Deep Vein Thrombosis - What You Should Know

 

The blood has an inherent ability to change its liquid condition to a more solid form, basically to cement from the inside any tear or cut in arteries and veins: this is called a clot. When the clot on the vessel wall has done its job, natural anticoagulants go ahead and dissolve it. This two way process comes about by a very fine balance between procoagulant and anticoagulant factors (the former is known as the clotting cascade, and the latter as the fibrinolytic system: one forms fibrin and the other destroys it). These actors are called into play by chemical messengers from the damaged artery or vein, and from the very small cells called platelets which circulate in the blood exclusively to this end: to stick to the lesion and help seal the wound. They also turn on chemical messengers to amplify the response, and as the job gets done, other chemical messengers do the opposite, “clean up the mess”, but avoid harming the sealed result.

 

When the scale tips in favour of the first group, we have a thrombotic condition, clotting is exaggerated, and extends from the small area of sealing of the wound, can occupy all the diameter of the vein involved and so, obstructing the flow of blood. When it tips to the opposite side, we have a potential hemorrhagic condition, with a high risk of bleeding.

 

Dr. Rudolf Virchow, a world famous German pathologist, was the first to describe the condition in 1848. He coined the word thrombus for the clot, and embolus for the part (or whole) of the clot which floats upstream from the veins towards the right side of the heart and, from there onwards, to impact in the lung. This is a life threatening condition, known as pulmonary embolism or more recently as thromboembolic disease.

 

Dr. Rudolf Virchow - 1821-1902

Coágulo de sangre venoso

A clot in a vein

 

There are a number of predisposing conditions that favour the formation of clots, and occur mainly in the deep veins in the legs: thus Deep Vein Thrombosis (DVT).      

 

  • Major surgery: knee and hip replacements, surgery for cancer, surgery for fractures, and any surgery lasting more than 30 minutes in patients at risk for thrombosis;
  • Prolonged bed rest, especially in patients with strokes or other forms of paralysis, and in patients with heart failure and similar conditions;
  • The use of oral contraceptives;
  • Obesity;
  • Sitting for long hours (usually more than 10) in confined spaces, such as in long distance air travel;
  • In pregnant women immediately after delivery;
  • Cancer;
  • Inherited or acquired conditions which make the blood hypercoagulable: only identified after the first occasion of having a deep vein thrombosis;
  • Illnesses associated to the excess production of red blood cells, which determine that the blood has higher viscosity.

 

Though redness and swelling of a leg can be the main symptom, more often than not it is a painless condition, and can escape detection even of the most experienced physician after a very careful examination. A high degree of suspicion is mandatory, and leads the doctor to requesting tests to confirm or rule out the diagnosis. The principal test used today is ultrasound scanning of the deep veins, which is non-invasive and has quick and reliable results.

 

Prevention of thrombosis is both possible and indispensable today. In surgical conditions, or those that involve prolonged bed rest, low doses of anticoagulants –either heparin preparations injected under the skin once or twice a day, or oral warfarin- administered just before or just after whatever the condition is, have made a dramatic impact both on deep vein thrombosis as on its dreaded complication, pulmonary embolism. Though it has not eliminated the incidence completely, rates for DVT in surgery for hip fractures have been brought down from over 40% to less than 10%. This strategy can also be used in air travel to prevent what is known as “economy class thrombosis” (it happens also in business and first class!), as also the frequent walking up and down the passages of the aircraft during the flight. Other measures that Hospitals use: intermittent calf compression with stockings that inflate and deflate rhythmically with a little electrical pump, and elastic stockings compressing the legs.

 

When pulmonary embolism (PE) develops, the patient experiences variable degrees of shortness of breath, and occasionally chest pain. Depending on the number and size of the clots and on the size of the arteries stopped up by these clots, the patients may have mild symptoms, which tests the ability of the treating physicians to identify it, or can have abrupt onset of severe symptoms, including sudden death. A positive ultrasound test for DVT with these symptoms is highly suspicious of the condition, though occasionally the ultrasound may be normal, if a solitary clot was dislodged and floated up to the lung. Other studies help to identify pulmonary embolism, such as an X ray of the chest, an electrocardiogram, an echocardiogram (cardiac ultrasound), ventilation and perfusion studies of the lungs. The most important non-invasive study with a high degree of accuracy is a CAT scan (computed tomography) of the lungs, whilst the definitive test is a pulmonary angiogram It involves the insertion of a catheter up to the lungs and the injection of contrast dyes, which highlights the clots stuck in the pulmonary circulation. This can only be done in a sophisticated Laboratory with the pertinent equipment, whilst CAT scans are widespread and readily accessible.

 

Treatment of DVT and of PE consists of using heparin initially, and switching in a few days to one of the oral anticoagulants. For many years heparin was administered intravenously for a week, for which Hospital admission was inevitable. With the development of newer heparins, known as low molecular weight heparins, one or two injections under the skin daily has been found to be safer and just as effective. Thus, milder cases of DVT and of PE, in the right setting, can be treated at home with minimum need for nursing care. The treatment lasts three to six months, depending on factors which each case merits.

 

In major orthopedic surgery, be it joint replacements or fractures, prevention of DVT with heparin lasted for a week until walking was begun and the patient was discharged. It has been proven beyond any doubt that prolonging heparin administration at home for a further four weeks eliminates the moderate number of cases (some of them fatal) who developed DVT and PE whilst at home after Hospital treatment was stopped.

 

Dr. John Emery MD

Hospital Británico de Buenos Aires

jemery@hbritanico.com.ar