These two terms are largely interchangeable designations for venous thrombosis accompanied by inflammation. Other sites where venous thrombi may form are the periprostatic venous plexus in males and the pelvic venous plexus in females, as well as the large veins in the skull and the dural sinuses (especially in the setting of infection or inflammation). Peritoneal infections, including peritonitis, appendicitis, salpingitis, and pelvic abscesses, as well as certain conditions associated with hypercoagulability (e.g., polycythemia vera) (Chapter 12) can lead to portal vein thrombosis.
In deep venous thrombosis (DVT) of the legs, prolonged immobilization resulting in venous stasis is the most important risk factor. This can occur with extended bed rest or even just sitting during long plane or automobile trips. The postoperative state is another independent risk factor for DVT, as are congestive heart failure, pregnancy, oral contraceptive use, malignancy, obesity, male sex, and age over 50 years. Inherited defects in coagulation factors (Chapter 4) often predispose affected individuals to development of thrombophlebitis. Venous thrombi also can result from elaboration of procoagulant factors from cancers (Chapter 6); the resulting hypercoagulable state can manifest as evanescent thromboses in different vascular beds at different times, so-called “migratory thrombophlebitis” or “Trousseau syndrome.”
Thrombi in legs tend to produce few, if any, reliable signs or symptoms. When present, local manifestations include distal edema, cyanosis, superficial vein dilation, heat, tenderness, redness, swelling, and pain. In some cases, pain is elicited by pressure over affected veins, squeezing the calf muscles, or forced dorsiflexion of the foot (Homan sign). However, many DVTs are asymptomatic, especially in bedridden patients, and the absence of findings does not exclude their presence.
Pulmonary embolism is a common and serious clinical complication of DVT, resulting from fragmentation or detachment of the venous thrombus. In many cases, the first manifestation of thrombophlebitis is a pulmonary embolus. Depending on the size and number of emboli, the outcome can range from resolution with no symptoms to death.
The superior vena cava syndrome usually is caused by neoplasms that compress or invade the superior vena cava, such as bronchogenic carcinoma or mediastinal lymphoma. The resulting obstruction produces a characteristic clinical complex consisting of marked dilation of the veins of the head, neck, and arms associated with cyanosis. Pulmonary vessels also can be compressed, causing respiratory distress.
The inferior vena cava syndrome can be caused by neoplasms that compress or invade the inferior vena cava or by a thrombus from the hepatic, renal, or lower-extremity veins that propagates cephalad. Certain neoplasms— particularly hepatocellular carcinoma and renal cell carcinoma—show a striking tendency to grow within veins, and these tumors may ultimately occlude the inferior vena cava. Obstruction of the inferior vena cava induces marked lower-extremity edema, distention of the superficial collateral veins of the lower abdomen, and— with renal vein involvement—marked proteinuria.
Primary disorders of lymphatic vessels are extremely uncommon. Much more commonly, lymphatic vessels are secondarily involved by inflammatory, infectious, or malignant processes.
Lymphangitis refers to an acute inflammation caused by bacterial seeding of the lymphatic vessels (Chapter 3). Clinically, the inflamed lymphatics appear as red, painful subcutaneous streaks, usually associated with tender enlargement of draining lymph nodes (acute lymphadenitis). If bacteria are not contained within the lymph nodes, they can pass into the venous circulation and cause bacteremia or sepsis.