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| Pulmonary Embolism | ||
| Etiology • Most pulmonary emboli are from deep leg vein thrombi • Unclear what causes the thrombi to break loose and travel to the heart | ||
| Pathogenesis • Conditions which promote deep vein stasis such as immobility, hypercoagulable states, and endothelial damage lead to thrombosis, | ||
| Epidemiology • Causes death in approximately 10% of adults dying in the hospital • 50,000 U.S. deaths/annum | ||
| General Gross Description • Large or medium sized pulmonary artery involved • Deep reddish purple firm material containing some fibrin strands or lines of Zahn (alternating platelet and red cell layers) • May be quite adherent to vessel wall if organization has begun • Smaller strands of thrombus may extend into smaller vessels •Examples: | ||
| General Microscopic Description • Mixture of red blood cells, platelets and fibrin • Over a few days capillaries, smooth muscle cells and fibroblasts grow into the embolus from the pulmonary vessel wall • Surface of the embolus will become endothelialized • Recanalization may occur •Examples: | ||
| Clinical Correlation • Large emboli obstructing more than 1/2 pulmonary circulation may cause sudden death • Smaller emboli may result in nothing more severe than hemorrhage if sufficient bronchial vascular or collateral supply to distal parenchyma • If no other supply to the distal lung or underlying chronic pulmonary disease infarct results | ||
| References • Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th edition. Philadelphia, W.B. Saunders, 1994, pp. 105-109, 111-112, 679. Please be patient during transfer. Medline will open in a new window. To return, close the Medline Window Pulmonary Embolism
| Synopsis by: Melinda Sanders M.D. (T28000M35300)[115]
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