Approach

The mainstay of treatment for DVT is anticoagulation. Interim therapeutic anticoagulation should be started (as long as there are no contraindications) pending results of investigations if:[19]

  • The patient is categorized as "DVT likely" (Wells score ≥2) and the result of venous ultrasound is not available within 4 hours

  • The patient is categorized as "DVT unlikely" (Wells score <2) and:

    • D-dimer level has been taken but the result is not available within 4 hours OR

    • D-dimer result is positive, and a venous ultrasound has been arranged with the result available within 24 hours

  • DVT is clinically suspected in a pregnant patient.[41]​​

Before starting interim therapeutic anticoagulation for suspected DVT, baseline blood tests should be ordered, including complete blood count, renal and hepatic function, prothrombin time, and activated partial thromboplastin time (aPTT).[19][40]

The results of these tests do not need to be seen before starting anticoagulation.[19] The results should be reviewed (and acted on if necessary) within 24 hours of starting anticoagulation.[19] If possible, an interim anticoagulant should be chosen that can be continued if DVT is confirmed.[19]

If venous ultrasound is negative, anticoagulation can be stopped.[19]

Phlegmasia cerulea dolens

Phlegmasia cerulea dolens (PCD) is a life- and limb-threatening emergency. If it is suspected, quick action is needed; the results of investigations should not be waited for before treatment is started.[40]

Supportive therapies and anticoagulation should be started immediately, and the patient should be referred to a vascular surgeon or interventional radiology. Treatment options include catheter-directed thrombolysis, pharmacomechanical-directed thrombolysis, and surgical thrombectomy (which may be combined with fasciotomy and iliac stenting), although these are generally used for PCD due to iliac vein DVT.[40][159][160][161]​​​​​​​

The affected limb should be elevated. Local resuscitation protocols should be followed, and urgent advice should be sought from the critical care team about appropriate resuscitation measures.[40]

Interventional therapies

Most cases of DVT are managed with anticoagulation alone. Guidelines differ regarding selection of patients for whom an interventional therapy, usually catheter-directed thrombolysis or pharmacomechanical intervention, is warranted. Apart from patients with limb-threatening PCD (for whom interventional therapy is indicated), patients should be selected on the basis of a large burden of thrombus affecting the ileofemoral veins, significant symptoms, low bleeding risk, and a preference for intervention.[18][162]​​ The long-term outcomes are likely similar in patients treated with intervention versus those treated with anticoagulation alone.[163]​ Interventional therapy, even with complete thrombus resolution, does not negate the need for standard anticoagulant therapy.

Proximal versus distal lower extremity DVT

Proximal DVT of the leg

  • For patients with proximal DVT of the leg, anticoagulant therapy is recommended.[18]​​

Isolated distal DVT of the leg

  • For patients with severe symptoms or risk factors for extension, anticoagulation is recommended.

  • Risk factors for extension include:[18]

    • Positive D-dimer

    • Extensive thrombosis (e.g., >5 cm long; involving multiple veins; >7 mm in maximum diameter)

    • Thrombosis close to the proximal veins

    • Absence of any reversible provoking factor

    • Active cancer

    • Past history of venous thromboembolism (VTE)

    • Inpatient status.

  • For patients with an acute isolated distal DVT of the leg but without severe symptoms or risk factors for extension, or with a high risk for bleeding, serial imaging (e.g., once weekly or with worsening of symptoms) of the deep veins for 2 weeks is suggested over anticoagulation.[18][164]​ Anticoagulation is given only if the thrombus propagates on serial ultrasound examinations.[18]

Anticoagulant therapy: general principles

Anticoagulation is the mainstay of therapy for the treatment of DVT, in both the lower and upper extremities.[41]​ Patients are treated with anticoagulants to:

  • Prevent propagation/progression of the thrombus in the deep veins in the legs

  • Reduce the risk of pulmonary embolism (PE)

  • Reduce the risk of recurrent DVT.

Anticoagulant therapy for DVT has been described in three phases: initiation, treatment (also referred to as "long-term"), and extended.[18]​​[22][41][165]​​​​

  • Initiation (from presentation to up to 5-21 days following diagnosis): goals of care are to arrest the active prothrombotic state and to inhibit thrombus propagation and embolization.

  • Treatment (initiation to 3 months): goals are to prevent new thrombus while the original clot is stabilized and intrinsic thrombolysis is under way.

  • Extended (3 months to indefinite): goal is secondary prevention of new VTE.

The recommended treatment regimens for patients with DVT have changed rapidly as new anticoagulants have become available. Care should be taken to minimize the risk of major hemorrhage throughout the treatment period and monitor for the development of heparin-induced thrombocytopenia (HIT) if unfractionated heparin (UFH) or low molecular weight heparin (LMWH) is used.[23][80]

Initiation phase of anticoagulation (from suspected diagnosis to up to 21 days)

Patients diagnosed with DVT, or who present with suspected DVT and have a high probability of disease, should receive an anticoagulant dosed according to the initiation phase of therapy, unless contraindicated.[18]

The choice of agent depends on patient factors such as clinical stability, bleeding risk, hepatic function, renal function, pregnancy, presence of cancer, obesity, concomitant drugs and the ability to monitor drug-drug interactions, and the risk of bleeding. Choice may also depend on individual physician or patient preference or recommendations in local guidelines.[18]

If treatment was initiated before diagnostic confirmation and DVT is subsequently excluded, anticoagulation can be discontinued.[18]

Recommendations for initial choice of antithrombotic therapy

  • UFH is recommended when interventional therapies (e.g., catheter-directed thrombolysis or pharmacomechanical intervention) may be utilized, or if the patient is at high risk of bleeding.

  • In stable patients, the choice of initial anticoagulant is guided by the choice for the most appropriate longer-term therapy. Generally this will be a direct oral anticoagulant (DOAC), but there are exceptions for specific patient populations.

  • DOACs (e.g., apixaban, edoxaban, rivaroxaban, dabigatran) are generally recommended over vitamin K antagonists (usually warfarin). If a DOAC is chosen, there is either an initiation phase at a higher oral dose (apixaban and rivaroxaban), or lead-in treatment with a parenteral anticoagulant for 5-10 days while treatment is established (edoxaban and dabigatran). This is then followed by oral monotherapy at treatment-phase dosing of the chosen agent.

  • For patients where warfarin is more appropriate, treatment with LMWH or fondaparinux alongside the starting dose of warfarin is needed in the initiation phase, while therapeutic anticoagulation is established.

  • Fondaparinux and argatroban are generally reserved for patients with HIT or those with a history of this condition.[166][167]

Considerations for specific anticoagulants

DOACs

  • DOACs are as effective as UFH, LMWH, and warfarin for the treatment of DVT, and are generally recommended over warfarin, UFH, and LMWH outside of special populations.[168]​ No monitoring of coagulation profile is necessary, and bleeding complications are similar or less than those of warfarin, but there is a lower or similar incidence of VTE.[169][170]​​​​​ All have a longer half-life than UFH or LMWH and a shorter half-life than warfarin, and all have a rapid onset of action.

  • Apixaban and rivaroxaban are initiated at a higher initial oral dose with no need for lead-in therapy with a parenteral anticoagulant. Edoxaban and dabigatran require lead-in therapy with a parenteral anticoagulant for 5-10 days before oral monotherapy.

  • DOACs do not interact with food; however, they do undergo some drug-drug interactions. Notable drug interactions include: strong inhibitors or inducers of P-glycoprotein (with edoxaban and dabigatran); and strong inhibitors or inducers of P-glycoprotein and CYP3A4 (with apixaban and rivaroxaban).

  • Specific reversal agents for dabigatran (idarucizumab) and the DOACs apixaban and rivaroxaban (recombinant coagulation factor Xa [andexanet alfa]) have been approved. Reversal of warfarin, in the setting of major or life-threatening bleeding, is recommended with vitamin K and prothrombin complex concentrates.[171]

Warfarin

  • In patients who will transition from UFH, LMWH, or fondaparinux to warfarin, warfarin should be started the same day that these drugs are started, unless there is a very high risk for bleeding. If bleeding risk is high, observing the patient for 1-2 days on UFH alone is advisable.

  • Three strategies can be used to select the initial dose of warfarin:[172][173] [ Cochrane Clinical Answers logo ] ​​​​​

    • A clinical algorithm calculates the estimated stable and starting dose based on several patient characteristics.

    • A genetic algorithm calculates the estimated stable and starting dose based on the results of genetic tests such as CYP450-2C9 genotype and VKORC1 haplotype, as well as clinical variables.

    • A fixed-dose approach uses initiation nomograms.

  • Use of an individualized nomogram for selecting the initial warfarin dose, and for subsequent titrations, is likely to result in better outcomes than a fixed-dose initiation, and is preferred.[173][174]​​ Tests are available that determine the genotype of the patient for cytochrome 2C9 variants and vitamin K epoxide reductase variants. However, overall, this information has not led to more rapid or safe anticoagulation compared with routine dosing. Genotyping is expensive and it takes several days to receive results.[175][176][177][178]​​ When available, employing an individualized approach to warfarin initiation may be preferred. An online tool is available to assist with warfarin initiation dosing, which utilizes clinical variables with or without the addition of genetic information. Warfarin dosing Opens in new window 

  • Once warfarin is started, it is continued concomitantly with the parenteral anticoagulant while the dose is titrated. Subsequent dosing of warfarin is based on the international normalized ratio (INR) response to each dose. The therapeutic INR range is 2-3 (target 2.5, unless concomitantly being used for anticoagulation of mechanical heart valves). UFH, LMWH, or fondaparinux should be continued for a minimum of 5 days, and until INR is 2 or greater for at least 24 hours, at which point the UFH, LMWH, or fondaparinux can be discontinued.[18]​​[179]

Heparin

  • UFH treatment is usually initiated with an intravenous weight-based loading bolus followed immediately by initiation of a weight-based continuous infusion. It also requires monitoring of aPTT or heparin-calibrated anti-Xa activity, which is used to titrate dosing to the target range.

  • LMWH and fondaparinux are dosed subcutaneously, according to patient weight.

  • Platelet count is regularly measured during treatment with any heparin (e.g., UFH, LMWH) therapy because of the possibility of HIT as a complication.

For more information on initiating anticoagulation, see Anticoagulation management principles.

Specific patient populations

Severe disease

  • For patients with higher severity of disease in whom interventional therapy is being planned or considered, UFH is preferred as most studies of interventional therapies were performed with this anticoagulant. It can also be adjusted if needed during intervention and has a relatively short half-life if bleeding occurs.[18][180]

  • Once stabilized the patient can be transitioned onto an anticoagulant guided by the choice for the most appropriate longer-term therapy.

Increased risk of bleeding

  • It may be preferable to treat patients who are at increased risk of bleeding (e.g., recent surgery, peptic ulceration) with intravenous UFH initially because it has a short half-life and its effect can be reversed quickly with protamine.[41]​ Once it is clear anticoagulation is tolerated, selection of an appropriate anticoagulation regimen can take place.

Active cancer

  • In patients with VTE and active cancer (cancer-associated thrombosis), guidelines from the American College of Chest Physicians (ACCP) and the UK National Institute for Health and Care Excellence (NICE) recommend a DOAC (apixaban, edoxaban, rivaroxaban) over LMWH.[18]​​[19]​​

  • Guidance from the American Society of Clinical Oncology suggest using LMWH, UFH, fondaparinux, rivaroxaban, or apixaban for initial anticoagulation.[42]

  • DOACs (particularly edoxaban and rivaroxaban) are associated with a higher risk of gastrointestinal bleeding than LMWH. In patients with luminal gastrointestinal cancer, the ACCP recommends apixaban or LMWH as the preferred agents.[18][181]

Renal impairment

  • For patients with renal impairment (i.e., creatinine clearance <30 mL/minute), intravenous or subcutaneous UFH, followed by warfarin, is the preferred anticoagulant regimen.

  • Apixaban is approved for use in severe renal disease and has outcomes similar to UFH followed by warfarin, and represents an alternative option.[182]

  • LMWH has unpredictable renal clearance among patients with renal failure. For patients on LMWH, laboratory monitoring of the anticoagulant effect (i.e., by anti-factor Xa assay) is generally not necessary, but should be considered in patients with severe renal impairment and those with moderate renal impairment if LMWH use is prolonged (i.e., >10 days).[183]

  • Fondaparinux, rivaroxaban, edoxaban, and dabigatran are generally not recommended in people with severe renal impairment, and patients with creatinine clearance <25 to 30 mL/minute were excluded from large randomized controlled trials. Apixaban, edoxaban, and rivaroxaban may be used in some patients with renal impairment; however, consult local guidance as recommendations vary between countries.

Hepatic impairment

  • LMWH or UFH are recommended in these patients, and should be overlapped with warfarin, unless cancer is present.[18]

  • Warfarin should be used cautiously if the baseline INR is elevated; extended-duration LMWH may be preferred.​[20][184]

  • DOACs are generally not recommended in patients with hepatic impairment, especially those with moderate-to-severe impairment (Child-Pugh class B or C).[18]​​[41]​​

Obesity

  • UFH or LMWH are options in patients living with obesity. The use of actual body weight is appropriate when calculating the therapeutic dose in obese patients. Laboratory monitoring of the anticoagulant effect of LMWH (i.e., by anti-factor Xa assay) is generally not necessary, but should be considered in patients with class III obesity (body mass index [BMI] 40 or above).[20]​​[81][183]

  • There is no known weight limit for the use of DOACs; however, they have not been extensively studied in patients with extreme weights. The Scientific and Standardization Committee of the International Society on Thrombosis and Haemostasis recommends dabigatran and edoxaban are avoided in patients with BMI >40 kg/m² or weight >120 kg given the lack of clinical outcomes data. Rivaroxaban and apixaban can be considered in these patients.[185]​ Two large, retrospective, matched cohort studies showed similar outcomes in patients receiving rivaroxaban, apixaban, or dabigatran versus warfarin, though no prospective comparative evidence exists.[186][187]​​​​ If DOACs are used in these patients, appropriate drug-specific monitoring may be considered, though there is limited evidence that drug-specific levels predict important clinical outcomes.[81]

Pregnancy

  • Women who develop VTE and who are pregnant or may become pregnant can be treated with subcutaneous UFH or LMWH monotherapy.[188] Because of changes in the pharmacodynamics of subcutaneous UFH during pregnancy, LMWH is preferred.[18]​​[189]​ Routine measurement of peak anti-Xa activity for pregnant or postpartum patients on LMWH is not recommended except in women at extremes of body weight (i.e., <50 kg or >90 kg) or with other complicating factors (e.g., renal impairment or recurrent VTE) that put them at high risk.

  • Warfarin is known to cause teratogenic effects when used in pregnancy and should be avoided.

  • If breastfeeding is planned, then LMWH is the agent of choice. Warfarin is an alternative; it is minimally secreted in breast milk, but there is extensive clinical experience suggesting no ill effect in the breastfeeding infant.[153][190]

  • The safety of DOACs in pregnancy and lactation is not known, and these should be avoided in both situations (but can be used in the postpartum period if the patient is not breastfeeding).

Heparin-induced thrombocytopenia (HIT)

  • In patients with HIT, the recommended anticoagulant is argatroban. Fondaparinux, apixaban, rivaroxaban, and dabigatran have also been suggested, although they are not approved for patients with active HIT.[166][167]​ Argatroban is preferred for patients with HIT with high bleeding risk or renal impairment. See Heparin-associated thrombocytopenia.

For more information on initiating anticoagulation, see Anticoagulation management principles.

Treatment phase of anticoagulation (initiation to 3 months)

The ACCP guidelines recommend that patients who do not have a contraindication are given a 3-month treatment phase of anticoagulation. DOACs are recommended over warfarin.[18]

During the treatment phase, follow-up and reevaluation are based on the patient's level of risk for bleeding, comorbidities, and the anticoagulant agent selected.[18]

  • Patients taking dabigatran or edoxaban should remain on the same dose started during the initiation phase with a parenteral agent, unless renal function substantially declines, warranting discontinuation.[41]​​

  • Patients taking apixaban and rivaroxaban should have their dose adjusted to the treatment-phase dose.[41]

  • Patients treated with warfarin should continue to report for INR measurements. The frequency of measurements depends on the stability of INR values at each visit. Commonly, INR is measured 1-2 times weekly after initial dose titration, with the time between measurements progressively extending if values remain in range. The target range of 2-3 (target INR 2.5) is maintained, unless concomitantly being used for anticoagulation of mechanical heart valves.[41]

  • If extended LMWH is used (e.g., in patients who cannot take oral drugs, patients with cancer with concomitant drugs that have significant drug-drug interaction that precludes DOAC use, patients with an intraluminal gastrointestinal [GI] malignancy and high risk of GI bleeding, and patients with severe liver disease where neither warfarin nor DOACs can be used), the dose depends upon the agent:

    • If dalteparin is chosen, the dose is reduced after 1 month.

    • If enoxaparin is chosen, some experts suggest reducing the initial dose after 1 month, though this is based on opinion only, and the initial dose can be continued.

  • LMWH dose should be adjusted to change in the patient's weight or creatinine clearance.

The treatment phase of anticoagulation differs in pregnant patients. Patients with pregnancy-associated VTE undergo treatment-phase anticoagulation for at least 3 months, or until 6 weeks postpartum, whichever is longer.[188][189]​​ At the conclusion of this phase in the postpartum, decisions are made according to whether the patient is planning to breastfeed. Guidelines differ on offering extended anticoagulation for VTE associated with pregnancy, as there is an intermediate risk of future unprovoked VTE.[21][180]

Once the treatment phase has been completed, all patients should be evaluated for extended-phase therapy.[18]

Extended phase of anticoagulation (3 months to indefinite)

The goal for continuation of anticoagulant therapy into the extended phase (i.e., beyond the first 3 months and with no scheduled stop date) is secondary prevention of VTE.

The ACCP guidelines recommend that patients who are diagnosed with DVT in the absence of transient provocation (unprovoked DVT or provoked by a persistent risk factor) are given extended-phase anticoagulation.[18]​ These patients should be given a DOAC, unless contraindicated, in which case they should be given warfarin.​

Extended-phase anticoagulation is not recommended in patients with DVT who are diagnosed in the context of a major or a minor transient risk factor.[18]

The ACCP guidelines recommend using reduced-dose apixaban or rivaroxaban for patients receiving apixaban or rivaroxaban; the choice of a particular drug and dose should consider the patient's BMI, renal function, and adherence to the dosing regimen.[18] The decision to start or continue extended therapy should be based on patient preference and the predicted risk of recurrent VTE or bleeding.[18]

The continued use of extended-phase anticoagulation should be reassessed at least annually, as well as at any time there is a significant change in the patient's health status.[18]​​

  • The evidence to continue extended therapy beyond 4 years is uncertain. The ACCP recommends shared decision-making, taking into account the patient's values and preferences. Patients should be periodically reassessed for bleeding risk, burdens of therapy, and any change in values and preferences.[18]

Provoked (minor or major transient risk factors) DVT

  • Anticoagulation is discontinued after a course of at least 3 months. There is consensus that patients who have an index DVT that occurs in the setting of a major transient provocation have a relatively low risk of developing recurrent VTE in the next 5 years, with estimates in the range of 15%.[18]​ In these patients, a time-limited course of anticoagulation of at least 3 months is suggested.[18]

  • The presence of a hereditary thrombophilia does not alter this recommendation, and guidelines recommend against testing for thrombophilias in patients with a DVT occurring following a major transient provocation.​[55][56]

  • The risk of recurrent VTE is modestly higher in patients who sustain DVT in the setting of a minor transient provocation. Guidelines differ on offering extended anticoagulation for VTE associated with minor transient provoking risk factors.[21][180]

Unprovoked (no identifiable risk factor) DVT

  • Patients with an unprovoked DVT of the leg who have been started on anticoagulation therapy should be assessed after 3 months for continued treatment.[18]​​

  • For patients with a first proximal DVT that is unprovoked and who have a low or moderate bleeding risk, extended anticoagulant therapy is recommended (with no scheduled stop date and reassessment of ongoing therapy at regular intervals, such as annually). For those patients with a high bleeding risk, 3 months' treatment only is recommended.

  • For patients with a second unprovoked DVT who have a low or moderate bleeding risk, extended anticoagulant therapy is recommended (with no scheduled stop date) over 3 months' treatment. In patients with a high bleeding risk, 3 months' treatment only is recommended.

  • Many studies have attempted to identify subgroups of patients with unprovoked VTE who do not need to be treated indefinitely with oral anticoagulation. There is strong evidence that the risk of recurrent VTE is higher in the following patients: male sex; those with a diagnosis of a proximal DVT (versus isolated calf DVT); those with ultrasound evidence of residual clot; those who have an elevated D-dimer 1 month after stopping a 3- to 6-month course of oral anticoagulation; and those who had an unprovoked DVT.[18][41]​​​ Several risk assessment models have been developed for this purpose, including the DASH score, the Vienna Prediction Model, and the “Men Continue and HER-DOO2” model.[191] The latter model identifies a subset of women with low risk for recurrent VTE after an initial unprovoked event, and one prospective validation study of this model was published.[192]

Cancer-associated VTE

  • Cancer represents a persistent provocation for VTE until cured. Among patients who are diagnosed with DVT and have an active cancer (e.g., cancer under any form of active therapy or palliation) there is a very high risk for recurrent VTE and indefinite anticoagulation is recommended. Guidelines recommend using a DOAC (e.g., apixaban, edoxaban, rivaroxaban) or LMWH for at least the initial 6 months of therapy.[18]​​[19] 

  • A DOAC (apixaban, edoxaban, rivaroxaban) or LMWH is the preferred agent for patients with a higher risk of bleeding, especially those with gastrointestinal cancers. LMWH is preferred for those with potential drug-drug interactions with DOACs.[18][181][193][194][195]

Bleeding risk

  • When assessing bleeding risk, the following factors should be considered:[18]​​

    • Age >65 years

    • Previous bleeding

    • Cancer (especially gastrointestinal cancer with DOACs)

    • Renal failure

    • Liver failure

    • Thrombocytopenia

    • Previous stroke

    • Diabetes mellitus

    • Anemia

    • Antiplatelet therapy

    • Poor anticoagulant control

    • Comorbidity with reduced functional capacity

    • Recent surgery

    • Frequent falls

    • Alcohol misuse

    • Use of nonsteroidal anti-inflammatory drugs

    • Uncontrolled hypertension.

  • Patients with none of these risk factors are considered low risk; one risk factor renders a patient moderate risk; and two or more risk factors renders a patient high risk.

  • Risk assessment models to assess bleeding risk derived from atrial fibrillation populations are not known to be accurate in patients with DVT. VTE-specific bleeding risk assessment models have been developed.[196][197][198]​​​​​

  • Drug-drug interactions may increase the risk of bleeding in patients receiving anticoagulants, and both the pharmacodynamic (e.g., nonsteroidal anti-inflammatory drugs, selective serotonin-reuptake inhibitors) and pharmacokinetic (e.g., amiodarone, rifampin) interactions should be thoroughly evaluated prior to initiation.[199][200]​​​

Inferior vena cava filters

An inferior vena cava (IVC) filter can be placed in patients with:​​[18][22][41]​​​​[201][202]​​​​

  • acute proximal DVT (e.g., diagnosed in the preceding 1 month) who have a contraindication to anticoagulation therapy (absolute contraindications to anticoagulation include active major bleeding, severe thrombocytopenia, high bleeding risk, central nervous system lesion)

  • acute PE and an absolute contraindication to anticoagulant therapy, such as active major bleeding

  • confirmed recurrent PE despite adequate anticoagulation.

The ACCP guidelines recommend using an IVC filter only for patients with acute PE (e.g., diagnosed in the preceding 1 month) and an absolute contraindication to anticoagulant therapy (e.g., active major bleeding, severe thrombocytopenia, high bleeding risk, central nervous system lesion). The ACCP recommends against the use of IVC filters in addition to anticoagulation in patients with acute DVT of the leg.​​[18]​ Other guidelines consider relative indications for IVC filter use to include massive PE with residual deep venous thrombus in a patient at risk for further PE, free-floating iliofemoral or IVC thrombus, and severe cardiopulmonary disease and DVT (e.g., cor pulmonale with pulmonary hypertension).[203]

Some centers insert IVC filters intraoperatively or immediately postoperatively in patients who undergo surgical pulmonary embolectomy.[204][205][206]​​​​

IVC filter placement should take place as early as possible if it is the only treatment that can be initiated. There is little evidence available to suggest the ideal time for placement. Observational studies suggest that insertion of a venous filter might reduce PE-related mortality rates in the acute phase but with an associated increase in the risk of filter-related VTE.[207][208]​​​

Complications associated with permanent IVC filters are common, although they are rarely fatal.[208] Early complications (including insertion-site thrombosis) occur in approximately 10% of patients. Late complications are more frequent and include recurrent DVT (approximately 20% of patients) and post-thrombotic syndrome (up to 40% of patients).[209][210]​​​​ Occlusion of the IVC filter affects approximately 22% of patients at 5 years and 33% at 9 years, regardless of the use and duration of anticoagulation.[210]

Post-filter anticoagulation should be considered on a case-by-case basis according to relative and absolute contraindications.[211]​ Anticoagulation should be initiated if the contraindication resolves or if a risk/benefit analysis suggests this to be a reasonable course.[18]​​​ When retrievable filters are used, they should be removed if anticoagulation has been instituted and once it is clearly being tolerated.[22]

Hospitalization versus outpatient therapy

Most cases of DVT are amenable to treatment at home, rather than in the hospital.[41]​​ Outcomes are at least as good as those achieved with hospitalization, including improved patient satisfaction.[212] [ Cochrane Clinical Answers logo ] [Evidence C]

A minority of patients with acute DVT require hospitalization. Criteria for hospitalization:

  • DVT that is best treated with intravenous UFH.

  • Suspected or confirmed concomitant PE, especially with cardiopulmonary compromise (tachycardia, tachypnea, signs of right heart failure); in many centers, patients with PE are hospitalized only if there is a high Pulmonary Embolism Severity Index (86 or greater).[19][213][214][215][216][217]​​ See Pulmonary embolism. 

  • DVT that will undergo interventional therapy (e.g., catheter-directed thrombolysis).

  • Highly symptomatic DVT (e.g., severe pain and edema in the presence of acute DVT requiring inpatient analgesia), or phlegmasia cerulea dolens.

  • Inability to educate the patient adequately in the outpatient or emergency department setting regarding ongoing anticoagulant therapy.

  • Coexisting comorbidity requiring hospital management.

  • Presence of risk factor for bleeding that requires close observation in the hospital (e.g., chronic liver disease with or without varices, recent or prior gastrointestinal bleeding, bleeding disorder, malignancy, recent stroke, or prior intracranial hemorrhage).

Antiplatelet therapy

If the decision is to stop extended-phase anticoagulation in patients with an unprovoked proximal DVT, the ACCP guidelines recommend aspirin (unless contraindicated) to prevent recurrent DVT.[18]​ The benefits of using aspirin should be balanced against the risk of bleeding and inconvenience of use. Aspirin should not, however, be considered a reasonable alternative for patients who are willing to undergo extended anticoagulation therapy, as aspirin is much less effective. The use of aspirin should in any case be reassessed when patients stop anticoagulant therapy because it might have been stopped when anticoagulant therapy was started.[18]

Gradient stockings and physical activity

Gradient (graduated compression) stockings are not recommended for the prevention of post-thrombotic syndrome by the ACCP guidelines. There is no evidence that their use reduces the risk for recurrent DVT, and the highest-quality randomized controlled trial on the topic did not demonstrate a reduction in the incidence of post-thrombotic syndrome.[218]​ However, they may be useful for patients with acute or chronic symptoms of DVT.[18]​​ [ Cochrane Clinical Answers logo ] ​​​​ Studies of gradient stockings have usually employed 30-40 mmHg stockings, worn while upright, for 2 years. However, patients may have difficulty complying with this regimen, and shorter-duration therapy or lower degrees of compression can be considered.[219]​ It is important to remember that there are possible risks and complications associated with use of compression stockings; they should only be used if benefits outweigh risks.[220]

Early walking exercise is considered safe in patients with acute DVT.​[41]​​[221]​​ It does not increase leg symptoms acutely in patients with a previous DVT, and may help to reduce post-thrombotic syndrome.[221][222][223][224]

Patients with recurrent VTE on anticoagulant therapy

Recurrent VTE is unusual among patients receiving therapeutic-dose anticoagulant therapy, except in cancer (7% to 9% on-therapy recurrence with LMWH).[18]​​[22][225]​​ In addition to definitively establishing the presence of recurrent VTE, consideration should be given to compliance with anticoagulant therapy or the presence of underlying malignancy and the presence of any drugs that may diminish the anticoagulant effect of therapy.[18]

ACCP guidelines recommend a temporary switch to LMWH (for at least 1 month) for patients with recurrent VTE who are thought to be compliant with a non-LMWH anticoagulant (or within the therapeutic range if receiving warfarin therapy).[18]​ An increased dose of LMWH is appropriate for patients with recurrent VTE who have been receiving LMWH.[18]

Recurrent VTE following discontinuation of anticoagulant therapy

For patients who are no longer receiving anticoagulant therapy and experience a second VTE with no identifiable risk factor (i.e., unprovoked), guidelines recommend the following anticoagulant treatment durations:[18][22]

  • Low or moderate bleeding risk: extended anticoagulant therapy with periodic reassessment to review risk-benefit ratio

  • High bleeding risk: stop anticoagulation after 3 months.

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