Fig. 4.13A ), and rheumatic heart disease may engender atrial mural thrombi by causing atrial dilation and fibrillation. Both cardiac and aortic mural thrombi are prone to embolization. Although any tissue can be affected, the brain, kidneys, and spleen are particularly likely targets because of their rich blood supply.
ThrombusdevelopmentisusuallyrelatedtooneormorecomponentsofVirchow’striad: endothelialinjury(e.g.,bytoxins,hypertension,inflammation,ormetabolicproducts) abnormalbloodflow,stasis,orturbulence(e.g.,resultingfromaneurysms,atheroscleroticplaque) hypercoagulability:eitherprimary(e.g.,factorVLeiden,increasedprothrombinsynthesis,anti-thrombinIIIdeficiency)orsecondary(e.g.,bedrest,tissuedamage,malignancy)
Thrombimaypropagate,resolve,becomeorganized,orembolize.
Thrombosiscausestissueinjurybylocalvascularocclusionorbydistalembolization.
DIC is widespread thrombosis within the microcirculation that may be of sudden or insidious onset. It may be seen in disorders ranging from obstetric complications to advanced malignancy. To complicate matters, the widespread micro-vascular thrombosis consumes platelets and coagulation proteins (hence the synonym consumptive coagulopathy), and at the same time, fibrinolytic mechanisms are activated.
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The net result is that excessive clotting and bleeding may co-exist in the same patient. It is discussed in greater detail along with other bleeding diatheses in Chapter 12.
An embolus is a detached intravascular solid, liquid, or gaseous mass that is carried by the blood from its point of origin to a distant site, where it often causes tissue dysfunction or infarction. The vast majority of emboli derive from a dislodged thrombus—hence the term thromboembolism. Less commonly, emboli are composed of fat droplets, bubbles of air or nitrogen, atherosclerotic debris (cholesterol emboli), tumor fragments, bits of bone marrow, or amniotic fluid. Inevitably, emboli lodge in vessels too small to permit further passage, resulting in partial or complete vascular occlusion; depending on the site of origin, emboli can arrest anywhere in the vascular tree. The primary consequence of systemic embolization is ischemic necrosis (infarction) of downstream tissues, whereas embolization in the pulmonary circulation leads to hypoxia, hypotension, and right-sided heart failure.
Pulmonary emboli originate from deep venous thromboses and are responsible for the most common form of thromboembolic disease. The incidence of pulmonary embolism (PE) is 2 to 4 per 1000 hospitalized patients. Although the rate of fatal PE has declined considerably since the early 1990s, PE still causes about 100,000 deaths per year in the United States. In more than 95% of cases, venous emboli originate from thrombi within deep leg veins proximal to the popliteal fossa; embolization from lower leg thrombi is uncommon.
Fragmented thrombi from DVTs are carried through progressively larger channels and usually pass through the right side of the heart before arresting in the pulmonary vasculature. Depending on size, a PE can occlude the main pulmonary artery, lodge at the bifurcation of the right and left pulmonary arteries (saddle embolus), or pass into the smaller, branching arterioles (