Correspondence

Management of Venous Thromboembolism

N Engl J Med 1997; 336:1528-1529May 22, 1997

Article

To the Editor:

In his review of the management of venous thromboembolism (Dec. 12 issue),1 Ginsberg failed to mention the role of echocardiography in the diagnosis of this disorder. Despite the importance of ventilation–perfusion lung scanning, it has its limitations. It usually necessitates the transfer of the patient, who may be acutely dyspneic, to the radiology department and occasionally to a different hospital. On the other hand, echocardiography, whether transthoracic or transesophageal, is widely available, carries a minimal risk or none, and can help in making the diagnosis at the bedside. In the absence of chronic pulmonary disease, echocardiographic features that suggest pulmonary embolism include a dilated hypokinetic right ventricle and the presence of tricuspid regurgitation with increased velocity, suggesting an elevation of the pulmonary arterial systolic pressure. The absence of left ventricular dysfunction helps rule out the cardiac disease as a cause of acute dyspnea. Visualization of a right atrial thrombus confirms the diagnosis.2

Bedside echocardiography is a practical diagnostic procedure that in some patients eliminates the need for further studies.

Bassem S. Ibrahim, M.R.C.P.
National Heart Institute, Cairo, Egypt

2 References

1
Ginsberg JS. Management of venous thromboembolism. N Engl J Med 1996;335:1816-1828
Full Text | Web of Science | Medline

2
van Kuyk M, Mols P, Englert M. Right atrial thrombus leading to pulmonary embolism. Br Heart J 1984;51:462-464
CrossRef | Web of Science | Medline

To the Editor:

We think Ginsberg failed to emphasize the importance of recurrent embolism. All patients with pulmonary embolism are at risk for further embolism, and therefore, diagnosing pulmonary embolism is not enough. Instead, every patient should be evaluated for residual large thrombi, from the popliteal vein to the vena cava, by Doppler ultrasonography or venography. Patients with large residual thrombi may die from recurrent embolism, whereas patients without thrombi will not. Whether thrombolytic therapy prevents recurrent embolism is unknown. Vena caval filters are effective in preventing pulmonary embolism.1 Placement of a vena caval filter may be the pivotal step to prevent death — by preventing further embolism in patients with pulmonary embolism who have residual venous thrombi.

Christoph Pechlaner, M.D.
Thomas Buratti, M.D.
Michael Joannidis, M.D.
Innsbruck University Hospital, A-6020 Innsbruck, Austria

1 References

1
Greenfield LJ, Proctor MC. Current indications for caval interruption: should they be liberalized in view of improving technology? Semin Vasc Surg 1996;9:50-58
Medline

To the Editor:

We agree with Ginsberg that the duration of anticoagulant therapy in patients who have venous thromboembolism should be determined by balancing the risks of continuing therapy against the risk of recurrent thrombosis and the complications of therapy. He points out that there are no data to assist us in making decisions about the use of anticoagulation therapy in asymptomatic carriers of a thrombophilic defect (i.e., anticoagulation treatment restricted to high-risk situations vs. life-long prophylaxis) or in these same patients after a first thrombotic event (i.e., treatment for three to six months vs. life-long treatment). However, there is evidence that overall mortality in families with antithrombin deficiency and protein C deficiency does not differ from that in the general population.1,2 The mortality rates in these families were calculated back into the previous century, before thrombophilia was recognized and before anticoagulation therapy existed. These results also hold true for the most severe type of thrombophilia, type I antithrombin deficiency.3

Although these results are general and cannot guide management in the case of patients with recurrent thrombosis or families that appear to be extremely prone to thrombosis, they are reassuring and do not support the use of prophylactic anticoagulation solely on the basis of the presence of the biochemical defect, especially in the light of the known risks of the therapy (a 1 to 3 percent risk of major hemorrhage per year and a 0.3 to 0.6 percent risk of fatal hemorrhage per year).4,5

On the basis of these retrospective data, we believe that asymptomatic patients with heritable thrombophilia should not receive anticoagulant agents except in situations in which the risk of thrombosis is increased — for example, after surgery and during immobilization.

Frits R. Rosendaal, M.D.
Felix J.M. van der Meer, M.D.
Jan P. Vandenbroucke, M.D.
University Hospital Leiden, NL-2300 RC Leiden, the Netherlands

5 References

1
Rosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262
CrossRef | Web of Science | Medline

2
Allaart CF, Rosendaal FR, Noteboom WMP, Vandenbroucke JP, Briet E. Survival in families with hereditary protein C deficiency, 1820 to 1993. BMJ 1995;311:910-913
CrossRef | Web of Science | Medline

3
van Boven HH, Olds RJ, Thein S-L, et al. Hereditary antithrombin deficiency: heterogeneity of the molecular basis and mortality in Dutch families. Blood 1994;84:4209-4213
Web of Science | Medline

4
van der Meer FJM, Rosendaal FR, Vandenbroucke JP, Briet E. Assessment of a bleeding risk index in two cohorts of patients treated with oral anticoagulants. Thromb Haemost 1996;76:12-16
Web of Science | Medline

5
Palareti G, Leali N, Coccheri S, et al. Bleeding complications of oral anticoagulant treatment: an inception-cohort, prospective collaborative study (ISCOAT). Lancet 1996;348:423-428
CrossRef | Web of Science | Medline

Author/Editor Response

Dr. Ginsberg replies:

To the Editor: Ibrahim suggests that echocardiography is a practical procedure that eliminates the need for further studies in some patients with suspected pulmonary embolism. In a patient with suspected pulmonary embolism and a clear-cut right atrial thrombus, a diagnosis of pulmonary embolism can be made. However, the frequency of this finding is probably very low, since the source of pulmonary embolism in most patients is leg-vein thrombosis.1 Although in the absence of chronic pulmonary disease, a dilated, hypokinetic right ventricle with or without tricuspid insufficiency may be diagnostic of pulmonary embolism, the accuracy of this finding has not been established. Overall, the clinical utility of echocardiography in the evaluation of patients with suspected pulmonary embolism is not known. Furthermore, clinicians should not be distracted from performing tests that have a clear-cut utility in diagnosing pulmonary embolism, such as lung scanning, venous ultrasonography, or pulmonary angiography.

Pechlaner and colleagues suggest that all patients with established pulmonary embolism should undergo extensive evaluation to determine the presence (and extent) of deep-vein thrombosis, with the placement of a vena caval filter if large residual thrombi are present. Such an approach is costly and associated with side effects (of venography, cavography, and insertion of the filter) and in view of the clear-cut efficacy of anticoagulant therapy, cannot be justified. Although some experts recommend insertion of a filter in patients with free-floating thrombi, the necessity for this measure (above and beyond anticoagulant therapy) has never been demonstrated.

I agree with Rosendaal and colleagues that routine anticoagulant therapy is not indicated in asymptomatic patients with thrombophilia,2 but the data are retrospective, and a small but clinically important increase in mortality in these patients cannot be ruled out. Furthermore, although mortality is the most important complication of venous thromboembolism, there is substantial associated morbidity (the post-thrombotic syndrome and chronic thromboembolic pulmonary hypertension), which may be reduced by long-term anticoagulant therapy.

Jeffrey S. Ginsberg, M.D.
McMaster University, Hamilton, ON L8N 3Z5, Canada

2 References

1
Hull RD, Hirsh J, Carter CJ, et al. Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan. Ann Intern Med 1983;98:891-899
Web of Science | Medline

2
Rosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262
CrossRef | Web of Science | Medline

Citing Articles (1)