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Deep Vein Thrombosis



Introduction

Deep vein thrombosis (DVT) is a common but elusive illness that can result in suffering and death if not recognized and treated effectively.Death can occur when the venous thrombi break off and form pulmonary emboli, which pass to and obstruct the arteries of the lung. DVT and pulmonary embolism PE, most often complicate the course of sick, hospitalized patients but may also affect ambulatory and otherwise healthy persons.

Since venous thrombosis is difficult to recognize clinically, these hospitalized cases probably represent the tip of the iceberg.Unfortunately, the death rate from PE and DVT is substantial, and the probability of survival of affected individuals is decreased when compared with unaffected ones.

Epidemiology

Women are a prime target for PE, being affected more often then men. It is estimated that the number of female patients who die from pulmonary embolism’ complications in one year, exceeds the number of women who die from breast cancer each year in the USA.

In instances when DVT and PE develop as complications of a surgical or medical illness, in addition to the mortality risk, hospitalization is prolonged and healthcare costs are increased.

Etiology of PE/DVT

The main hypothesis on etiology of PE/DVT is that most patients who suffer idiopathic PE/DVT (e.g., no associated cancer ) have a genetic predisposition, which remains subclinical until an additional stress occurs (e.g., immobilization during a long period ). Currently, only 25% of these underlying inherited hypercoagulable states are identified. The most common of them is resistance of Factor V to inactivation by activated Protein C (it is due to a single aminoacid mutation in Factor V- known as Factor V Leiden ). See Table 1

.

TABLE 1

Hypercoagulable States Associated
With Venous Thrombosis

  • Mutation in Factor V gene
  • Mutation in Protein C gene
  • Protein S deficiency
  • Antithrombin III deficiency
  • Antiphospholipid antibodies
  • Elevated concentration of Factor VIII

    • Pathogenesis of venous thromboembolism

    Venous thrombi consist mostly of red cell, a few platelets, and leucocyte component held together with fibrin. The disorder usually starts as a pure thrombotic process, and inflammation occurs secondary to the presence of the thrombus.

    The thrombi often break off and migrate to the lungs causing PE. The formation, development, and dissolution of thrombi depend on the balance between the effects of thrombogenic stimuli and a variety of protective mechanisms.

    Three mechanisms are involved in the pathogenesis of venous thrombosis, they are: venous stasis, injury to the venous wall, and hypercoagulable states. Venous stasis predisposes the patients to venous thrombosis mainly by impairing the clearance of activated coagulation factors from the local where thrombus is formed, and vascular damage contributes to the genesis of venous thrombosis through either direct trauma , or activation of endothelial cells by cytokines.

    Risk factors

    There are some clinical conditions ( see Table 2 )that predispose patients to DVT.In those circumstances prophylaxis should be done in the way to reduce complications, specially PE.These conditions are directly or indirectly involved with those pathogenic mechanisms described above.

    TABLE 2

    Risk Factors for
    Venous Thromboembolism (VT)

  • Age > 60 y
  • Extensive surgery
  • Previous VT
  • Marked immobility, pre or postoperative
  • Major orthopedic surgery
  • Fracture of pelvis, femur or tibia
  • Malignancies
  • Hypercoagulable states
  • Obesity
  • Pregnancy
  • Estrogen use
  • Venulitis
  • Postoperative sepsis
  • Heart failure
  • Inflammatory bowel disease
  • Sepsis
  • Myocardial infarction

    • Signs and symptoms

    DVTis often first noticed as an insidious, progressive, annoying “pulling sensation” at the insertion of the lower calf muscle into the posterior portion of the lower leg.This feeling can than become more pronounced and accompanied by warmth, swelling, and erythema. Tendernessmay be present along the course of the involved veins, and a cord may be palpable. Other signs include: increased tissue turgor,distension of superficial veins,proeminent venous collaterals. “Homans’sign” (increase resistance or pain during dorsiflexion of the foot) is unreliable and nonspecific.

    Part II will consists of Deep Vein Thrombosis’ diagnosis, differential diagnosis, treatment, complications, and prophylaxis.

    References

    Creager M.A., Dzau V.J.:Vascular Diseases of the Extremities. In: Isselbacher K.L., Braunwald E., Wilson J.D., Martin J.B., Fauci A.S., Kasper D.L. [eds]. Harisson’s Principles of Internal Medicine, pp. 1140-1142. Mc Graw Hill, 1994.

    Goldhaber S.Z. : Deep Vein Thrombosis and Pulmonary Embolism. Harvard Medical School - Board Review Course, 1996.

    Hirsh J., Hoak J.: Management of Deep Venous Thrombosis and Pulmonary Embolism. In Circulation, 1996; 93: 2212-2245.

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