Back to INTERNAL MEDICINEThree tests have good accuracy for diagnosing Deep Vein Thrombosis (DVT) in symptomatic patients : venography, impedance plethismography (IPG) and duplex venous ultrasound (B - mode imaging ). In most patients with clinically suspected venous thrombosis, venous ultrasound is the diagnostic method of choice.
In addition, the simpli -red -D-dimer test, which is performed on blood obtained by finger prick at the patient’s side and which has high sensitivity and moderate specificity, shows considerable promise as a test to rule out venous thrombosis. The D-dimer test is often false-positive after surgery or trauma, thereby limiting its value in these clinical situations
Computed Tomography (CT) and Magnetic Resonance Imaging (MRI) are also useful in some circumstances (see TABLE 1 ). Venography, although invasive, is the “gold standard” diagnostic procedure, and the best noninvasive substitute for venography is duplex ultrasound.
| Exam | Main use |
|---|---|
| Venography | Considered “gold standard”. Used when other test results are not conclusive |
| Duplex ultrasound | Most sensitive for thrombosis above the knee |
| MRI, Contrast CT | Most sensitive for thrombosis of pelvic veins |
| IPG | Good alternative to duplex ultrasound, but less specific/sensitive |
There are many other conditions that cause localized pain or edema in the lower extremities, and may be confused with DVT. These differential diagnosis include: ruptured popliteal synovial membrane or cyst (Baker’cyst), ruptured calf muscles or tendons, a severe muscle cramp, cellulitis and lymphedema. The examiner should be attempt to the patient’s history and physical signs, because in the situations described above some signs of DVT may be present but not all of them, and in each one of these conditions the management is different.
Pulmonary embolism (PE ) is a serious and frequent complication of DVT. Pulmonary emboli are detected by perfusion lung scanning in approximately 50% of patients with documented DVT, and asymptomatic venous thrombosis is found in 70% of patients with confirmed clinically symptomatic PE. Although DVT may begin frequently in the veins of the calf, it is only when the thrombosis extends above the knee that serious pulmonary embolism occurs.
Postthrombotic syndrome occurs in about 25% of cases. It is caused by venous hypertension, which occurs as a consequence of recanalization of major venous thrombi leading to patent but scarred and incompetent valves, or less frequently, persistent outflow obstruction produced by large proximal vein thrombi. This high pressure results in edema and impaired viability of subcutaneous tissues and, in its most severe forms, ulceration of venous origin.
In patients with extensive thrombosis involving the ileofemoral veins, swelling may never disappear, while in patients with less severe proximal vein thrombosis, swelling may subside after the initial event but may return in the next few years. Other manifestations of postthrombotic syndrome are pain in the calf relieved by rest and elevation of the leg, pigmentation and induration around the ankle and the lower third of the leg, and, less commonly venous claudication, a bursting calf pain that occurs during exercise (mainly in ileofemoral thrombosis).
The diagnosis of postthrombotic syndrome is sometimes obvious on clinical grounds if the symptoms are gradual in onset. However, patients can have subacute symptoms of leg pain and swelling, which may mimic acute recurrence of DVT. Although these symptoms are usually superimposed on a background of chronic pain and swelling, it may be difficult to exclude acute recurrence on clinical grounds alone, and a diagnosis of postthrombotic syndrome as the cause of the patient’ symptoms can be made only after acute recurrent venous thrombosis has been excluded (the best exam to do this is MRI ).
As soon as the diagnosis of DVT has been made, treatment (which consists of anticoagulation ) should begin, in the way to prevent local extension of the thrombus, prevent the thrombus from embolizing, and, in certain clinical circumstances, accelerate fibrinolysis. Full anticoagulation is the best treatment for DVT. Heparin is preferred to initiate treatment because of its immediate action, whereas warfarin-type drugs may not become fully effective for a considerable period of time. See TABLE 2 with the guidelines for use of anticoagulants in the treatment of DVT. Furthermore, patients should be encourage to use graduated compression stockings after the acute episode of DVT to prevent postthrombotic syndrome.
| Treatment of DVT |
|---|
| Bolus dose of heparin: 5000-10000 U EV |
| Initial maintenance dose of heparin: 32000 U EV per 24h by continuous infusion or 17000 U subcutaneously to be repeated after adjustment at 12h |
| Adjust dose of heparin at 6h according to normogram. Maintain aPTT 2 times the control |
| Repeat aPTT 6 times every hour until in therapeutic range and then daily (see nomogram) |
| Start warfarin 10mg at 24h and 10mg next day. |
| Overlap heparin and warfarin for at least 4 days |
| Perform PT daily and adjust warfarin dose to maintain INR at 2.0-3.0 |
| Continue heparin for a minimum of 5 days, then stop if INR has been in therapeutic range for at least 2 consecutive days. |
| Continue warfarin for 3 months and monitor PT daily until in therapeutic range, then 3 times during first week, twice weekly for 2 weeks , or until dose response is stable, and then every 2 weeks |
| Obtain pretreatment hemoglobin level, platelet count, PT, and aPTT. Repeat platelet count daily until heparin stopped. |
The most effective way of reducing death from PE and morbidity from postthrombotic syndrome is to institute primary prophylaxis in patients at risk for venous thromboembolism (VTE). Safe and effective forms of prophylaxis are available for patients at high risk, and primary prophylaxis is cost-effective.
Prophylaxis is achieved by either modulating activation of blood coagulation or preventing venous stasis The following prophylactic approaches are of proven value: low dose subcutaneous heparin, intermittent pneumatic compression of legs, oral anticoagulants, adjusted doses of subcutaneous heparin, (low doses which means 5000u every 12 hours), graduated compression stockings, and LMWH (low molecular weigh heparin). Antiplatelet agents such as aspirin are less effective for preventing VTE. See TABLE 3 with some clinical situations of risk for VTE and their suitable prophylaxis
| Risk for DVT | Patients | Recommendations |
|---|---|---|
| Low Risk | Hospitalized medical patients without risk factors | Ambulatory leg exercises |
| Surgical patients under age 40, surgery lasting < 30 minutes, no additional risk factors | Ambulatory leg exercises | |
| Moderate risk | Hospitalized medical patients with one or more risk factors | Low-dose heparin |
| Surgical patients over age 40 having abdominal or thoracic surgery lasting > 30 minutes | Low-dose heparin | |
| Neurosurgery or others patients with high bledding risk | Intermittent pneumatic compression of legs | |
| High risk | Hip fracture | Warfarin(low dose regimen) |
| Hip replacement | Warfarin(low dose regimen) or LMWH | |
| Knee replacement | Warfarin(low dose regimen) and intermittent pneumatic compression of the legs | |
| Open prostatectomy | intermittent pneumatic compression of the legs | |
| Ginecology Malignancy | Intermittent |
Kontos H.A.: Vascular diseases of the limbs. In: Bennett J.C., Plum F.[eds].Cecil Textbook of Medicine, pp. 353-356. W.B.Saunders Company, 1996
Creager M.A., Dzau V.J.:Vascular Diseases of the Extremities. In: Isselbacher K.L., Braunwald E., Wilson J.D., Martin J.B., Fauci A.S., Kasper D.L. [eds]. Harisson’s Principles of Internal Medicine, pp. 1140-1142. Mc Graw Hill, 1994.
Goldhaber S.Z. : Deep Vein Thrombosis and Pulmonary Embolism. Harvard Medical School - Board Review Course, 1996.
Hirsh J., Hoak J.: Management of Deep Venous Thrombosis and Pulmonary Embolism. In Circulation, 1996; 93: 2212-2245.
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