Cause of common hypercoaguable state leading to venous thrombi in leg and pelvic veins unknown.
Genetic deficiencies of anti-thrombin III, proteins S and C are rare causes of hypercoaguable states.
A combination of stasis, a hypercoaguable state, and endothelial injury leads to the formation of small thrombi in the venous valve pocket.
Normally, venograms have revealed that revolving eddies of static blood persist in valve pockets in the upright position, with clearing by elevating leg.
Hypercoaguable state risk factors include metastatic cancers, smoking, obesity, advanced age, and systemic lupus erythematosus.,
Massive pulmonary embolization (PE) causes 50,000 deaths per year.
Incidence of all cases much higher with 60% of adult autopsies showing PE, mostly asymptomatic.
Incidence probably rising with increasing surgical interventions, longevity, and capabilities of intensive care.
|General Gross Description|
A dark red clot, similar to clotted blood in a test tube, completely occluding the artery as a firm cast.
Embolus may be folded on itself if completely occluding artery with a greater diameter.
Impressions of venous valve pockets may be seen on surface of embolus.
Postmortem thrombi in pulmonary arteries are loose in the lumens with thread like branches loosely extending into adjoining smaller branches, and are soft and elastic when manipulated gently.
|General Microscopic Description|
Bulk of the venous thrombus is red cell and fibrin constituted because it is a stasis thrombus, with focal lines of Zahn formation on outer layers, appearing on surface as thin patches of light tan areas.
Without focal surface patches of lines of Zahn, fresh ante- and postmortem venous thrombi can not be distinguished microscopically. Both appear as sheets of red cells.
Cotran RS et al: Robbins Pathologic Basis of Disease. 5th edition. Philadelphia, W.B. Saunders, 1994, pp. 679-680.
Harrison's Principles of Internal Medicine, 13th Edition: Isselbach et. al. (eds). New York, McGraw-Hill, 1994, pp. 1214-20.
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||Synopsis by: J. Hasson, MD (T32000M35300)