, weak recommendations on limited evidence[37] were offered on VTE prevention. For at risk long-haul travelers—those with "previous VTE, recent surgery or trauma, active malignancy, pregnancy, estrogen use, advanced age, limited mobility, severe obesity, or known thrombophilic disorder"—recommendations for prevention include frequent walking, calf exercizes, and aisle seating in airplanes to facilitate walking.[30][38] The use of "properly fitted, below-knee [graduated compression stockings] providing 15 to 30 mm Hg of pressure at the ankle during travel" was recommended though use of aspirin or anticoagulants were not.[30]

Compression stockings have sharply reduced the levels of asymptomatic DVT in airline passenters, but the effect on symptomatic VTE is unknown as no individuals studied developed symptomatic VTE.[39]

[edit] Management

[edit] Anticoagulation

Anticoagulation is the usual treatment for DVT. In general, patients are initiated on a brief course (i.e., less than a week) of heparin treatment while they start on a 3- to 6-month course of warfarin (or related vitamin K inhibitors). Low molecular weight heparin (LMWH) is preferred,[40] though unfractionated heparin is given in patients who have a contraindication to LMWH (e.g., renal failure or imminent need for invasive procedure). In patients who have had recurrent DVTs (two or more), anticoagulation is generally "life-long." The Cochrane Collaboration has meta-analyzed the risk and benefits of prolonged anti-coagulation.[41] Once the thrombosis is treated with RBC-thinning agents, the affected area has a fair chance of returning to its normal proportions. However, thinning agents do not lessen the chance of embolism to the pulmonary or coronary arteries. Thus, while the area affected with deep venous thrombosis (i.e. the legs) may cease coagulation, pulmonary embolism is still as possible. In a 2008 Cochrane review, it was found that anticoagulation used in combination with leg compression is a more effective therapy than anticoagulation alone.[42]

An abnormal D-dimer level at the end of treatment might signal the need for continued treatment among patients with a first unprovoked proximal deep-vein thrombosis.[43]

Despite the fact that no one disputes this, based on a meta analysis done by the Cochrane Collaboration where they found only one randomized trial of anti coagulation vs placebo in the treatment of VTE in which there was no significant difference between the two.[44]

Current recommendations for initial treatment of acute DVT include initiation of a vitamin K antagonist (VKA) together with LMWH or UFH on the first treatment day.[45] Heparin may be discontinued when the international normalized ratio (INR) is stable and greater than 2.0. For the duration and intensity of treatment for acute DVT of the leg, the recommendations include the following:

  • for patients with a first episode of DVT secondary to a transient (reversible) risk factor, long-term treatment with a VKA for 3 months.
  • for patients with a first episode of idiopathic DVT, treatment with a VKA for at least 6 to 12 months. The dose of VKA is adjusted to maintain INR in the range of 2.0 to 3.0.
  • for the prevention of the post-thrombotic syndrome, the use of an elastic compression stocking is recommended.

[edit] Thrombolysis

Thrombolysis is generally reserved for extensive clot, e.g. an iliofemoral thrombosis. Although a meta-analysis of randomized controlled trials by the Cochrane Collaboration shows improved outcomes with thrombolysis,[46] there may be an increase in serious bleeding complications. In July 2008, the American College of Chest Physicians (ACCP) published evidence-based clinical guidelines for the treatment of venous thromboembolic (VTE) disease which for the first time suggested the use of pharmacomechanical thrombolysis in the treatment of certain cases of acute DVT. Complete 2008 ACCP VTE guidelines can be downloaded at no charge at: TheNewGuidelines.org

[edit] Thrombectomy

Thrombus can be removed with a mechanical thrombectomy device. Combination therapy that uses mechanical thrombectomy to deliver localized thrombolytics has recently received considerable attention as a treatment for DVT.

[edit] Compression stockings

Elastic compression stockings should be routinely applied "beginning within 1 month of diagnosis of proximal DVT and continuing for a minimum of 1 year after diagnosis".[40] Starting within one week may be more effective.[47] They reduce the risk of postthrombotic syndrome.[48] The stockings in almost all trials were stronger than routine anti-embolism stockings and exerted a pressure of either 20–30 mm Hg or 30–40 mm Hg. Most trials used knee-high stockings. A meta-analysis of randomized controlled trials by the Cochrane Collaboration showed reduced incidence of post-thrombotic syndrome.[49] The number needed to treat is relatively high, at 4 to 5 patients needing to have been treated to prevent one case of post-thrombotic syndrome.[50]

[edit] Compression Systems

Intermittent pneumatic compression (IPC) can be of benefit to patients deemed to be at risk of deep vein thrombosis. IPC is an accepted treatment method for preventing blood clots or deep venous thromboses (DVTs) and complications of venous stasis in persons after trauma, orthopaedic surgery, neurosurgery, or in disabled persons who are unable to walk or mobilise effectively.

Intermittent pneumatic compression (IPC) uses an air pump to inflate and deflate an airtight bag wrapped around the leg. This technique is also used to stop blood clots developing during surgery. However, the review of trials found conflicting evidence about whether or not IPC is better than compression bandages and hosiery. Intermittent pneumatic compression (IPC) is better for healing leg ulcers than no compression but it is uncertain if it improves healing when bandages or hosiery are already used [51]

[edit] Inferior vena cava filter

Inferior vena cava filter reduces pulmonary embolism[52] and is an option for patients with an absolute contraindiciation to anticoagulant treatment (e.g., cerebral hemorrhage) or those rare patients who have objectively documented recurrent PEs while on anticoagulation, an inferior vena cava filter (also referred to as a Greenfield filter) may prevent pulmonary embolisation of the leg clot. However these filters are themselves potential of thrombosis,[53] IVC filters are viewed as a temporizing measure for preventing life-threatening pulmonary embolism.[54]

[edit] Hospitalization

Treatment at home is an option according to a meta-analysis by the Cochrane Collaboration.[55] Hospitalization should be considered in patients with more than two of the following risk factors as these patients may have more risk of complications during treatment:[56]

  • bilateral DVT
  • renal insufficiency
  • low body weight (<70 kg/154 lbs)
  • recent immobility
  • chronic heart failure
  • cancer

[edit] Prognosis

Main article: Post-thrombotic syndrome

In the one to two year period after the initial development of symptoms of deep vein thrombosis (DVT), post-thrombotic syndrome occurs in between as few as a fifth, and as many as half of cases. A "severe" post-thrombotic syndrome likewise varies in frequency between a twentieth and a tenth of individuals diagnosed with DVT. This malady is sometimes characterized by varicose ulceration.[57]

[edit] Epidemiology

DVTs occur in about 1 per 1000 persons per year. It is estimated that approximately 350,000 to 600,000 Americans each year suffer from DVT and pulmonary embolism and at least 100,000 deaths may be directly or indirectly related to these diseases.[58]

DVT is much less common in the pediatric population. About 1 in 100,000 people under the age of 18 experiences deep vein thrombosis, possibly due to a child's high rate of heartbeats per minute, relatively active lifestyle when compared with adults, and fewer comorbidities (e.g. malignancy).

In pregnant women, it has an incidence of 0.5 to 7 per 1,000 pregnancies, and is the second most common cause of maternal death in developed countries after bleeding.[59]

[edit] History

In 1851, German physician Rudolf Virchow published a paper[60] which formed the basis of what is referred to today as Virchow's triad. It contained a triad of factors to explain why venous thrombi form. Virchow also noted that more deep venous thrombosis occurred in the left leg than in the right and proposed compression of the left common iliac vein by the overlying right common iliac artery as the underlying cause (see May-Thurner syndrome).

[edit] References

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