Deep Venous Thrombosis (DVT)

Common complications of deep venous thrombosis include

Much less commonly, acute DVT leads to phlegmasia alba dolens or phlegmasia cerulea dolens, both of which, unless promptly diagnosed and treated, can result in venous gangrene.

In phlegmasia alba dolens, a rare complication of DVT during pregnancy, the leg turns milky white. Pathophysiology is unclear, but edema may increase soft-tissue pressure beyond capillary perfusion pressures, resulting in tissue ischemia and wet gangrene.

In phlegmasia cerulea dolens, massive iliofemoral venous thrombosis causes near-total venous occlusion; the leg becomes ischemic, extremely painful, and cyanotic. Pathophysiology may involve complete stasis of venous and arterial blood flow in the lower extremity because venous return is occluded or massive edema cuts off arterial blood flow. Venous gangrene may result.

Infection rarely develops in venous clots. Jugular vein suppurative thrombophlebitis (Lemierre syndrome), a bacterial (usually anaerobic) infection of the internal jugular vein and surrounding soft tissues, may follow tonsillopharyngitis and is often complicated by bacteremia and sepsis. In septic pelvic thrombophlebitis, pelvic thromboses develop postpartum and become infected, causing intermittent fever. Suppurative (septic) thrombophlebitis, a bacterial infection of a superficial peripheral vein, comprises infection and clotting that usually is caused by venous catheterization.

Ultrasonography identifies thrombi by directly visualizing the venous lining and by demonstrating abnormal vein compressibility or, with Doppler flow studies, impaired venous flow. The test is > 90% sensitive and > 95% specific for femoral and popliteal vein thrombosis but is less accurate for iliac or calf vein thrombosis.

D-Dimer is a byproduct of fibrinolysis; elevated levels suggest recent presence and lysis of thrombi. D-Dimer assays vary in sensitivity and specificity; however, most are sensitive and not specific. Only the most accurate tests should be used. For example, a highly sensitive test is enzyme-linked immunosorbent assay (ELISA), which has a sensitivity of about 95%.

If pretest probability of DVT is low, DVT can be safely excluded in patients with a normal D-dimer level on a sensitive test. Thus, a negative D-dimer test can identify patients who have a low probability of DVT and do not require ultrasonography. However, a positive test result is nonspecific; because levels can be elevated by other conditions (eg, liver disease, trauma, pregnancy, positive rheumatoid factor, inflammation, recent surgery, cancer), further testing is necessary.

If pretest probability of DVT is moderate or high, D-dimer testing can be done at the same time as duplex ultrasonography. A positive ultrasound result confirms the diagnosis regardless of the D-dimer level. If ultrasonography does not reveal evidence of DVT, a normal D-dimer level helps exclude DVT. Patients with an elevated D-dimer level should have repeat ultrasonography in a few days or additional imaging, such as venography, depending on clinical suspicion.

Contrast venography was the definitive test for the diagnosis of DVT but has been largely replaced by ultrasonography, which is noninvasive, more readily available, and almost equally accurate for detecting DVT. Venography may be indicated when ultrasonography results are normal but pretest suspicion for DVT is high. The complication rate is 2%, mostly because of contrast agent allergy.

Noninvasive alternatives to contrast venography are being studied. They include MRI venography using an intravenous contrast agent and direct MRI of thrombi using T1-weighted gradient-echo sequencing and a water-excitation radiofrequency pulse; theoretically, the latter test can provide simultaneous views of thrombi in deep veins and subsegmental pulmonary arteries (for diagnosis of pulmonary embolism).

If symptoms and signs suggest PE, additional imaging (eg, CT pulmonary angiography or, less often, ventilation/perfusion [V/Q] scanning) is required.

Patients with confirmed DVT and an obvious cause (eg, immobilization, surgical procedure, leg trauma) need no further testing. Testing to detect hypercoagulability Diagnosis In healthy people, homeostatic balance exists between procoagulant (clotting) forces and anticoagulant and fibrinolytic forces. Numerous genetic, acquired, and environmental factors can tip... read more is controversial but is sometimes done in patients who have idiopathic (or unprovoked) DVT or recurrent DVT, in patients who have a personal or family history of other thromboses, and in young patients with no obvious predisposing factors. Some evidence suggests that presence of hypercoagulability does not predict DVT recurrence as well as clinical risk factors.

Screening patients with DVT for cancer has a low yield. Selective testing guided by complete history and physical examination and basic "routine" tests (complete blood count, chest x-ray, urinalysis, liver enzymes, and serum electrolytes, blood urea nitrogen [BUN], creatinine) aimed at detecting cancer is probably adequate. In addition, patients should have any age- and gender-appropriate cancer screening (eg, mammography, colonoscopy) that is due.

(For details on drugs and their complications, see Drugs for Deep Venous Thrombosis Drugs for Deep Venous Thrombosis All patients with deep venous thrombosis (DVT) are given anticoagulants and in rare cases thrombolytics. A number of anticoagulants are effective for management of deep venous thrombosis (see... read more )

All patients with DVT are given anticoagulants (1 Treatment references Deep venous thrombosis (DVT) is clotting of blood in a deep vein of an extremity (usually calf or thigh) or the pelvis. DVT is the primary cause of pulmonary embolism. DVT results from conditions... read more , 2 Treatment references Deep venous thrombosis (DVT) is clotting of blood in a deep vein of an extremity (usually calf or thigh) or the pelvis. DVT is the primary cause of pulmonary embolism. DVT results from conditions... read more ). Typically, patients are initially given an injectable heparin (unfractionated or low molecular weight) for 5 to 7 days, followed by longer term treatment with an oral drug. For patients who are to start warfarin, warfarin is started within 24 to 48 hours after the start of the injectable heparin. For patients who are to start an oral factor Xa inhibitor (edoxaban) or dabigatran etexilate, the oral agent is started on the day after the 5 to 7 days of injectable heparin is completed.

The reason for this different approach is that when starting warfarin, it takes about 5 days to attain a therapeutic effect; hence, the need to overlap with rapidly acting heparin for 5 to 7 days. On the other hand, oral factor Xa inhibitors and dabigatran attain a therapeutic effect within 2 to 3 hours of intake and there is no need to overlap these drugs with an injectable heparin.

Select patients may continue treatment with a low-molecular-weight heparin rather than switching to an oral drug, eg, patients with extensive iliofemoral DVT or selected patients with cancer. Alternatively, anticoagulation may be initiated with selected direct oral anticoagulants (rivaroxaban or apixaban) without first giving an injectable heparin; however, use of these drugs may be limited due to higher cost compared to warfarin.

Inadequate anticoagulation in the first 24 to 48 hours 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.

An IVC filter may help prevent pulmonary embolism in patients with lower extremity DVT who have contraindications to anticoagulant therapy or in patients with recurrent DVT (or emboli) despite adequate anticoagulation. An IVC filter is placed in the inferior vena cava just below the renal veins via catheterization of an internal jugular or femoral vein. Some IVC filters are removable and can be used temporarily (eg, until contraindications to anticoagulation subside or resolve).

IVC filters reduce risk of acute embolic complications but can have longer-term complications (venous collaterals can develop, providing a pathway for emboli to circumvent the filter, and there is also an increased risk of recurrent DVT). Also, IVC filters 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 IVC filter.

A clotted filter may cause bilateral lower extremity venous congestion (including acute phlegmasia cerulea dolens), lower body ischemia, and acute kidney injury Acute Kidney Injury (AKI) Acute kidney injury is a rapid decrease in renal function over days to weeks, causing an accumulation of nitrogenous products in the blood (azotemia) with or without reduction in amount of urine... read more . Treatment for a dislodged filter is removal, using angiographic or, if necessary, surgical methods. Despite widespread use of IVC filters, efficacy in preventing PE is understudied and unproved. IVC filters should be removed whenever possible.

Thrombolytic drugs, which include alteplase, tenecteplase, and streptokinase, lyse clots and may be more effective than anticoagulation alone in selected patients, but the risk of bleeding is higher than with heparin. Consequently, thrombolytics should be considered only in highly selected patients with DVT. Patients who may benefit from thrombolytics include those < 60 years with extensive iliofemoral DVT who have evolving or existing limb ischemia (eg, phlegmasia cerulea dolens) and do not have risk factors for bleeding.

Surgery is rarely needed. However, thrombectomy, fasciotomy, or both are mandatory for phlegmasia alba dolens or phlegmasia cerulea dolens unresponsive to thrombolytics to try to prevent limb-threatening gangrene.