Fig. 4.14 Anorganizedthrombus.Low-powerviewofathrombosedarterystainedforelastictissue.Theoriginallumenisdelineatedbytheinter-nalelasticlamina(arrows)andiscompletelyfilledwithorganizedthrombus.
vascularized mass of connective tissue that is eventually incorporated into the wall of the remodeled vessel. Occasionally, instead of organizing, the center of a thrombus undergoes enzymatic digestion, presumably because of the release of lysosomal enzymes from entrapped leukocytes. If bacterial seeding occurs, the contents of degraded thrombi serve as an ideal culture medium, and the resulting infection may weaken the vessel wall, leading to the formation of a mycotic aneurysm (Chapter 10).
Thrombi are significant because they cause obstruction of arteries and veins and may give rise to emboli. The effect that is of the greatest clinical importance depends on the site of thrombosis. Thus, although venous thrombi can cause congestion and edema in vascular beds distal to an obstruction, they are most worrisome because of their potential to embolize to the lungs and cause death. Conversely, whereas arterial thrombi can embolize and cause tissue infarction, their tendency to obstruct vessels (e.g., in coronary and cerebral vessels) is considerably more important.
Most venous thrombi occur in the superficial or the deep veins of the leg. Superficial venous thrombi usually arise in the saphenous system, particularly in the setting of varicosities; these rarely embolize but they can be painful and can cause local congestion and swelling from impaired venous outflow, predisposing the overlying skin to the development of infections and varicose ulcers. Deep venous thromboses (DVTs) in the larger leg veins at or above the knee joint (e.g., popliteal, femoral, and iliac veins) are more serious because they are prone to embolize. Although such DVTs may cause local pain and edema, collateral channels often circumvent the venous obstruction. Consequently, DVTs are entirely asymptomatic in approximately 50% of patients and are recognized only after they have embolized to the lungs.
Lower-extremity DVTs are associated with stasis and hypercoagulable states, as described earlier (
Table 4.2 ). Thus, common predisposing factors include congestive heart failure, bed rest, and immobilization; the latter two factors reduce the milking action of leg muscles and thus slow venous return. Trauma, surgery, and burns not only immobilize a patient but also are associated with vascular injury, procoagulant release, increased hepatic synthesis of coagulation factors, and reduced t-PA production. Many factors contribute to the thrombotic diathesis of pregnancy; in addition to the potential for amniotic fluid infusion into the circulation at the time of delivery, pressure produced by the enlarging fetus and uterus can produce stasis in the veins of the legs, and late pregnancy and the postpartum period are associated with hypercoagulability. Tumor-associated procoagulant release is largely responsible for the increased risk of thromboembolic phenomena seen in disseminated cancers. These are sometimes referred to as migratory thrombophlebitis, because of the tendency to involve several different venous beds transiently, or as Trousseau syndrome, for the physician who both described the disorder and suffered from it. Regardless of the specific clinical setting, the risk of DVT is increased in persons older than 50 years.
Atherosclerosis is a major cause of arterial thromboses because it is associated with the loss of endothelial integrity and with abnormal blood flow (
Fig. 4.13B ). Myocardial infarction can predispose to cardiac mural thrombi by causing dyskinetic myocardial contraction and endocardial injury (