Acute Deep Vein Thrombosis

Acute Deep Vein Thrombosis

Vishal Kapur and Sagar Goyal

Division of Cardiology, The Zena and Michael A. Weiner Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA


Acute deep venous thrombosis (DVT) is a life‐threatening condition that can have serious potential consequences. Early diagnosis and treatment form the cornerstone of disease management. The introduction of direct oral anticoagulation and advancement in invasive techniques have improved the outcomes in this subgroup of patients. This chapter overviews the comprehensive management of patients with acute DVT.

Accurate diagnosis of lower‐extremity DVT is extremely important, given the potentially fatal risks of untreated DVT in the form of pulmonary embolism (PE) and the risks of anticoagulation used for its treatment (e.g. major or life‐threatening bleeding).

Lower‐extremity DVT and PE are two manifestations of venous thromboembolism (VTE). The diagnosis of VTE is made in a sequence of steps including assessment of the pretest probability, followed by D‐dimer testing and imaging as appropriate (Figure 14.1).

Overall, VTE can be excluded in 29% (95% CI, 20–40%) of patients with suspected DVT and 28% (95% CI, 20–37%) of those with suspected PE using diagnostic algorithms including pretest probability assessment and D‐dimer testing (Figure 14.1) [2, 3]. The remaining patients require compression ultrasonography or computed tomography pulmonary angiography (CTPA) to determine whether VTE is present [46].

When VTE is diagnosed, immediate initiation of anticoagulant therapy is imperative.

Schematic illustration of diagnostic management of patients with suspected DVT or PE [1].

Figure 14.1 Diagnostic management of patients with suspected DVT or PE [1].

Treatment Strategy

There are three phases of VTE treatment: the initial (first 5–10 days), long‐term (from the end of acute treatment to 3–6 months), and extended (beyond 3–6 months) periods. The benefits of anticoagulation, including prevention of clot extension, PE, recurrent VTE, hemodynamic collapse, and death, should be carefully weighed against the risk of bleeding to determine the choice of anticoagulant and the duration of therapy (Figure 14.2).

VTE events are often classified as being “provoked” by a transient or persistent risk factor or as “unprovoked” in the absence of any identifiable risk factors for VTE to estimate the risk of recurrent VTE and guide decisions on treatment duration [7]. In patients with VTE provoked by surgery, the risk of recurrence after treatment is low (<1% after one year and 3% after five years); those with VTE caused by a nonsurgical transient risk factor, such as immobilization, pregnancy, or estrogen therapy, have an intermediate risk of recurrent VTE (5% after one year and 15% after five years) [8]. In both situations, anticoagulation is recommended for only three months, as previous randomized trials showed that major bleeding risk during extended anticoagulant treatment beyond this period outweighed the risk of recurrent VTE [5, 6, 8, 9]. Patients with cancer‐associated VTE have a high risk of recurrence (15% annualized), and therapy may be given until the cancer is cured [5, 6, 8].

Schematic illustration of approach to initial treatment of venous thromboembolism (onset through days 5–10).

Figure 14.2 Approach to initial treatment of venous thromboembolism (onset through days 5–10).

When a patient does not have any identifiable risk factors for VTE, the event is classified as unprovoked.

Patients with a first unprovoked VTE have a high risk of recurrence of VTE (10% after one year and 30% at five years) and should therefore receive indefinite therapy unless the bleeding risk is high [5, 6, 8]. The risk in men is at least double than that in women (Figure 14.3).

Schematic illustration of approach to long-term and extended treatment of VTE (after initial treatment).

Figure 14.3 Approach to long‐term and extended treatment of VTE (after initial treatment).

Initial and Long‐Term Treatment of VTE

Oral Anticoagulants

Over the past decade, direct oral anticoagulants (DOACs), including the direct thrombin inhibitor dabigatran and the factor Xa inhibitors rivaroxaban, apixaban, and edoxaban, have been studied and are now recommended by the 2016 American College of Chest Physicians and the 2014 and 2017 European Society of Cardiology guidelines for both DVT and PE [5, 8, 9]. However, vitamin K antagonists remain the preferred treatment for patients with severe renal impairment. Similarly, DOACs are generally avoided in patients with concomitant use of potent P‐glycoprotein inhibitors or cytochrome P4503A4 inhibitors or inducers, including azole antimycotics (e.g. ketoconazole), several protease inhibitors used for human immunodeficiency virus treatment (e.g. ritonavir), and antiepileptic drugs (in particular, phenytoin and carbamazepine), because they can alter plasma levels of DOACs.

Compared with initial LMWH followed by long‐term VKA treatment, DOACs are noninferior for recurrent VTE and are associated with a lower risk of major bleeding, as defined by the International Society on Thrombosis and Hemostasis [10] (absolute risk, 1.1% vs. 1.8%; risk ratio, 0.62; 95% CI, 0.45–0.85) in the first months of VTE treatment [11]. All‐cause mortality and case‐fatality rates of recurrent VTE or major bleeding with DOACs are comparable with rates with LMWH/VKA [12]. DOAC therapy is currently more expensive than treatment with VKAs. Monthly costs range between $333 and $419 with DOACs, whereas generic VKAs cost $8 per month [13].

These agents were developed according to two different regimens for the treatment of VTE (Table 14.1) [1419]. The single‐drug approach consists of an initial treatment period with high‐dose DOACs followed by a maintenance dose of the same agent with no need for parenteral anticoagulation. The sequential approach includes an initial treatment with LWMH or fondaparinux for 5–10 days followed by a maintenance dose of DOACs. Apixaban and rivaroxaban have been developed according to the single‐drug approach, and dabigatran and edoxaban have been developed according to the sequential approach [20].


Catheter‐directed thrombolysis as initial treatment of acute DVT is currently recommended only for patients with threatened limb loss [8]. A Cochrane review including patients with acute proximal DVT showed that thrombolysis plus anticoagulation compared with anticoagulation alone may reduce postthrombotic syndrome by one‐third (risk ratio, 0.66; 95% CI, 0.53–0.81) [21]. However, thrombolysis appeared to have no effect on the occurrence of PE, recurrent DVT, or death and, moreover, has an increased bleeding risk [11]. Results did not differ between thrombolytic agents and route of administration (systemic vs. locoregional vs. catheter‐directed) [21]

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Oct 25, 2023 | Posted by in CARDIOLOGY | Comments Off on Acute Deep Vein Thrombosis

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