•Only rare hypercoaguable states due to genetic deficiencies of anticoagulants (antithrombin III, protein C and protein S) are known specific causes.

•Multiple factors involved in the pathogenesis of most thromboses, including a probable state of hypercoaguability, due to causes unknown. In contrast to hypocoaguable states, there are no current objective quantitative measures of hypercoaguability available.

•Endothelial injury: Thrombi on atheromatous plagues, overlying myocardial infarcts, valvular endocarditis, hemodynamic trauma due to high pressures, or stenosis of valves.

•Stasis: Leg DVT^s begin in valve pockets where eddies persist in upright position and washed out by elevation of legs. Abetted by immobility. Atrial thrombi with mitral stenosis and /or AF.

•Hypercoaguable states: See Etiology. Metastatic cancers, smoking, obesity, advanced age, SLE.

•RE: Deep vein thrombosis (DVT) and pulmonary emboli (PE). Massive PE cause 50,000 deaths per year. Actual incidence much higher, with 60% of autopsies showing PE (1963), which are mostly asymptomatic. Incidence probably rising with increasing surgical interventions, advances in intensive care, and longevity.

•Epidemiology of other effects of thrombosis, i.e. arterial thrombi complicating atherosclerosis & mural thrombi, vary with associated syndrome.

•Venous: May be asymptomatic or have leg edema and/or calf tenderness due to distension of veins. Pulmonary emboli may be asymptomatic or cause unexplained dyspnea and/or sudden death.

•Mural thrombi: Can embolize to brain, spleen, kidneys and limbs with associated syndromes. Vegetations of endocarditis can also embolize to coronary arteries with myocardial infarction.

•Arterial: Common cause of acute syndromes of visceral infarction and gangrene of extremities.

•Venous: A dark red clot forming a cast, equivalent to clotted blood in a test tube, due to stasis. Postmortem clots are ruled out by gross features, lacking cast form, wall and valve impressions.

•Mural thrombi: Friable brown discrete adherent
mounds with typical uniformly wrinkled surfaces, the lines of Zahn due to genesis in flowing blood. Occur in cardiac chambers, aorta, and iliacs.

•Arterial: Usually a completely occlusive, dark red clot. Postmortem clots are cord like and elastic.

•Venous: Sheets of red cells. Fibrin component not visible. Outer rims may show a few lines of Zahn.

•Mural thrombi: Classical lines of Zahn with even layers of ridges of platelets with adherent wbc^s separated by valleys of red cells. This is proof of antemortem genesis because blood flow needed.

•Arterial: Mostly venous-like when due to injuries
of atherosclerosis. But, meticulous study of total thrombus will reveal focus of endothelial injury with nidus of platelet and fibrin thrombus.

• Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 105-12.

• Harrison^s Principles of Internal Medicine, 13th Ed: Isselbach et. al. (eds). New York, McGraw-Hill, 1994, pp.1214-5.

• Current literature from PubMed at National Library of Medicine