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  1. Which hospitalized patients are at risk for venous thromboembolism?

  2. Who is at increased risk for complications from thromboprophylaxis?

  3. How do you make sure that thromboprophylaxis is prescribed to all patients who should get it?

Many patients have an increased baseline propensity for thrombosis due to underlying hypercoagulable states, the majority of which are acquired. An acute insult may then result in hospitalization, which usually further increases the risk due to immobilization, procedures including central venous catheter placement or pacemaker, and/or administration of certain drugs. The main question in most patient groups detailed below is whether they can expect a net benefit from pharmacologic thromboprophylaxis, mainly low-molecular-weight heparins (LMWHs). Ideally, one has to balance the risk and consequences of venous thromboembolism (VTE) with the risk of bleeding and other complications of anticoagulants in every patient, while also taking the values and preferences of that patient into consideration. To facilitate this balancing process, institutions and national and international organizations have developed guidelines for the use of thromboprophylaxis. The use of these guidelines and local protocols has greatly improved patient outcomes, mainly by increasing the use of pharmacologic thromboprophylaxis in patients at risk for VTE. The authors strongly advise the development and implementation of a local protocol.

Deficiencies of Natural Inhibitors of Coagulation

Less than 1% of the general population has a congenital deficiency of one of the natural inhibitors of coagulation: antithrombin, protein C, and protein S. These deficiencies are associated with a high lifetime risk of VTE (60–70% in a recent study) and with a high risk of recurrence after a first event (50% after 10 years). A limitation to these data is that they are derived from highly selected families, which might have led to an overestimation of risk. No population-based data are available.

Acquired protein C deficiency may be seen with disseminated intravascular coagulation (DIC), extensive deep vein thrombosis (DVT), severe liver disease, infection, malignancy, acute respiratory distress syndrome (ARDS), the hemolytic uremic syndrome, thrombotic thrombocytopenic purpura (TTP), and following L-asparaginase therapy. Although levels of protein C may decrease postoperatively, the significance is unknown. Acquired protein S deficiency may be seen with DIC and severe liver disease. Total and free protein S decrease steadily during pregnancy, with the lowest levels at term. Acquired antithrombin deficiency may be seen due to decreased synthesis (liver disease, following L-asparaginase therapy), malnutrition, or consumptive states (acute thrombosis, DIC, malignancy, pre-eclampsia). Most patients, however, will have normal antithrombin levels within 24 hours of initiation of heparin therapy. A clue to antithrombin deficiency may be inadequate or failure of activated partial thromboplastin time (PTT) to prolong during intravenous heparin therapy. Because protein C and protein S are vitamin K–dependent factors, warfarin-induced skin necrosis may occur with these deficiencies.

Patients with a known deficiency, primarily of antithrombin but to some extent also protein C and protein S, have a strong indication for pharmacologic thromboprophylaxis in ...

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