Inferior Vena Cava Filters: A Surgeon’s Perspective

PAMELA A. LIPSETT

Since 1934, a thrombosis of the deep vein has been recognized as causing pulmonary embolism.¹ Pulmonary embolism (PE) and deep venous thrombosis (DVT) should be considered part of the same pathological process. For almost seven decades, the beneficial effects of heparin have been recognized as preventing PE, and heparin therapy remians the cornerstone of therapy for patients with DVT. Several authors have suggested that the risks of heparin therapy may exceed its benefits, especially in elderly patients.²^,³ Early experience with heparin anticoagulation documented a recurrent fatal PE rate of only 0.14%.⁴ Today the emphasis remains away from a primary role of mechanical interruption in the inferior vena cava (IVC). Rather, the role of surgery in vena cava interruption devices for pulmonary emboli has shifted to circumstances in which anticoagulation could not be used.

In 1973 the Greenfield filter was introduced.⁵ The design of the filter allowed more secure fixation, with the conical shape allowing maintenance of blood flow, even with 70 to 80% occlusion. Later, sustained flow allowed gradual resolution of entrapped emboli. Long-term patency of greater than 97% has been achieved.⁶^,⁷ The introduction of percutaneous methods of placement since the mid-1980s improved the ease, safety, and reliability of vena cava interruption devices.⁸^,⁹ Currently, these devices are placed by interventional radiologists or surgeons. The following sections highlight the clinical indications and short- and long-term outcome following placement of these devices.

Indications

In clinical and surgical practice in particular, venous thrombosis is a common cause of both morbidity and mortality, with thrombosis occurring in about 1 in 1000 patients per year in a general patient population; for each 10-year increase in age, the incidence of venous thromboembolism doubles.¹⁰ Postoperative patients at particularly high risk of DVT include those who have undergone recent major surgery or trauma and those who have had a previous thrombosis; this risk is generally in the range of 15 to 35%.¹¹ Several other factors, such as obesity, cancer, infection, congestive heart failure, varicose veins, pregnancy, the use of oral contraceptives, genetic predisposition, and prolonged sitting or bed rest, each contribute to the risk of developing DVT. Each of these conditions affect blood coagulability, venous stasis, or vascular injury, and the presence of multiple risk factors increases the risk of DVT.

The mortality of PE remains high. The 3-month mortality rate has been reported to be in the range of 10 to 17.5%.¹⁰ Of the 15 to 35% of surgical patients who develop DVT, 20 to 30% will suffer a potentially lethal PE.¹⁰ Deep venous prophylaxis therapy is warranted in all high-risk patients, as indicated in the National Institute of Health (NIH) consensus statement.¹¹ In patients who have not received prophylaxis or for whom prophylaxis has failed, subsequent treatment of DVT or pulmonary emboli by using anticoagulation, thrombolysis, or a filter interruption device must be considered.¹⁰^–¹³

Anticoagulation Therapy

Unless there are specific contraindications, anticoagulation with heparin (unfractionated or fractionated) remains the standard treatment for DVT.⁴^,¹⁰^,¹¹ Heparin accelerates the action of antithrombin III, thereby preventing additional thrombus from forming and permitting endogenous thrombolysis to dissolve some of the clot. For patients treated with unfractionated heparin, the partial thromboplastin time (PTT) is maintained in the range of 60 to 80 seconds, and heparin levels may be measured in patients with a circulating anticoagulant or an apparent heparin resistance.¹⁰ Monitoring the platelet count for the development thrombocytopenia is essential. Calf thrombi are noted to propagate to the femoral popliteal system about 20% of the time, and about half of these will embolize. If these patients do not receive anticoagulation therapy, the calf thrombosis must be monitored for proximal propagation.

In many patients, simultaneous initiation of warfarin therapy can be initiated once a therapeutic PTT (or heparin level) has been achieved. The prothrombin time International Normalized Ratio (INR) should be monitored and kept at about three times normal while the patient is on heparin therapy. Warfarin is necessary in combination with heparin for depletion of factor II (thrombin), which usually takes about 5 days. The optimal duration of anticoagulation is uncertain, with a treatment period of 6 months preventing more recurrences of a PE that 6 weeks.¹⁰ An indefinite period of anticoagulation should be considered in patients with recurrent PE if the risk of bleeding is low.

Systemic administration of thrombolytic agents such as streptokinase, urokinase, or tissue plasmogen activator is an alternative medical therapy for DVT.¹⁰ Thrombolysis can be lifesaving in patients with, massive pulmonary embolus, cardiogenic shock, or overt hemodynamic instability; however, bleeding is a major complication associated with thrombolytic therapy, and cessation of administration must occur immediately. Clotting factors are corrected by fresh-frozen plasma or cryoprecipitate. Absolute and relative contraindications to systemic thrombolytic therapy are listed in Table 41–1.

For pulmonary emboli, anticoagulation has a proven benefit.¹⁰^,¹⁴ A retrospective study of 516 patients found a survival rate of 92% and a recurrence rate of only 16%; in contrast, survival was 42% and the incidence of recurrence 55% among patients not treated with heparin.⁴ In patients without hemodynamic instability with right ventricular dysfunction and PE, rapid correction of right ventricular function in addition to heparin therapy may lead to a lower rate of recurrent PE than heparin therapy alone.¹⁰ Because of the increased risk of hemorrhage and substantial economic impact of thrombolytic therapy, this therapy should be weighed carefully for its potential benefit and the risk of hemorrhage, which rises with increasing age and increasing body mass index.¹⁰

Interruption of the IVC to reduce PE as a consequence of DVT generally is performed for two reasons: first, recurrent PE, which occurs under adequate anticoagulation; secondly, patients who have a contraindication to anticoagulation therapy. Additionally, vena cava interruption may be considered in patients with floating thrombus in the IVC, in patients with massive or previous PE who are at high risk of losing additional lung function, in patients with spinal cord injury, and in patients surviving successful pulmonary embolectomy. Prophylactic placement of IVC devices also may be considered for high-risk trauma patients. In a trial of 400 patients with DVT, IVC filters plus anticoagulation did not reduce the 2-year mortality rate compared with anticoagulation alone.¹⁵ This study clearly documented a lower rate of PE at 12 days (odds ratio, 0.22; 95% CI, 0.05–0.90) in patients treated with the filter and anticoagulation arm.¹⁵

**TABLE 41–1. Contraindications to Thrombolytic Therapy of Deep Venous Thrombosis**
Absolute Active internal bleeding Recent (2 mo) history of stroke or intracranial pathology Relative-major Recent surgery (10 days) Recent organ biopsy (10 days) Gastrointestinal bleeding (within 6 mo) Active peptic ulcer disease Visceral malignancy Uncontrolled hypertension Obstetric delivery (2 mo) Relative-minor Recent cardiopulmonary resuscitation Minor surgery Minor trauma Atrial mural thrombosis

Unique Clinical Considerations

Brain Tumor

Patients with brain tumors suffer a high incidence of DVT or PE, with reported incidences of 19% outside the perioperative period in a fully ambulatory practice.¹⁶ Of course, the incidence of DVT increases in the perioperative period and also when the patients are hemiplegic. Many studies documented an increased risk of intracranial bleeding in patients with primary and secondary tumors.¹⁷^,¹⁸ In many institutions, this patient population, if noted to have a PE or DVT, are automatically treated with vena cava filter. Although no large study has addressed the risk of hemorrhage from anticoagulation in patients with metastatic tumor, Levin et al ¹⁹ suggested that patients do not have a remarkably increased risk of anticoagulation and appear to do poorly with a vena cava filter. The high rate of definite or probable PE or IVC filter thrombosis (31%), along with recurrent DVT, occurred in more than 50% of patients. Other studies, however, documented a much lower complication rate following filter placement.¹⁶ At this point, the data support both the concept of anticoagulation risk and anticoagulation safety. Thus, filter placement may be reasonable; however, a controlled trial has not been done. The risk of anticoagulation may decrease whenever more specific therapeutic agents are available, but at institutions where vena cava filters are safely placed, this is probably the treatment of choice.

Patients with Cancer

The risk of DVT in patients with cancer has been reported as high as 41%.²⁰ Postoperatively, patients with neoplastic disease have a twofold risk of DVT and PE.²¹ Postoperatively, hypercoagulability can be caused by deficiency of antithrombin III, protein C, protein S, and prostacyclins. These defects are not seen in patients with cancer, however. Neoplastic cells can generate thrombin or synthesize various procoagulants.¹⁰^,²² In contrast to the hypercoagulable state of the cancer patient, the postoperative or traumatized patient is also at risk of bleeding. Raw tumor surfaces are more likely to bleed, and clotting factors may be impaired because of thrombocytopenia, hypoproteinemia, malnutrition, circulating immune complexes, or low-grade consumptive coagulopathy. After chemotherapy, patients may be at particular risk of bleeding. Many authors concluded that a vena cava filter device is a superior treatment modality for patients with cancer and a DVT or PE.²³^,²⁴

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