Deep vein thrombosis (DVT) is a condition in which blood clots form in a vein deep within the body. The word thrombosis means forming a blood clot. The clot itself is called a thrombus.

David Bloom, the late NBC News correspondent, was a dedicated and talented television journalist. During his last assignment in Iraq, he rode for hours at a time along with U.S. troops in an M-88 tank, determined to provide the best coverage of the war as possible. Tragically, the 39-year-old reporter’s zeal might have contributed to his untimely death earlier this year.

Mr. Bloom’s cause of death was reported to be a pulmonary embolism (PE), which occurs when part of a blood clot breaks off and travels to the lung, blocking a pulmonary artery. PE is the third most common cause of death in the United States. In Mr. Bloom’s case, one theory is that his length of time and limited mobility in the tank might have resulted in a condition that affects about 1 in 1,000 people, deep vein thrombosis, (DVT), which led to the embolism.

DVT is an abnormal blood clot that occurs in one of the body’s deep veins; it is one of a broader classification of vascular conditions called venous thrombosis. While DVT can develop anywhere, it most typically originates in the legs or pelvic area. One contributing factor is immobility. “Movement causes muscles to contract, sending blood back up to the heart. When there’s limited movement, the blood pools and is more likely to form clots,” says Dr. Jonathan Harrison, associate professor of medicine at New Jersey Medical School and a hematologist at University Hospital. The so-called Economy Class Syndrome refers to people who develop blood clots during long airplane flights. “The problem isn’t the length of the flight itself, but when people sit during the flight and don’t move their legs or arms.”

Anytime mobility is limited or there’s an obstruction to blood flow, DVT is a possibility. Patients who are immobilized following surgery (particularly orthopaedic procedures) are at risk for developing clots, as are pregnant women, when the uterus presses down on pelvic veins and suppresses blood flow. Estrogen?whether taken as hormone replacement therapy or an oral contraceptive?increases the chance of clot development. Diseases such as diabetes and certain cancers interfere with the synthesis of blood clotting factors, also.

For some, a family matter

Some people have a genetic predisposition to venous thrombosis conditions such as DVT. “When a person has a DVT or other thrombotic event without any apparent reason, there’s often an underlying genetic cause,” says Dr. Marvin Schwalb, director of the Center for Human and Molecular Genetics at New Jersey Medical School. For example, when people who had DVT or PE were tested after the event, 25 percent had the Factor V Leiden mutation.

Factor V Leiden, identified in 1994, is the most common DVT mutation, occurring in between 3 percent to 8 percent of the general population, but there are others. The prothrombin II mutation and Protein S and Protein C deficiencies can occur alone, or very rarely, in combination with each other. “These are variants in important proteins necessary to the complex coagulation cascade,” says Dr. Schwalb. “And while coagulation?the blood’s ability to clot and prevent excessive bleeding?is certainly in itself not bad, these mutations cause an increase in coagulation that can be life threatening.”

It’s not necessary for everyone to be screened for these mutations, says Dr. Schwalb. However, they are dominant disorders, meaning that the son or daughter of a person with an inherited thrombophilic factor such as Factor V Leiden has a 50 percent chance of also carrying the mutated gene. “If a first-degree relative?mother, father, sister, or brother?has one of these disorders, it’s wise to be tested,” says Dr. Schwalb. “A person with an otherwise unexplainable DVT or PE, and anyone with a personal or family history of DVT or PE, especially at young ages, should be screened.”

A person who has had a DVT and, after testing, shows a genetic predisposition for the condition, will typically be advised to take anticoagulant medication for the rest of his or her life. However, it’s a different case for family members of that patient who are found to have a mutation but have no history or indication of clotting. They would be educated about the signs and symptoms of DVT, but not generally be started on any medication, says Dr. Harrison.

Dr. Schwalb notes that some of the same mutations that cause DVT can also lead to very serious complications in pregnancy. Clotting in the placenta can reduce blood flow to the fetus, which can contribute to growth retardation, stillbirth, or miscarriage.

	Ultrasonographic testing identifies even the smallest of blood clots.

With or without warning

In about 50 percent of the cases, DVT patients develop warning signs. When DVT occurs in the leg, the classic symptoms include pain or swelling in the calf, thigh, or both, and a warmth or discoloration at the site. “However, the other half of the time, patients report no symptoms at all,” says Dr. Harrison. “They might not realize there’s anything wrong until they are having a PE. The symptoms of a PE include a sudden shortness of breath, sharp chest pain upon taking a deep breath, a rapid pulse, sweating, and coughing up blood. Patients with these symptoms should seek immediate medical care.”

A doctor will take a medical history and perform a physical exam of a patient with possible DVT. Doppler ultrasound is a non-invasive and effective method of assessing blood flow, but other tests, such as a venogram, which utilizes contrast dye and X-ray, might also be done.

There are different approaches to treating DVT. “Not all cases of DVT have the same high risk for developing an embolism, and some of the clots that form naturally dissolve,” says Dr. Harrison. “If the clot is below the knee, it might be enough to monitor the patient over a few months.”

When medication is warranted, the typical DVT patient will be prescribed heparin, which reduces blood’s clotting ability. Heparin doesn’t dissolve the clot, but it can prevent a clot from getting worse. Heparin used to be most commonly given intravenously, requiring the patient to be hospitalized. But with the emergence of low molecular weight heparin, which is given by injection, that’s no longer the case.

“With low molecular weight heparin, the patient can avoid the hospitalization and the need for blood test monitoring,” says Dr. Harrison. “Low molecular weight heparin is started as therapy for DVT once the clot is identified. It is continued during the first few days of Coumadin® (warfarin) therapy until the patient has a therapeutic level of anticoagulation. This level is determined by a blood clotting assay called prothrombin time, which is measured in a unit called the International Normalization Ratio (INR). Low molecular weight heparin is continued until the INR is between 2.0 and 3.0; lower than 2.0 carries a high risk of clot extending, and an INR above 4.0 presents a risk of life-threatening bleeding.”

If after three to six months on warfarin there are no signs of clotting, then the patient is taken off of the blood thinner. The outcomes are very individualized: some people remain on warfarin for life, while others are taken off the drug and monitored by their physician.

There’s another relatively new approach to treating DVT, one that Dr. Peter Pappas, associate professor of surgery and director of the division of vascular surgery at New Jersey Medical School and a vascular surgeon at University Hospital, believes is underutilized. It is called lytic therapy. Just as medication can be delivered via catheter to arteries to break up blood clots that could cause a stroke, clot-busting drugs can be delivered to veins. “With lytic therapy, we can very quickly get rid of the clot, which decreases the incidence of PE,” says Dr. Pappas. There’s another benefit of lytic therapy. “Years after a DVT has been treated with heparin and warfarin, there can be serious damage to the vein known as chronic venous insufficiency (CVI),” explains Dr. Pappas. “Veins have tiny one-way valves that direct the blood back to heart. A clot inside a vein damages these valves, causing some of the blood to flow backward and creating an abnormal pressure in the vein. The ankle and leg can swell and ulcers can form and become infected. It can be very difficult for the patient to walk or stand. With lytic therapy, the clot is destroyed without long-term damage to the vein.”

Blood-thinning drugs still have an important role in treating DVT; patients can be given heparin and warfarin after lytic therapy. However, says Dr. Pappas, a new drug, ximelagatran, currently being reviewed by the Food and Drug Administration, could significantly change the treatment of DVT. “Ximelagatran comes in pill form, eliminating the need for injection, and has a slow, steady release into the bloodstream. There’s no need for blood tests to monitor levels of the drug, as is the case with warfarin,” says Dr. Pappas. “It’s not an exaggeration to say that this drug could be revolutionary.”

To arrange for a consultation regarding DVT, contact Dr. Jonathan Harrison at 973-972-5108, Dr. Peter Pappas at 973-972-9372 or Dr. Marvin Schwalb at 973-972-3300.