Blood clots are the body’s first step in healing injuries. Sometimes, however, unnecessary blood clots form inside the bloodstream and cause problems such as a pulmonary embolism, heart attack or stroke, all of which may result in death. Deep vein thrombosis happens when a blood clot forms inside a deep vein. Although not immediately hazardous, a deep vein blood clot can develop into a serious condition if it breaks loose. If it’s diagnosed in time, treatment can keep the hazard in check while the blood clot slowly breaks apart.
Deep vein thrombosis (DVT) is a blood clot (thrombus) that forms on the inner tissue of a deep vein. Deep vein blood clots most commonly form in the calf, thigh, or pelvis, but can also form in the arms, intestinal area, or head.
Many deep vein clots resolve without complications. However, the deep vein blood clot could detach from the vein, travel through the heart, and block arteries in the lungs, a potentially fatal condition called pulmonary embolism (PE). Also, about 20% to 50% of deep vein blood clots advance to post-thrombotic syndrome, a potentially debilitating condition marked by intense pain, swelling, and ulcers.
Deep vein thrombosis is caused by a combination of one or more factors: blood pooling in a vein, damage to a vein, or increased blood coagulation, called hypercoagulation. Blood pooling can result from immobility, bed rest, long-distance travel, or vein problems, such as varicose veins. Injury, surgery, or catheters can cause vein damage. Finally, hypercoagulation can be triggered by dehydration, older age, excessive salt intake, illness, medications, or genetics.
It often takes a combination of these factors to induce a deep vein blood clot. For instance, surgery puts people at risk for DVT because surgery can damage veins and several days of bed rest causes blood to pool in the legs.
Deep vein thrombosis strikes about one out of every 1,000 people every year. Fortunately, DVT can be successfully treated with anticoagulants, medications that help to thin blood and reduce the body’s ability to form future blood clots. Early diagnosis, however, is critical in preventing potentially fatal complications.
Deep vein thrombosis is diagnosed based on risk factors, symptoms, a D-dimer test, and ultrasonography.
A healthcare professional can’t diagnose DVT with certainty from just taking a medical history and performing a physical exam—both are only able to contribute to the likelihood of DVT.
The history will help the physician identify risk factors such as:
The healthcare provider will use a scoring method to determine the clinical probability of DVT. The initial exam can be performed by a general practitioner or urgent care doctor, but they might refer the patient to a hematologist (an internist who specializes in blood conditions) or even a vascular surgeon for further assessment and management.
A D-dimer test alone cannot be used to confirm a DVT but can help rule out a DVT in patients who are at low to intermediate risk based on the history and physical. D-dimer is a left-over product of the blood clotting process, so a D-dimer test can determine if blood clots are forming in a person’s body. If the test comes back negative in a low risk patient, there is a very minimal chance the patient has a DVT. If the test comes back positive, the doctor will order an ultrasound for confirmation.
An ultrasound is a fairly accurate test for DVT. It cannot only determine the presence of a blood clot, it can determine the size of the blood clot and how much of the vein is blocked. It is the first test given for patients with a high probability of DVT or to any patient with a positive D-dimer test.
Venography is an expensive and more invasive procedure that is only performed when an ultrasound is uncertain, which may happen if the clot is in the calf. A contrast dye is injected into the bloodstream and the nearby veins are imaged by X-ray to assess blood flow through the veins.
DVT treatment focuses on preventing complications such as pulmonary embolism or post-thrombotic syndrome using anticoagulant medications to prevent further blood clotting. For severe cases or patients who cannot take anticoagulants, a small blood clot filter can be implanted in the vein that runs to the heart.
Anticoagulants are the central pillar of DVT treatment. Depending on whether the DVT episode requires hospitalization, treatment may begin in a hospital setting with injectable anticoagulants versus oral anticoagulants due to their fast onset of action and predictable duration of action. Once the patient is stabilized, patients can be treated on an outpatient basis withusually oral anticoagulants. Patients who do not require hospitalization may avoid injectable anticoagulants altogether and be initiated on an oral anticoagulant with close monitoring. The usual duration of therapy is at least three to six months. Patients with recurrent DVTs and/or other underlying conditions, such as cancer, will receive therapy for longer.
For severe DVT, a vascular surgeon will insert a catheter into a vein and inject a clot-breaking medication directly on to the blood clot - called a thrombolytic. Clot-breaking medications have a high risk of causing internal bleeding, so CDT allows for a very small dose to be used. This approach has demonstrated a reduction in progression to PTS by preventing venous scarring.
Mechanical devices are often used to improve blood flow as a preventative measure. These include compression stockings, intermittent pneumatic compression (IPC), and the venous foot pump.
In severe cases or for patients who cannot safely take anticoagulants, surgery may be used to remove the blood clot via thrombectomy. Patients who cannot be put on anticoagulants will most likely have a filter implanted in the inferior vena cava (IVC), the large vein in the middle of the body that carries blood from the lower body to the heart. The inferior vena cava filter is implanted with a catheter and catches any blood clot that comes loose, preventing that blood clot from reaching the lungs and causing a pulmonary embolism. Depending on the patient’s risk for forming blood clots, the IVC filter may be installed permanently or removed after a few months.
Deep vein thrombosis is treated with anticoagulants, drugs that suppress the formation or function of various clotting factors normally present in the blood. In severe cases, deep vein thrombosis will also be treated with medications that dissolve blood clots.
Blood clot formation is a complex process. To make a blood clot, platelets—small, disk-shaped cells in the bloodstream—clump and glue themselves together in a web made out of a protein called fibrin.
The process involves activating a series of proteins one after another, known as the coagulation cascade. These proteins are known as blood clotting factors, each one having an inactive state and an active state. Each active blood clotting factor activates the next clotting factor in line of the cascade. At the end of this line is factor X (“factor 10”) which is activated into factor Xa (“activated factor 10”). Activated factor X converts an inert protein called prothrombin into thrombin, the last switch in the process. Thrombin activates fibrinogen to form fibrin, the “glue” that catches platelets circulating within the bloodstream to form the clot.
The formation of many of these active clotting factors require a reserve of vitamin K. In addition, the human body produces proteins that function to shut down the coagulation cascade as a form of checks and balances. The most important of these is antithrombin, a protein that attaches to thrombin and prevents that crucial last step, the activation of fibrinogen into fibrin.
The whole process, then, is like a factory line that can be shut down at any step. That is what anticoagulants do. Some push antithrombin into action (called antithrombin activators), some shut down the formation of vitamin K (called vitamin K antagonists), and some just flip the off switch on factor Xa or thrombin (called direct factor Xa inhibitors and direct thrombin inhibitors).
Antithrombin activators are fast-acting blood thinners and a first-line therapy for DVT. They are intended to quickly slow down and stabilize blood clotting. The most commonly prescribed are low molecular weight heparins (LMWH) such as enoxaparin, but unfractionated heparin (UFH) may be used in certain patients, such as those with kidney failure. Heparins, however, can have serious side effects, which if arise doctors may prescribe a similar acting drug called fondaparinux.
Vitamin K antagonists prevent cells from converting vitamin K into a version that can be used to form active blood clotting factors. Warfarin has historically been the first-line anticoagulant prescribed after a patient has been treated with enoxaparin or fondaparinux. Warfarin, however, has a narrow therapeutic range, so patients require close monitoring of the drug through regular blood work.
Direct oral anticoagulants block proteins involved in blood clot formation. For DVT, the most commonly prescribed oral anticoagulant is Pradaxa (dabigatran), a direct thrombin inhibitor. Factor Xa inhibitors include Xarelto (rivaroxaban), Eliquis (apixaban), and Savaysa (edoxaban). All have similar efficacy to warfarin, but have a wider therapeutic range and do not require continual blood work monitoring.
Thrombolytic (“clot-dissolving”) medications break up blood clots and are most commonly prescribed for patients immediately after a stroke or heart attack due to a clot. Alteplase is one thrombolytic used in DVT patients, but only in very small doses injected directly on to the blood clot using catheter-directed thrombolysis (CDT).
Anticoagulant treatment of DVT follows well-researched protocols and is closely monitored. The “best” medication may vary depending on pre-existing conditions and side effects.
Best medications for Deep Vein Thrombosis | ||||
---|---|---|---|---|
Drug Name | Drug Class | Administration Route | Standard Dosage | Common Side Effects |
Lovenox (enoxaparin) | Low molecular weight heparin | Injection | Dosage depends on weight | Bleeding, anemia, heparin-induced thrombocytopenia (HIT) |
Arixtra (fondaparinux) | Factor Xa inhibitor | Injection | Dosage depends on weight | Bleeding, anemia, insomnia |
Coumadin (warfarin) | Vitamin K antagonist anticoagulant | Oral | Dosage will depend on response and will be regularly adjusted | Bleeding, stomach pain, skin rash |
Pradaxa (dabigatran) | Direct thrombin inhibitor | Oral | One 150 mg capsule twice daily | Bleeding, nausea, stomach pains |
Xarelto (rivaroxaban) | Direct Factor Xa inhibitor | Oral | One 15 mg tablet taken twice daily with food for the first 21 days followed by one 20 mg taken once daily with food for the remaining treatment | Bleeding, back pain, stomach pain |
Eliquis (apixaban) | Direct Factor Xa inhibitor | Oral | Two 5 mg tablets taken orally twice a day for seven days, followed by one 5 mg tablet taken orally twice daily | Bleeding, anemia, nausea |
Savaysa (edoxaban) | Direct Factor Xa inhibitor | Oral | One 60 mg tablet taken once daily | Bleeding, rash, anemia |
Activase (alteplase) | Tissue plasminogen activator | Oral | Regimens vary based on local protocols | Bleeding low blood pressure, skin rash |
Many of the standard dosages above are from the U.S. Food and Drug Administration (FDA). Dosage is determined by your doctor based on your medical condition, response to treatment, age, and weight. Other possible side effects exist. This is not a complete list.
Anticoagulants block the body’s ability to form blood clots, so the most frequently experienced side effects are bleeding problems, bruising, and potentially life-threatening internal bleeding in the brain or other organs. Some blood-thinning medications have antidotes to control bleeding episodes.
The type and severity of side effects will vary based on the medication. This is not a complete list, and you should consult with a healthcare professional for possible side effects and drug interactions based on your specific situation.
Antithrombin activators are particularly fast-acting and potent blood thinners, so bleeding is a common problem. The risk of bleeding in the brain or other life-threatening internal hemorrhage is high. Protamine sulfate is a heparin antidote and can reverse bleeding problems or be administered if a patient requires emergency surgery. Fondaparinux, however, does not have an antidote. The most serious side effect of heparin is heparin-induced thrombocytopenia (HIT), an immune response to heparin that can cause hazardous blood clots.
Like other anticoagulants, the vitamin K antagonist warfarin raises the risk of bleeding and internal hemorrhage. In addition, warfarin has a narrow therapeutic range. If the dose is a little bit off, the patient is in danger of blood clots or hemorrhage, so warfarin requires continual blood monitoring of a marker measuring how thin blood is, called the INR (international normalised ratio). Warfarin also has many drug and food interactions that interfere with its effectiveness. For bleeding episodes or medical procedures, warfarin does not have a specific antidote but its effects can be reversed in approximately 24 hours with a vitamin K injection.
Direct oral anticoagulants cause bleeding, bruising, and potentially fatal internal hemorrhaging. There is no antidote currently available for any of these drugs.
Thrombolytic (“clot-dissolving”) drugs are powerful medications that carry a very high risk of internal hemorrhaging, particularly in the brain. For bleeding episodes, the effects of thrombolytics may be suppressed with an intravenous injection of aminocaproic acid or tranexamic acid, and may be given in conjunction with other supportive blood products.
Deep vein thrombosis treatment focuses on preventing the growth of the blood clots or the formation of new blood clots. However, blood pooling in the veins is another factor in the formation of deep vein blood clots. Home treatments can help improve blood movement.
Frequent short walks as well as simple sitting exercises such as knee pulls, ankle circles, and foot pumps can get the blood moving out of the lower legs.
Raising the legs to hip level or higher can help prevent blood from pooling in the lower extremities.
Compression socks increase blood pressure and improve blood flow.
NSAIDs are blood thinners. Even a single dose of a non-steroidal anti-inflammatory drug (NSAID), such as aspirin, ibuprofen, or naproxen, can nearly double the risk of a bleeding event for patients taking anticoagulants.
Medications that increase the risk of deep vein thrombosis include birth control pills; hormone replacement therapy for menopause; tamoxifen, an estrogen blocker; and erythropoietin, a medication that stimulates the body’s production of red blood cells and platelets.
The greatest risk of untreated DVT is pulmonary embolism, a condition that results when the blood clot breaks loose, travels through the heart, and lodges in a lung artery. Untreated deep vein thrombosis resulting in pulmonary embolism has a 30-day mortality rate of one out of three patients.
No food dissolves blood clots. Thrombolysis—the breaking apart of blood clots— is a natural process that is activated by proteins produced in the body.
Some foods are high in substances, such as salicylates, that prevent clotting by blocking platelets from clumping together. These foods, such as cherries, berries, and avocados, are not recommended for patients taking blood thinners.
Patients taking the blood thinner warfarin, which depletes vitamin K dependent clotting factors, should avoid foods high in vitamin K such as leafy vegetables.
Deep vein blood clots form when blood moves too slowly or pools in the leg veins. Elevating the lower legs to the hip level or higher prevents blood from pooling in the lower legs.
DVT in the lower leg is treated with anticoagulants.
Deep vein thrombosis results from a lack of blood movement, damage to veins, and increased coagulation of the blood. Home treatment for DVT can improve blood flow in the legs. This includes leg exercises, walking, leg elevation, and use of compression stockings.
Venous blood clots do dissolve naturally. The body produces an enzyme, plasmin, which breaks up blood clots. There is no natural remedy or home treatment that can speed up this process.
Deep vein thrombosis can be cured. Patients are put on anticoagulant medications for three to six months while the body naturally breaks up the blood clot.
Dehydration thickens the blood and raises the risk of blood clotting.
Deep vein thrombosis is an urgent medical condition that requires prompt diagnosis and treatment.
Deep vein thrombosis results from a combination of slow blood movement in the leg veins, vein damage, and greater blood coagulation. Leg exercises, including walking, increases the rate of blood flow through the legs. Exercise is a standard component of DVT therapy to prevent the blood clot from growing or new blood clots from forming.
Despite popular claims, lemon juice does not dissolve, prevent, or affect deep vein blood clots in any way.
Marissa Walsh, Pharm.D., BCPS-AQ ID, graduated with her Doctor of Pharmacy degree from the University of Rhode Island in 2009, then went on to complete a PGY1 Pharmacy Practice Residency at Charleston Area Medical Center in Charleston, West Virginia, and a PGY2 Infectious Diseases Pharmacy Residency at Maine Medical Center in Portland, Maine. Dr. Walsh has worked as a clinical pharmacy specialist in Infectious Diseases in Portland, Maine, and Miami, Florida, prior to setting into her current role in Buffalo, New York, where she continues to work as an Infectious Diseases Pharmacist in a hematology/oncology population.
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