|Thrombosis of Artery|
•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
•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.
|General Gross Description|
•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
•Arterial: Usually a completely occlusive, dark red
clot. Postmortem clots are cord like and elastic.
|General Micro Description|
•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
• 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.