Venous thrombosis refers to the formation of a blood clot in any vein. While this condition may interfere with blood drainage from dependent tissues, morbidity and mortality are primarily associated with thromboembolism.
Presentation
Symptoms presented by VT patients depend on the site and degree of thrombotic vessel occlusion. Individuals suffering from deep vein thrombosis, an entity typically compromising the veins of the lower limbs, may present with edema and erythema of the affected region. Tissues damaged by venous stasis may be tender or painful, and patients typically claim their discomfort to intensify after prolonged standing or walking. Homans' sign may be present. In severe cases, phlegmasia cerulea dolens or gangrene may be observed [6].
The occlusion of pulmonary arteries by thrombi that formed in the venous system causes acute-onset chest pain, dyspnea, tachycardia, and cyanosis. Affected individuals may also claim dizziness, sweating, and cough. A low-grade fever may be detected. A considerable subset of patients suffering from pulmonary embolism has a medical history of deep vein thrombosis.
Workup
Thrombi interfering with venous blood flow may be depicted employing duplex sonography, magnetic resonance imaging or computed tomography [7]. The former is preferred if the affected vein can be visualized by means of sonography, e.g., in patients suffering from thrombosed varicose veins or deep vein thrombosis of the extremities. Certain sites may not be accessible, so, for example, magnetic resonance flow imaging or contrast-enhanced computed tomography scans have to be carried out to depict cerebral vein thrombosis [8]. Of note, imaging techniques as described before have largely replaced contrast venography, an invasive approach to diagnosing VT. Still, venograms may provide useful information in case of subacute or chronic VT [8] [9].
Anamnestic data may reveal a predisposition for VT. For instance, thrombosis of isolated veins may be related to catheter insertion, surgery or trauma. In contrast, patients suffering from thrombophilia or other systemic conditions facilitating thrombus formation generally present with multiple VT. The underlying disease may be associated with additional disorders that should be considered when planning diagnostic measures:
- Laboratory analyses of blood samples may reveal thrombophilia, enhanced levels of D-dimer [10], or altered concentrations of coagulation factors.
- Coagulation studies should be conducted to test for a systemic prothrombotic condition.
- Diagnostic imaging is helpful to assess the condition of lungs and heart.
- Genetic screenings may be indicated to diagnose hereditary diseases.
Treatment
Prognosis
Etiology
Epidemiology
Pathophysiology
Prevention
Summary
Venous thrombosis (VT) refers to the formation of a blood clot in any vein. In general, VT may be triggered by endothelial lesions or may be the result of a systemic prothrombotic state. The latter may be observed in patients suffering from certain hereditary disorders (e.g., protein C deficiency, protein S deficiency, hereditary deficiency of antithrombin III) or acquired conditions associated with venous stasis (e.g., forced immobilization, pregnancy, neoplasms, cardiac disease) [1] [2]. In this context, VT may be considered as a manifestation of an underlying disorder. It is of utmost importance to identify this pathology if causative treatment is to be provided.
On the other hand, VT may lead to serious complications. The formation of small thrombi within venous vessels does not necessarily cause venous stasis, but it does provoke alterations of local fluid mechanics. At such sites, erythrocytes are likely to form so-called red thrombi. These are secondary thrombi that increase the volume of the initial blood clot. Eventually, dependent tissues may be compromised and patients may develop symptoms consistent with chronic venous insufficiency [3], postphlebitic syndrome, or Budd-Chiari syndrome [4], among others. Venous thrombi may also be dragged away, reach the right heart and pulmonary circulation. As the blood clot advances through the pulmonary circulation, the diameter of arteries is constantly declining. This increases the likelihood of the thrombus becoming lodged in these vessels, thus causing a potentially fatal pulmonary embolism, pulmonary infarction or chronic thromboembolic pulmonary hypertension [5].
References
- Khan S, Dickerman JD. Hereditary thrombophilia. Thromb J. 2006;4:15.
- Trenor CC, 3rd, Chung RJ, Michelson AD, et al. Hormonal contraception and thrombotic risk: a multidisciplinary approach. Pediatrics. 2011;127(2):347-357.
- Yamaki T, Nozaki M. Patterns of venous insufficiency after an acute deep vein thrombosis. J Am Coll Surg. 2005;201(2):231-238.
- Shin N, Kim YH, Xu H, et al. Redefining Budd-Chiari syndrome: A systematic review. World J Hepatol. 2016;8(16):691-702.
- Goldhaber SZ. Venous thromboembolism: epidemiology and magnitude of the problem. Best Pract Res Clin Haematol. 2012;25(3):235-242.
- Bhatt S, Wehbe C, Dogra VS. Phlegmasia cerulea dolens. J Clin Ultrasound. 2007;35(7):401-404.
- Steven A, Raghavan P, Altmeyer W, Gandhi D. Venous Thrombosis: Causes and Imaging Appearance. Hematol Oncol Clin North Am. 2016;30(4):867-885.
- Saposnik G, Barinagarrementeria F, Brown RD, Jr., et al. Diagnosis and management of cerebral venous thrombosis: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2011;42(4):1158-1192.
- Mendichovszky IA, Priest AN, Bowden DJ, et al. Combined MR direct thrombus imaging and non-contrast magnetic resonance venography reveal the evolution of deep vein thrombosis: a feasibility study. Eur Radiol. 2016.
- Riley RS, Gilbert AR, Dalton JB, Pai S, McPherson RA. Widely Used Types and Clinical Applications of D-Dimer Assay. Lab Med. 2016;47(2):90-102.