What Is the Optimal Therapy for Acute DVT?

Key Points

  • Anticoagulate immediately with LMWH or fondaparinux (IV heparin with renal insufficiency), and transition to warfarin with goal INR of 2.0 to 3.0.
  • Treat three months for most patients with a provoked or distal DVT and indefinitely for most patients with an unprovoked or cancer-related DVT.

The Case

A 55-year-old female undergoes cholecystectomy. On post-operative Day 2, she develops right-lower-extremity swelling and pain; venous ultrasound detects a proximal deep venous thrombosis (DVT). The patient denies smoking or use of hormonal medications. She has no history of venous thromboembolism (VTE), although her brother had a DVT at age 60. The hospitalist team is consulted for management of acute DVT.

Doppler ultrasound scan showing an acute deep venous thrombosis (DVT) blocking a vein.

Doppler ultrasound scan showing an acute deep venous thrombosis (DVT) blocking a vein.


VTE, including lower- and upper-extremity DVT and pulmonary embolism (PE), is one of the most common and preventable hospital diseases. DVT with PE is associated with a 10% mortality rate, and DVT with post-thrombotic syndrome can be associated with significant morbidity, including pain, edema, skin/pigment change, venous dilation, and ulcer development.1,2 Recognition of clinical symptoms and risk factors for DVT (see Table 1) in conjunction with validated clinical scoring predictors (such as the Wells Prediction Rule) and a high-sensitivity D-dimer assay can help diagnose the condition and determine the need for ultrasound.3-7

Table 1. Risk factors for VTE3

Acquired risk factors

  • Surgery
  • Immobility
  • Trauma (major trauma
  • or lower-extremity injury)
  • Hospitalization
  • Obesity
  • Malignancy (active or occult)
  • Cancer therapy (hormonal, chemotherapy, angiogenesis inhibitors)
  • Previous VTE
  • Increased age
  • Pregnancy and postpartum period
  • Estrogen-containing oral contraceptives or hormone replacement therapy
  • Selective estrogen receptor modulators
  • Erythropoiesis-stimulating agents
  • Acute medical illness
  • Inflammatory bowel disease
  • Nephrotic syndrome
  • Meyloproliferative disorders
  • Paroxysmal nocturnal hemoglobinuria
  • Central venous catheterization

Hereditary risk factors for VTE

  • Factor V Leiden mutation
  • Prothromin gene mutation
  • Protein C, S deficiency
  • Antithrombin (AT) deficiency

Pharmacologic Treatment

Anticoagulation should be initiated in all patients with VTE, regardless of patient symptoms. Anticoagulant options include:

  • Intravenous (IV) or subcutaneous (SC) unfractionated heparin (UFH);
  • SC low-molecular-weight heparins (LMWH), such as enoxaparin and dalteparin; and
  • Fondaparinux (as effective as LMWH for acute treatment of VTE).8

These agents can be used while transitioning to oral vitamin K antagonists (VKA), such as warfarin.3

The 2012 American College of Chest Physicians (ACCP) guidelines on antithrombotic therapy for VTE recommend initial therapy with LMWH or fondaparinux (rather than IV or SC UFH). The guidelines suggest that LMWH once-daily dosing is favored over twice-daily dosing, based mainly on patient convenience, although this is a weak recommendation (2C) based on the overall quality of the data. The recommendation applies only if the daily dosing of the LMWH, including tinzaparin, dalteparin, and nadroparin, is equivalent to the twice-daily dosing (i.e., dalteparin may be dosed at 100 units/kg BID vs. 200 units/kg daily). Of importance, enoxaparin has not been studied at a once-daily dose (2 mg/kg), which is equivalent to the twice-daily dosing regimen (1 mg/kg twice daily). Additionally, one study suggests that once-daily dosing of enoxaparin 1.5mg/kg might be inferior to 1 mg/kg twice-daily dosing; therefore, caution must be exercised in applying this recommendation to the LMWH enoxaparin at this time.3,27,28 (updated Aug. 28, 2012)

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