All patients with DVT are given anticoagulants, initially an injectable heparin (unfractionated or low molecular weight) for a brief period, followed by longer term treatment with an oral drug (eg, warfarin) started within 24 to 48 h. Select patients may continue treatment with a low molecular weight heparin rather than switching to an oral drug. Inadequate anticoagulation in the first 24 to 48 h may increase risk of recurrence or PE. Acute DVT can be treated on an outpatient basis unless severe symptoms require parenteral analgesics, other disorders preclude safe outpatient discharge, or other factors (eg, functional, socioeconomic) might prevent the patient from adhering to prescribed treatments.
Low molecular weight heparins (LMWHs)
Unfractionated heparin (UFH)
Non-warfarin oral anticoagulants: factor Xa inhibitors (eg, rivaroxaban, apixaban), direct thrombin inhibitors (dabigatran)
LMWHs (eg, enoxaparin, dalteparin, tinzaparin—see Table: Some Low Molecular Weight Heparin Options in Thromboembolic Disease) are the initial treatment of choice because they can be given on an outpatient basis. LMWHs are as effective as UFH for reducing DVT recurrence, thrombus extension, and risk of death due to PE. Like UFH, LMWHs catalyze the action of antithrombin (which inhibits coagulation factor proteases), leading to inactivation of coagulation factor Xa and, to a lesser degree, factor IIa. LMWHs also have some antithrombin–mediated anti-inflammatory properties, which facilitate clot organization and resolution of symptoms and inflammation.
LMWHs are typically given sc in a standard weight-based dose (eg, enoxaparin 1.5 mg/kg sc once/day or 1 mg/kg sc q 12 h or dalteparin 200 units/kg sc once/day). Patients with renal insufficiency may be treated with UFH or with reduced doses of LMWH. Monitoring is buy nolvadex d astrazeneca careers not reliable because LMWHs do not significantly prolong the results of global tests of coagulation. Furthermore, they have a predictable dose response, and there is no clear relationship between the anticoagulant effect of LMWH and bleeding. Treatment is continued until full anticoagulation is achieved with warfarin (typically about 5 days). However, evidence suggests that LMWH is effective for long-term DVT treatment in high-risk patients, such as those with cancer. Thus, LMWH may become an acceptable alternative to warfarin for some patients, although warfarin is likely to be the treatment of choice for most patients because of its low cost and oral route of administration.
UFH may be used instead of LMWH for hospitalized patients and for patients who have renal insufficiency or failure (creatinine clearance 10 to 30 mL/min) because UFH is not cleared by the kidneys. UFH is given as a bolus and infusion (see Figure: Weight-based heparin dosing.) to achieve full anticoagulation, (eg, activated PTT [aPTT] 1.5 to 2.5 times that of the reference range). For outpatients, UFH 333 units/kg initial bolus, then 250 units/kg sc q 12 h can be substituted for IV UFH to facilitate mobility; the dose does not appear to need adjustment based on aPTT. Treatment is continued until full anticoagulation has been achieved with warfarin.
Complications of heparins include bleeding, thrombocytopenia (less common with LMWHs), urticaria, and, rarely, thrombosis and anaphylaxis. Long-term use of UFH causes hypokalemia, liver enzyme elevations, and osteopenia. Rarely, UFH given sc causes skin necrosis. Inpatients and possibly outpatients should be screened for bleeding with serial CBCs and, where appropriate, testing for occult blood in stool.
Bleeding due to overheparinization can be stopped with protamine sulfate. The dose is 1 mg protamine for each milligram of LMWH given as 1 mg in 20 mL of normal saline infused slowly over 10 to 20 min. If a 2nd dose is required, it should be one half the first dose. However, the precise dose is undefined because protamine only partially neutralizes LMWH inactivation of factor Xa. During all infusions, patients should be observed for hypotension and a reaction similar to an anaphylactic reaction. Because UFH given IV has a half-life of 30 to 60 min, protamine is not given to patients receiving UFH (eg, if UFH was given > 60 min beforehand) or is given at a dose based on the amount of heparin estimated to be remaining in plasma, based on the half-life of UFH.
Fondaparinux, a parenteral selective factor Xa inhibitor, may be used as an alternative to UFH or LMWH for the initial treatment of DVT or PE. It is given in a fixed dose of 7.5 mg sc once/day (10 mg for patients> 100 kg, 5 mg for patients <</span> 50 kg). It has the advantage of fixed dosing and is less likely to cause thrombocytopenia.
Parenteral direct thrombin inhibitors (argatroban, bivalirudin, desirudin) are available but do not have a role in treatment or prevention of DVT or PE. Argatroban may be useful to treat DVT in patients with heparin-induced thrombocytopenia.
Vitamin K antagonists,including warfarin, are the drugs of choice for long-term anticoagulation for all patients except pregnant women (who should continue to take heparin) and patients who have had new or worsening venous thromboembolism during warfarin treatment (who may be candidates for an inferior vena cava filter). Warfarin 5 to 10 mg can be started immediately with heparin because it takes about 5 days to achieve desired therapeutic effect. The elderly and patients with a liver disorder typically require lower warfarin doses. Therapeutic goal is an INR of 2.0 to 3.0. INR is monitored weekly for the first 1 to 2 mo of warfarin treatment and monthly thereafter; the dose is increased or decreased by 0.5 to 3 mg to maintain the INR within this range. Patients taking warfarin should be informed of possible drug interactions, including interactions with foods and nonprescription medicinal herbs.
Non-warfarin oral anticoagulants, also called direct oral anticoagulants (DOACs), are available as alternatives to warfarin as a 1st-line treatment for the treatment of DVT and PE; not all DOACs are currently FDA-approved for this indication (see Table: Oral Anticoagulants). Drugs include factor Xa inhibitors (rivaroxaban, apixaban, edoxaban) and a direct thrombin inhibitor (dabigatran). Compared to warfarin, these drugs have been shown to give similar protection against recurrent DVT and have similar (or with apixaban, perhaps lower) risk of serious bleeding.
Their advantages are that they are effective within several hours (thus, except for dabigatran, do not require parenteral bridging treatment with a heparin), and they are given as a fixed dose (thus do not require ongoing laboratory testing).
Their disadvantages are that they are expensive, and currently (except for dabigatran and edoxaban) there are no available antidotes to reverse their anticoagulant effect in patients with life-threatening bleeding or who need urgent surgery. Idarucizumab is a humanized monoclonal antibody to dabigatran that is an effective antidote to dabigatran. Antidotes for the other direct oral anticoagulants are currently being developed. If life-threatening bleeding occurs, prothrombin complex concentrate (PCC) may be tried to decrease the anticoagulant effect of rivaroxaban and apixaban, and activated PCC may be used for dabigatran (if the antidote is not available). Rarely, hemodialysis or hemoperfusion may help decrease the anticoagulant effect of dabigatran, which is not highly protein bound; such measures are not effective on rivaroxaban and apixaban. Supportive care with intravenous fluids and packed RBC transfusions are sufficient for many bleeding episodes in patients who are receiving a DOAC.
If used, rivaroxiban 15 mg po bid is started immediately upon diagnosis and given for 3 wk followed by 20 mg po once/day for 9 wk. Apixaban 10 mg po bid is started immediately upon diagnosis and given for 7 days followed by 5 mg po bid for 6 mo. Dabigatran 150 mg po bid is given only after an initial 5 to 7 days of treatment with LMWH.
Duration of treatment varies. Patients with transient risk factors for DVT (eg, immobilization, surgery) can usually stop taking warfarin after 3 to 6 mo. Patients with nonmodifiable risk factors (eg, hypercoagulability), idiopathic (or unprovoked) DVT with no known risk factors, or recurrent DVT should take warfarin for at least 6 mo and, in selected patients, probably for life unless complications occur.
Bleedingis the most common complication. Risk factors for severe bleeding (defined as life-threatening hemorrhage or loss of ≥ 2 units of blood in ≤ 7 days) include
Age ≥ 65
History of prior GI bleeding or stroke
Coexisting anemia (Hct <</span> 30%), renal insufficiency (serum creatinine > 1.5 mg/dL), or diabetes
In patients who are actively bleeding or may be at increased risk of bleeding, anticoagulation can be reversed careers with vitamin K; the dose is 1 to 2.5 mg po if INR is 5 to 9, 2.5 to 5 mg po if INR is > 9, and 5 to 10 mg IV (given slowly to avoid anaphylaxis) if hemorrhage occurs. If hemorrhage is severe, a transfusion of coagulation factors, fresh frozen plasma, or prothrombin complex concentrate should also be given. Selected patients with overanticoagulation (INR 5 to 9) who are neither actively bleeding nor at increased risk of bleeding can be managed by omitting 1 or 2 warfarin doses and monitoring INR more frequently, then giving warfarin at a lower dose. Rarely, warfarin causes skin necrosis in patients with protein C or S deficiency or factor V Leiden mutations.
Anticoagulants and their sites of action.
LMWH = low molecular weight heparin; TF = tissue factor; UFH = unfractionated heparin.
An IVCF may help prevent PE in patients with lower extremity DVT who have contraindications to anticoagulant therapy or in patients with recurrent DVT (or emboli) despite adequate anticoagulation. An IVCF is placed in the inferior vena cava just below the renal veins via catheterization of an internal jugular or femoral vein. Some IVCFs are removable and can be used temporarily (eg, until contraindications to anticoagulation subside or resolve).
IVCFs reduce risk of acute embolic complications but can have longer-term complications (eg, venous collaterals can develop, providing a pathway for emboli to circumvent the IVCF, and increased risk of recurrent DVT). Also, IVCFs can dislodge or become obstructed by a clot. Thus, patients with recurrent DVT or nonmodifiable risk factors for DVT may still require anticoagulation despite the presence of an IVCF. A clotted filter may cause bilateral lower extremity venous congestion (including acute phlegmasia cerulea dolens), lower body ischemia, and acute kidney injury. Treatment for a dislodged filter is removal, using angiographic or, if necessary, surgical methods. Despite widespread use of IVCFs, efficacy in preventing PE is unstudied and unproved. IVCFs should be removed whenever possible.
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