On this page

About VTE

The most common manifestations of venous thrombotic disease are superficial-vein thrombosis (SVT), deep vein thrombosis (DVT) and pulmonary embolism (PE), collectively known as venous thromboembolic events (VTEs).

Incidence of VTE

Although the exact number of people affected each year by VTE is difficult to determine, however, reliable estimates have been obtained from epidemiological studies that suggest the annual incidence of VTE is about 1 per 1,000 of the population.[1] VTE is estimated to be the third-most common cardiovascular disorder (after coronary heart disease and stroke). In the European Union alone, more than 540,000 patients are estimated to die each year from VTE, which is double the number of Europeans killed by breast cancer, prostate cancer, HIV/AIDS and road traffic accidents combined.[2]

Due to observational data the incidence of superficial-vein thrombosis (SVT), or thrombophlebitis, is estimated 0.6 per 1,000 of the population. SVT has widely been estimated to be an uncomfortable but benign disease. But several studies have shown that at first presentation to the doctor, one in four patients with SVT already have deep vein thrombosis (DVT) and one in 20 have pulmonary embolism. Furthermore, 5-10% of patients will develop a severe progression of the disease in the first three months if they are not adequately treated.[3]

VTE is a major health burden

Despite its high incidence, the true burden posed by VTE is typically underestimated. There has been a tendency to both under-recognize the condition and underestimate its clinical and health-economic impact.

In Europe, the size of the problem posed by VTE has been highlighted by the recent findings of an epidemiological modelling study, VITAE (VTE Impact Assessment Group in Europe). The approximate number of symptomatic VTE events per annum within the six participant EU countries was over 466,000 cases of DVT, 296,000 cases of PE, and 370,000 VTE-related deaths (range based on probabilistic sensitivity analysis).[2]

Based on European data, it has been estimated that the annual burden of fatal and non-fatal symptomatic VTE in 25 European countries exceeds 1.5 million events, a figure that includes over 543,000 deaths, 434,000 cases of PE, and 684,000 cases of DVT. Around 60% of these VTEs were hospital-acquired. The total direct costs of all these VTE events are estimated at EUR 3.07 billion each year.[4]

Risk factors for developing a VTE

The risk factors for developing VTE are varied and wide-ranging. Different risk factors or events can cause unnatural clotting; however, each factor may initiate clotting in a different way.  Under-recognition of the disease is caused in part by the fact that most VTEs are silent or asymptomatic. Data suggests that approximately 10% of hospital deaths are attributed to a pulmonary embolism (PE), but in 70–80% of these cases a diagnosis of PE was not even considered prior to death. Yet most hospitalized patients have one or more of the known and well-defined risk factors for VTE; and these risk factors are cumulative.[5]

Improving VTE prevention

The prevention of VTE is important to reduce the healthcare burden associated with SVT, DVT, PE and associated complications. There is now strong scientific evidence in support of VTE prevention, demonstrating the efficacy of anti-thrombotic medication in different patient groups. This evidence is effectively summarized in evidence-based guidelines on VTE prevention by the American College of Chest Physicians (ACCP), several national guidelines and an International Consensus group.

Expositional and dispositional risk factors determine risk of VTE

Expositional risk factors are major risk factors for VTE, to which patients may be temporarily exposed. Guidelines recommend that patients presenting with these conditions are given a preventive anti-thrombotic treatment (known as prophylaxis). Expositional risk factors include:[6]

Dispositional risk factors are certain patient-related risk factors, which can also increase the overall risk for developing VTE. Examples of dispositional risk factors include:[7]

  • Prior VTE of the patient
  • Prior VTE of a first degree relative
  • Age (patients over 40, and risk approximately doubles with each subsequent decade)
  • Obesity
  • Immobility
  • Pregnancy
  • Oral Contraceptives
  • Thrombophilia (a condition where the blood has an increased tendency to form clots), hereditary or acquired

Expositional and dispositional risk factors together determine the individual VTE risk of a patient, and have to be accounted for a sound decision for an appropriate VTE prevention. The combination of two or more moderate and/or weak risk factors may create sufficient cumulative risk to justify the provision of prophylaxis against VTE.

VTE prevention in low risk patients

Patients at low risk of a VTE such as those who must be temporarily inactive for long periods, as during an airplane flight, should be encouraged to walk or otherwise move their legs periodically. Usually, no medical treatment is needed in these circumstances (unless there are known severe dispositional VTE risk factors, in which case a doctor should be asked for advice) and flexing the leg around 10 times per hour is probably sufficient.

VTE prevention in pregnancy

The risk of VTE is increased during pregnancy and the postpartum period. DVT and pulmonary embolism are common during all trimesters of pregnancy and for 6-12 weeks after delivery. Sadly, pulmonary embolism is the leading cause of death in pregnancy. Failure to treat the mother properly is the most common cause of foetal demise. For advice, a specialised physician (an angiologist or a specialist in haemostasis) should be consulted.

VTE prevention in chronically immobile patients at home or in nursing homes

The American College of Chest Physicians (ACCP) guidelines (2012) recommend against the routine use of antithrombotic prophylaxis in chronically (long-term) immobilized persons residing at home or at a nursing home. Despite their similarities to medical inpatients, there have been few studies and no placebo-controlled trials investigating VTE prophylaxis for chronically immobilized outpatients. Any particular request should be cleared with a doctor.


ABOUT DEEP VEIN THROMBOSIS

Deep vein thrombosis (DVT) is the presence of a clot (or thrombus) in a deep vein of an extremity or the pelvis.

Deep vein thrombosis is the most common type of VTE

It most commonly occurs in the lower extremities such as the major vein of the leg (usually the calf or thigh).  A DVT restricts the return of de-oxygenated blood to the heart. A thrombus usually forms behind venous valve at points where the vein branches and blood flow is turbulent. As the blood gathers behind the thrombus, it causes pain and swelling.

DVT

Diagnosing DVT – signs and symptoms

A DVT can be very difficult to diagnose as its signs and symptoms vary dramatically from patient to patient and can be mild. There may not even be any symptoms (asymptomatic), particularly if DVT occurs in the small calf veins. However, early recognition and appropriate treatment of DVT can save many lives.

In general, symptoms of DVT may include:[8]

  • Fluid retention and swelling (edema)
  • Leg pain (occurs in 50% of patients but is nonspecific)
  • Tenderness (occurs in 75% of patients)
  • Warm, irritated or discoloured skin
  • Clinical symptoms of pulmonary embolism (see below)

Complications of DVT

Although DVT is uncomfortable, the main concern is with the complications, which include:

  • Chronic venous insufficiency – DVT causes damage to the vein wall as well as the vein valves, causing blood to flow backwards. This may result in discomfort, tissue breakdown and venous skin ulcers
  • Post-thrombotic syndrome (PTS) – complications that may occur after someone has previously experienced DVT. PTS covers a range of symptoms, including swelling of the leg, aching and discomfort on standing, pain on walking and damage to the skin of the leg, particularly in the lower part. Severe cases of PTS result in venous ulcers. PTS may not develop until several years after the initial DVT, as the symptoms often manifest slowly.
  • Paradoxic emboli – a very rare complication that can occur in patients with cardiac defects. These patients are at risk for venous emboli to pass through an abnormal passage into the arterial circulation where they may block an artery in another part of the body.
  • Recurrent DVT – without treatment, one half of patients have a recurrent, symptomatic VTE within 3 months.
  • Pulmonary embolism (PE) – occurs when an embolism becomes detached from the vein wall and travels with the blood along the venous system, through the right side of the heart and into the pulmonary artery. The embolism lodges within the pulmonary artery where it causes a partial or complete blockage.

Treating DVT: initial anticoagulation therapy

The objectives of DVT treatment include: preventing the clots from increasing in size, preventing complications and providing symptom relief. All patients with DVT are given anticoagulants (a category of medicines that inhibit further clotting and ease or stimulate clot dissolution (through a process known as fibrinolysis).

Initial anticoagulation therapy traditionally involves the subcutaneous administration of an injectable (parenteral) anticoagulant, either a heparin or a pentasaccharide until adequate systemic anticoagulation is achieved. Rapid anticoagulation is essential within the first 24 hours of diagnosis. This reduces the incidence of recurrent venous thrombosis during the first 3 months from 25% to 5%. In most cases, patients will be treated and monitored in the hospital setting.

Treating DVT: long term anticoagulation therapy

Long-term anticoagulation is necessary to prevent recurrent VTEs. Once acute anticoagulation is achieved, vitamin-k-antagonists (VKA), such as warfarin are the medicines of choice for long-term therapy to prevent clot recurrence. Alternatively, the use of a class of medicines known as direct oral anticoagulants (DOACs) can be considered, especially in patients with intolerance to warfarin, or insufficient anticoagulation under VKA treatment. The duration of anticoagulation can vary depending on: whether the patient has a first episode of DVT and ongoing risk factors for VTE.

Treating DVT: surgical interventions

In many patients, anticoagulation alone is highly effective, and it has become the primary treatment of choice for many forms of VTE. Unfortunately, when thrombosis is extensive, fibrinolysis alone may be inadequate to dissolve the volume of thrombus present. Surgical thrombus removal has traditionally been used in patients with complications resulting from massive swelling.

Treating DVT: inferior vena cava filters (IVCF)

An inferior vena cava filter (IVCF) is a small umbrella-shaped metal device (the filter) and is placed into the vena cava (a major vein) to catch any traveling blood clots before they can reach the heart or lungs. An IVCF may help prevent PE in patients with lower extremity DVT who have contraindications to anticoagulant therapy or in patients with recurrent DVT (or emboli) despite adequate anticoagulation.

Treating DVT: physical measures

In patients with symptomatic DVT, primary prevention of venous insufficiency and post-thrombotic syndrome (PTS) is recommended. Knee-high elastic compression stockings (ECS) providing pressure are used. These assist the calf muscle pump and reduce complications such as venous hypertension and venous reflux.  They also reduce swelling and aid circulation.

Controversy exists regarding the role of ambulation (walking) in the therapy of DVT. Early ambulation on day two after initiation of outpatient anticoagulant therapy in addition to effective compression is strongly recommended, but early ambulation without compression stockings is not recommended.


ABOUT PULMONARY EMBOLISM

A complication of DVT, rather than a disease in and of itself, a pulmonary embolism (PE) occurs when an embolism (a partial or complete blood clot or thrombus) becomes detached from a DVT in the vein wall and travels with the blood along the venous system, through the right side of the heart and into the pulmonary artery. The embolism lodges within the pulmonary artery where it causes a partial or complete blockage.

Pulmonary embolism – a serious and potentially fatal condition

The consequences of PE vary depending on the size and location of the embolism, the reaction and underlying condition of the lungs, and the body’s intrinsic ability to dissolve clots. However, PE is an extremely dangerous condition, which can be potentially fatal. As a cause of sudden death, massive pulmonary embolism is second only to sudden cardiac death. Approximately 10% of hospital deaths are attributed to PE.

Signs and symptoms of PE

The diagnosis of PE is often missed or delayed because patients with pulmonary embolism present with nonspecific signs and symptoms. Signs and symptoms of PE can vary greatly, depending on how much of the lung is involved, the size of the clots and overall health, including the presence or absence of underlying lung disease or heart disease.

Signs and symptoms for pulmonary embolism are nonspecific, meaning that these symptoms could be caused by other conditions than a pulmonary embolism. However, if you have any of the following, see your doctor. If symptoms are severe, call for emergency help:

  • Shortness of breath, typically appearing suddenly and always becoming worse with exertion
  • Chest pain which may become worse when breathing deeply (pleurisy), coughing, eating or bending over or exercise
  • Cough which may produce bloody or blood-streaked sputum
  • Leg pain or swelling, or both, usually in the calf
  • Clammy or discolored skin (cyanosis)
  • Fever
  • Excessive sweating
  • Rapid or irregular heartbeat
  • Lightheadedness or dizziness

Treating PE

Because PE is a complication of underlying venous thrombosis, there are many similarities in the treatment of both DVT and PE (see sections above under ‘Treating DVT’ for detailed information). However, the risk of early death (within one month) from VTE is much greater after presenting with PE than after DVT.

The increase risks associated with PE may justify more aggressive initial treatment of PE compared with DVT including: thrombolytic therapy, insertion of an inferior vena cava (IVC) filter and more intensive anticoagulant therapy. All patients with strongly suspected or confirmed PE should be hospitalized and, ideally, should also be continually monitored for life-threatening cardiovascular complications in the first 24 to 48 hours.


ABOUT SUPERFICIAL VEIN THROMBOSIS

Superficial venous thrombosis is a blood clot in a superficial vein of the upper or lower extremities. It can occur less commonly in one or more veins of the chest or breast (Mondor disease).

Risk factors for SVT

In the upper extremities, SVT most commonly results from IV infusions or catheterization; a risk factor for SVT occurring in the lower extremity is varicose veins (although most people with varicose veins do not develop thrombosis).

Diagnosing SVT – signs and symptoms

Typical signs and symptoms of SVT are pain, tenderness, or a palpable superficial vein. The overlying skin is usually warm and irritated. Tenderness of the vein may precede redness, and sometimes the clinical signs and symptoms may be less specific. The clinical diagnosis of SVT may be unreliable and extension of SVT is often underestimated clinically. An ultrasound examination is important to accurately assess SVT and to exclude any other complications of VTE (including deep vein thrombosis or pulmonary embolism)

Complications of SVT

SVT has widely been estimated to be an uncomfortable but benign disease. But several studies have shown that at first presentation to the doctor, one in four patients with SVT already have deep vein thrombosis (DVT) and one in 20 have pulmonary embolism. Furthermore, 5-10% of patients will develop a severe progression of the disease in the first three months if they are not adequately treated.[9]

Treating SVT

There are currently no standard guidelines for the treatment of SVT. Because the epidemiology, risk factors, and natural history of SVT are similar to deep vein thrombosis, a key rationale behind selecting therapy for SVT includes prevention of further VTE. Therapies may include:

  • Applying non-steroidal anti-inflammatory drugs (NSAIDs) to the affected area of skin
  • Elastic compression stockings
  • Surgical removal of the clot (thrombus)
  • Systemic NSAID therapy to reduce pain and inflammation
  • Administration of anticoagulant medicines

[1] Glynn R.J. et al. Ann Intern Med 2007; 147:525-33; Amin A, Stemkowski S, et al. J Thromb Haemost. 2007;5:1610-6.
[2] Cohen AT, et al. Thromb Haemost. 2007;98:756-64
[3] Bauersachs R.M., Hämostaseologie 2013; 33:2
[4] http://www.coalitiontopreventvte.org/…/THE_BURDEN_OF_VTE/….HTM
[5] Geerts WH, Pineo GF, et al. Chest. 2004;126 Suppl 3:338-400S
[6] Anderson F.A., et al, Circulation 2003; 107: I-9-I-16
[7] Anderson F.A., et al, Circulation 2003; 107: I-9-I-16
[8] http://emedicine.medscape.com/article/1911303-overview
[9] Bauersachs R.M., Hämostaseologie 2013; 33:2