Deep vein thrombosis
DEEP VEIN THROMBOSIS
DEEP VEIN THROMBOSIS DEFINITION
Deep vein thrombosis (DVT) occurs when a blood clot (thrombus) forms in one or more of the deep veins in your body, usually in your legs. Deep vein thrombosis can cause leg pain or swelling, but may occur without any symptoms.
Deep vein thrombosis can develop if you have certain medical conditions that affect how your blood clots. Deep vein thrombosis can also happen if you don’t move for a long time, such as after surgery, following an accident, or when you are confined to a hospital or nursing home bed.
Deep vein thrombosis is a serious condition because blood clots in your veins can break loose, travel through your bloodstream and lodge in your lungs, blocking blood flow (pulmonary embolism).
DEEP VEIN THROMBOSIS CAUSES
Deep vein thrombosis (DVT) is a blood clot that forms in a vein inside a muscle. It usually happens in your legs, but you can also get them in your arms, chest, and other areas of your body.
It can be serious. It may make your leg hurt and swell. The clot might move and get stuck in a blood vessel in your lungs, brain, or heart. That could cause organ damage and even death — within hours.
The main cause of DVT is poor blood flow. When it slows, blood can pool, which gives the cells a chance to stick together and start clotting. Someone whose blood clots easily is also at greater risk.
You’re more likely to get a clot after any surgery that reduces blood flow to a part of your body or after major surgery on your legs, belly, or chest. That includes orthopedic surgery, such as a hip replacement, and abdominal surgery where you’ll be under general anesthesia for more than 30 minutes.
The procedure could set tissue, protein, and fats loose in your veins. If the wall of a vein gets accidently damaged, it can release chemicals that trigger blood clotting.
Following major surgery, you’ll probably be on bed rest. You won’t be using your leg muscles, and that slows your blood flow.
DEEP VEIN THROMBOSIS PATHOPHYSIOLOGY
Over a century ago, Rudolf Virchow described 3 factors that are critically important in the development of venous thrombosis: (1) venous stasis, (2) activation of blood coagulation, and (3) vein damage. These factors have come to be known as the Virchow triad.
Venous stasis can occur as a result of anything that slows or obstructs the flow of venous blood. This results in an increase in viscosity and the formation of microthrombi, which are not washed away by fluid movement; the thrombus that forms may then grow and propagate. Endothelial (intimal) damage in the blood vessel may be intrinsic or secondary to external trauma. It may result from accidental injury or surgical insult. A hypercoagulable state can occur due to a biochemical imbalance between circulating factors. This may result from an increase in circulating tissue activation factor, combined with a decrease in circulating plasma antithrombin and fibrinolysins.
Over time, refinements have been made in the description of these factors and their relative importance to the development of venous thrombosis. The origin of venous thrombosis is frequently multifactorial, with components of the Virchow triad assuming variable importance in individual patients, but the end result is early thrombus interaction with the endothelium. This interaction stimulates local cytokine production and facilitates leukocyte adhesion to the endothelium, both of which promote venous thrombosis. Depending on the relative balance between activated coagulation and thrombolysis, thrombus propagation occurs.
Decreased vein wall contractility and vein valve dysfunction contribute to the development of chronic venous insufficiency. The rise in ambulatory venous pressure causes a variety of clinical symptoms of varicose veins, lower extremity edema, and venous ulceration.
Development of thrombosis
Thrombosis is the homeostatic mechanism whereby blood coagulates or clots, a process crucial to the establishment of hemostasis after a wound. It may be initiated via several pathways, usually consisting of cascading activation of enzymes that magnify the effect of an initial trigger event. A similar complex of events results in fibrinolysis, or the dissolution of thrombi. The balance of trigger factors and enzymes is complex. Microscopic thrombus formation and thrombolysis (dissolution) are continuous events, but with increased stasis, procoagulant factors, or endothelial injury, the coagulation-fibrinolysis balance may favor the pathologic formation of an obstructive thrombus. Clinically relevant deep venous thrombosis is the persistent formation of macroscopic thrombus in the deep proximal veins.
For the most part, the coagulation mechanism consists of a series of self-regulating steps that result in the production of a fibrin clot. These steps are controlled by a number of relatively inactive cofactors or zymogens, which, when activated, promote or accelerate the clotting process. These reactions usually occur at the phospholipid surface of platelets, endothelial cells, or macrophages. Generally, the initiation of the coagulation process can be divided into 2 distinct pathways, an intrinsic system and an extrinsic system
DEEP VEIN THROMBOSIS SYMPTOMS
Deep vein thrombosis signs and symptoms can include:
- Swelling in the affected leg. Rarely, there may be swelling in both legs.
- Pain in your leg. The pain often starts in your calf and can feel like cramping or a soreness.
Deep vein thrombosis may sometimes occur without any noticeable symptoms.
DEEP VEIN THROMBOSIS DIAGNOSIS
If you think that you may have deep vein thrombosis (DVT), see your GP as soon as possible.
Your GP will ask you about your medical history and your symptoms. However, it can be difficult to diagnose DVT from symptoms alone, so your GP may recommend one of the following tests:
A specialised blood test known as the D-dimer test is used to detect pieces of blood clot that have been broken down and are loose in your bloodstream. The larger the number of fragments found, the more likely it is that you have a blood clot in your vein.
However, the D-dimer test is not always reliable. Blood clot fragments can increase after an operation or injury, or if there is inflammation in your body (when your immune system reacts to an infection or disease). This means that additional tests, such as an ultrasound scan, need to be performed to confirm DVT.
If the D-dimer test is negative, it rules out the possibility of a DVT in up to 97% of cases.
An ultrasound scan can be used to detect clots in your veins. A special type of ultrasound known as a Doppler ultrasound can also be used to find out how fast the blood is flowing through a blood vessel. This helps doctors identify when blood flow is slowed or blocked, which could be caused by a blood clot.
If the results of a D-dimer test and ultrasound scan cannot confirm a diagnosis of DVT, a venogram might be used.
A special dye is injected into a vein in your foot, which travels up the blood vessels of your leg. An X-ray is taken to see the dye. If there is a blood clot in your leg, the dye will not be able to flow round it and will show up as a gap in your blood vessel.
DEEP VEIN THROMBOSIS TREATMENT
Deep vein thrombosis treatment is aimed at preventing the clot from getting any bigger, as well as preventing the clot from breaking loose and causing a pulmonary embolism. After that, the goal becomes reducing your chances of deep vein thrombosis happening again.
Deep vein thrombosis treatment options include:
- Blood thinners.Medications used to treat deep vein thrombosis include the use of anticoagulants, also sometimes called blood thinners, whenever possible. These are drugs that decrease your blood’s ability to clot. While they don’t break up existing blood clots, they can prevent clots from getting bigger or reduce your risk of developing additional clots.
Usually, you’ll first be given a shot or infusion of the blood thinner heparin for a few days. After starting heparin injections, your treatment may be followed by another injectable blood thinner, such as enoxaparin (Lovenox), dalteparin (Fragmin) or fondaparinux (Arixtra). Other blood thinners can be given in pill form, such as warfarin (Coumadin, Jantoven) or rivaroxaban (Xarelto). Newer blood thinners also may offer additional options in the near future.
You may need to take blood thinners for three months or longer. If you’re prescribed any of these blood thinners, it’s important to take your medication exactly as your doctor instructs. Blood-thinning medications can have serious side effects if you take too much or too little.
You may need periodic blood tests to check how long it takes your blood to clot. Pregnant women shouldn’t take certain blood-thinning medications.
- Clotbusters. If you have a more serious type of deep vein thrombosis or pulmonary embolism, or if other medications aren’t working, your doctor may prescribe different medications.
One group of medications is known as thrombolytics. These drugs, called tissue plasminogen activators (TPA), are given through an IV line to break up blood clots or may be given through a catheter placed directly into the clot. These drugs can cause serious bleeding and are generally used only in life-threatening situations. For these reasons, thrombolytic medications are only given in an intensive care ward of a hospital.
- Filters. If you can’t take medicines to thin your blood, a filter may be inserted into a large vein — the vena cava — in your abdomen. A vena cava filter prevents clots that break loose from lodging in your lungs.
- Compression stockings. These help prevent swelling associated with deep vein thrombosis. These stockings are worn on your legs from your feet to about the level of your knees.
This pressure helps reduce the chances that your blood will pool and clot. You should wear these stockings during the day for at least two to three years if possible. Compression stockings can help prevent postphlebitic syndrome.