Thrombosis and embolism

Not only replacement heart valve patients are reliant on long-term anticoagulation with vitamin K antagonists (Marcumar®, Sintrom®, Coumadin®); increasingly, patients with recidivating thrombosis (mostly in the legs) and/or with pulmonary embolism are taking these medications.

What is thrombosis?

Thrombosis is the occlusion (blockage) of a blood vessel through clotting. Veins carry blood that is low in oxygen from the body back to the heart. All of the veins in the lower half of the body feed into the inferior vena cava, while the veins in the upper half feed into the superior vena cava. Both of these venous trunks empty into the right atrium of the heart. From here the blood is pumped into the right ventricle and onward to the lung via the pulmonary artery. In the lung the blood is enriched with oxygen, then passes back via the pulmonary veins to the left side of the heart (atrium and ventricle), from where it is in turn pumped through the aorta to supply the body with oxygen (Fig. 1).

Occlusion of a vein in the leg causes a backlog. Blood continues to be pumped into the leg through the artery, but can no longer flow back through the vein.

Typical symptoms of deep vein thrombosis are:

  • swelling of the calf or lower leg
  • pain, especially under load
  • sometimes a reddish-blue colour
  • skin tension = "glossy skin"
  • tenderness of the calf
  • tenderness of the soles of the feet

Not all of the symptoms will necessarily be present. In many cases deep vein thrombosis causes only minor symptoms and is therefore overlooked by the patient as well as the treating physician.

Theoretically, thrombosis can occur in any vein, e.g. in the gut (mesenteric vein thrombosis), brain (sinus vein thrombosis), arm, etc. The commonest localization, however, is in the leg or pelvic region, as it is here that the fluid pressure of the blood is at its highest.

Fig 1

What is an embolism?

The thrombus (clot) that is occluding a vein can break away and travel through the venous system into the inferior vena cava, and from there to the right side of the heart and into the lung. In the pulmonary system the lumen of the blood vessels becomes smaller, so that the thrombus may become lodged in a pulmonary artery, where it blocks the flow of blood, interrupting oxygen exchange in the area supplied by the affected pulmonary artery.

Also, the blood may back up into the right side of the heart, causing pressure-induced heart failure (so-called acute cor pulmonale).

A pulmonary embolism is therefore potentially life-threatening and should be prevented from happening.

If a pulmonary embolism has occurred, a search is made for the thrombosis causing the problem. Generally it is located in the legs or in the pelvic veins. 

Symptoms of pulmonary embolism:

  • shortness of breath,
  • breathing-related chest pains,
  • coughing of blood,
  • unconsciousness and collapse.

With pulmonary embolism, too, not all symptoms will necessarily occur simultaneously; or symptoms may be very mild, making it difficult sometimes to formulate a diagnosis.

How common are thrombosis and pulmonary embolism?
The incidence of thrombosis is age-dependent. In childhood it only plays a role in severely ill children, e.g. during heart surgery involving the use of catheters.

From puberty onwards the incidence rises sharply.

In the general population the incidence of thrombosis is approximately 1-3 per thousand persons. It occurs much more frequently in certain risk situations (see table). Each year in Germany about 30,000 people die of pulmonary embolism.

Risk factors for thrombosis and pulmonary embolism

Generally, various factors are instrumental in causing thrombosis:


  1. Haemostasis (interruption of the flow of blood). Thrombosis is therefore particularly common following surgery, long periods of immobilization, when a vein has become twisted, e.g. as a result of restricted leg room in automobiles or on planes or during pregnancy through the uterus pressing on a vein.
  2. Haemostasis causes the composition of the blood to change and blood coagulation to become activated. The tendency for clots to form is raised significantly.
  3. Often there is damage to the wall of a blood vessel, e.g. through pressure or injury, but also caused by bacterial toxins or materials released by malignant tumours.

The typical risk factors are summarized in the table.

Sometimes several risk factors must be present to produce thrombosis or pulmonary embolism. For instance, congenital thrombophilia may go totally unnoticed until a female patient starts to take oestrogens and then undergoes surgery. Only then does the thrombosis develop.

Spontaneous thrombosis occurring in normal daily life is fortunately a rarity.

Risk factors for the occurrence of thromboembolic diseases:

  • acquired risk factors, blood/thrombophilia risk factors
  • malignant tumours
  • chromic inflammations (e.g. rheumatic heart disease, chronic bowel disease)
  • various rarer congenital and acquired dysfunctions
  • raised lipoprotein (a)
  • protein C/protein S/antithrombin deficit
  • antiphospholipid syndrome
  • prothrombin mutation G20210A
  • APC-Resistenz bzw. Faktor-V-Mutation-Leiden
  • raised homocysteine concentration and MTHFR-C677T mutation
  • surgery, especially artificial joint replacement
  • confinement in bed
  • obesity
  • pregnancy, confinement, the pill, hormone replacement in the menopause
  • old age
  • long flights > 4 hours, car journeys > 8 hours

How is thrombosis/embolism diagnosed?

There are several ways of diagnosing these conditions. Firstly, the symptoms described by the person presenting with the condition are checked, and also where appropriate the risk situation and hence the probability of thrombosis occurring are assessed.

If there is good reason to suspect thrombosis, the first line of action is generally to prescribe an ultrasound scan of the vessels (Doppler). This gives an image of the blood flow. Modern instruments and experienced operators are nowadays able to make a definitive statement.

Occasionally an additional x-ray examination is necessary (so-called phlebography). A contrast medium is injected into a vein in the foot and the return flow can be traced through x-ray imaging.

In the case of pulmonary embolism, an attempt is made to create an image of blood circulation in the lung, or of ventilation…

There is often increased clotting activity in the blood, which can be measured based on the so-called D-dimer value. In patients with thrombosis/embolism the D-dimer values are often significantly increased. However, a high D-dimer value is not conclusive proof of thrombosis, though an unremarkable value can rule it out.

What treatment is given?

1. Acute therapy:

The primary aim of acute therapy is to prevent pulmonary embolism where it has not yet occurred, and also to prevent the formation of thrombi.

This is achieved by diluting the blood as rapidly as possible. As soon as thrombosis/embolism has been diagnosed, the patient generally receives intravenous or subcutaneous heparin. The advantage of heparin is that it is fast-acting. The faster the blood can be diluted, the less chance there is of complications.

Additionally, in the case of deep vein thrombosis, so-called compression therapy is instituted, with tight-fitting stockings or bandages. This promotes the return flow of blood and eases the congestive symptoms.

2. Long-term therapy:

During treatment the patient is then normally put on long-term oral anticoagulation (vitamin K antagonists: Marcumar®, Sintrom®, Coumadin®). This long-term anticoagulation is very important as, in the first three months especially after thrombosis, new thrombi may form.

Compression therapy on the leg should be continued for a long time, preferably for one to two years following thrombosis depending on its severity. This is important, as compression therapy can help avoid a common complication of thrombosis: so-called post-thrombotic syndrome.

In post-thrombotic syndromes, changes occur to the skin with pigmentation and a general thinning of the skin, especially around the ankles. Ulceration of the legs may occur. Compression therapy is a very effective preventive measure and is thus also extremely important.

The duration of anticoagulation (blood dilution) depends on the localization of the thrombosis, on the patient’s history (risk profile) and also on possible thrombophilia, or tendency for thrombosis to occur. There will be a report on this in the next editions of “Coagulation”.)

Long-term or life-long therapy with vitamin K antagonists (Marcumar®, Sintrom®, Coumadin®) is generally necessary:

  • In the case of severe congenital coagulation defects. Thrombophilia does not always require life-long therapy.
  • In the condition following thrombosis or thromboembolism.
  • Following particularly severe life-threatening illness, e.g. sinus vein thrombosis, mesenteric vein thrombosis, and many other conditions.
  • Where there are additional risk factors such as cardiac arrhythmia (atrial fibrillation), foramen ovale apertus, and many others.

Patients needing long-term anticoagulation may be eligible to receive a Coagu-Check® monitor for INR self-testing. Please consult your health scheme for details.

The INR target range for long-term anticoagulation where there is a thrombotic risk: INR 2.0 – 3.0.

Dr. med. Hannelore Rott, Specialist in Transfusion Medicine, Königstr. 53, 47051 Duisburg/Germany (2005)