Thrombophlebitis
An acute condition characterized by inflammation and thrombus formation, thrombophlebitis may occur in deep or superficial veins. It typically occurs at the valve cusps because venous stasis encourages the accumulation and adherence of platelets and fibrin. Thrombophlebitis usually begins with localized inflammation alone (phlebitis), but such inflammation rapidly provokes thrombus formation. Rarely, venous thrombosis develops without associated inflammation of the vein (phlebothrombosis).
Deep vein thrombophlebitis affects small veins, such as the lesser saphenous vein, or large veins, such as the iliac, femoral, and popliteal veins and the vena cava. It’s more serious than superficial vein thrombophlebitis because it affects the veins deep in the leg musculature that carry 90% of the venous outflow from the leg. The incidence of deep vein thrombophlebitis involving the subclavian vein is rising with the increased use of subclavian vein catheters.
Some hospitalized patients are more at risk than others; however, the risk of developing deep vein thrombophlebitis increases dramatically after age 40. Many of the risk factors for thrombophlebitis are specific to females. (See Thrombophlebitis in females, page 900.) Superficial vein thrombophlebitis is usually self-limiting and, because these veins have fewer valves than the deep veins, is less likely to cause complications.
Causes
Deep vein thrombophlebitis may be idiopathic, but it’s more likely to occur in the presence of certain diseases, treatments, injuries, or other factors, such as the following:
hypercoagulable states—systemic infection, cigarette smoking, circulating lupus anticoagulant, disseminated intravascular coagulation, estrogen use, dysfibrinogenemia, myeloproliferative diseases, and deficiencies of antithrombin III, protein C, or protein S
intimal damage—infection, infusion of irritating I.V. solutions, trauma, and venipuncture
neoplasms—lung, ovary, pancreas, stomach, testicles, and urinary tract
surgery—abdominal, genitourinary, orthopedic, and thoracic
fracture—spine, pelvis, femur, or tibia
venous stasis—acute myocardial infarction, heart failure, dehydration, immobility, incompetent vein valves, postoperative convalescence, and stroke
venulitis—Behçet’s syndrome, homocystinuria, and thromboangiitis obliterans
other—pregnancy and previous deep vein thrombosis (DVT).
Complications
Pulmonary embolism and chronic venous insufficiency are the major complications of thrombophlebitis. (See Managing chronic venous insufficiency, page 901.)
Gender differencesThrombophlebitis in females
Hormonal contraceptives, pregnancy, and the postpartum period are recognized risk factors for thrombophlebitis in females.
Hormonal contraceptives
Research suggests that a female taking high-estrogen hormonal contraceptives is 3 to 12 times more likely to develop thrombosis than those not taking these agents. The incidence of deep vein thrombosis varies with the type and concentration of estrogen; even females taking low doses are at increased risk for thrombosis. The mechanism for thromboembolic disease in hormonal contraceptive use is multifactorial; however, studies have revealed the presence of numerous alterations in the coagulation systems of these patients. Such alterations promote a hypercoagulable state, thereby increasing risk of thrombosis.
Both estrogens and progestogens are implicated in promoting thrombosis. Furthermore, the risk of postoperative pulmonary embolism appears to be increased in females who use hormonal contraceptives, even with minimal amounts of estrogen.
