What causes thrombosis of the deep veins of the lower extremities?

Many factors can contribute to deep vein thrombosis of the lower extremities. Deep vein thrombosis of the lower limbs is most often the result of reduced venous return (for example, in immobilized patients), endothelial damage, impaired function (for example, after fractures of the leg) or hypercoagulation.

Risk factors for venous thrombosis

• Age over 60 years
• Smoking (including passive)
• Modulators of estrogen receptors (tamoxifen, raloxifene)
• Heart failure
• Hypercoagulation disorders
• Antiphospholipid Antibody Syndrome
• Deficiency of antithrombin III
• Factor V mutation (activated protein C resistance)
• Hereditary fibrinolytic defects
• Hyperhomocysteinemia
• Thrombocytopenia and thrombosis caused by heparin sodium
• Increase in the content of factor VIII
• Increase in the content of factor XI
• Increase in the content of von Willebrand factor
• Paroxysmal nocturnal hemoglobinuria
• Deficiency of Protein C
• Deficiency of Protein S
• Genetic variants of prothrombin G-A
• Inhibitor of tissue clotting factor
• Immobilization
• Introduction of venous catheters
• Injuries to the limb
• Malignant neoplasms
• Myeloproliferative diseases (high blood viscosity)
• Nephrotic syndrome
• Obesity
• Oral contraceptive use or estrogen therapy
• Pregnancy and the puerperium
• Previous venous thromboembolism
• Sickle-cell anemia
• Surgical interventions during the last 3 months.

Deep vein thrombosis of the upper extremities most often occurs due to damage to the endothelium during the placement of central venous catheters, pacemakers or injection of medications. Deep vein thrombosis of upper extremities is sometimes part of the syndrome of the inferior vena cava (SVVV), in other cases it occurs as a result of increased clotting or compression of the subclavian vein at the exit from the chest. The contraction may occur due to the normal or additional I rib, fibrous constriction (upper chest aperture syndrome), or arise with hard hands ("force thrombosis", or Paget-Shreter syndrome, which is 1-4% of all deep vein thrombosis of the upper limb ).

Many malignant neoplasms predispose to deep venous thrombosis, so GWT is a known marker of some hidden tumors. However, 85-90% of patients with deep venous thrombosis do not show any malignant neoplasm.

Usually deep venous thrombosis begins in the area of venous valves. Thrombi consists of thrombin, fibrin and erythrocytes with a relatively small number of platelets (red blood clots). Without treatment, these blood clots can spread proximally, give emboli for several days, or both.

Frequent complications include chronic venous insufficiency and post-phlebitis syndrome, as well as pulmonary embolism. Much less often, acute deep venous thrombosis leads to white or blue phlegmation. Both complications, in the absence of rapid diagnosis and treatment, provoke the development of venous (moist) gangrene.

With circulatory venous white gangrene, a rare complication of deep venous thrombosis during pregnancy, the leg becomes milky white. Pathophysiology is unclear, but edema can increase pressure in soft tissues without capillary perfusion pressure. Ischemia develops only if capillary blood flow becomes insufficient; the result is a moist gangrene.

With circulatory venous blue gangrene, a massive orofemoral venous thrombosis causes an almost complete venous occlusion. The blood supply to the leg is disturbed, it becomes extremely painful and cyanotic. Pathophysiology can include a complete stasis of venous and arterial blood in the lower extremity, since venous outflow is impossible or massive edema stops the flow of arterial blood. The result can be wet gangrene.

Other variants of deep venous thrombosis are rare. Purulent (septic) thrombophlebitis, bacterial infection of the superficial peripheral vein, usually develops after venous catheterization, which leads to infection and the formation of a thrombus. Purulent thrombophlebitis of the jugular vein (Lemierre syndrome) is a bacterial (usually anaerobic) infection of the internal jugular vein and surrounding soft tissues. It can be a consequence of tonsillitis and pharyngitis, often complicated by bacteremia and sepsis. In septic pelvic thrombophlebitis, pelvic thrombosis that occurs in the postpartum period causes periodic fever.

Thrombophlebitis without deep venous thrombosis is usually caused by venous catheterization, intravenous infusions or intravenous drug use.