Arterial thrombi arefrequentlyocclusive.Theyaretypicallyrichinplatelets,astheprocessesunderlyingtheirdevelopment(e.g.,endothelialinjury)leadtoplateletactivation.Althoughusuallysuperimposedonarupturedatheroscleroticplaque,othervascularinjuries(vasculitis,trauma)canalsobeunderlyingcauses.Venous thrombi (phlebothrombosis) arealmostinvariablyocclusive;theyfrequentlypropagatesomedistancetowardtheheart,formingalongcastwithinthevessellumenthatispronetogiverisetoemboli.Becausethesethrombiforminthesluggishvenouscirculation,theytendtocontainmoreenmeshedredcells,leadingtothemonikerred, or stasis, thrombi. Theveinsofthelowerextremitiesaremostcommonlyaffected(90%ofvenousthromboses);however,venousthrombialsocanoccurintheupperextremities,periprostaticplexus,orovarianandperiuterineveins,andunderspecialcircumstancestheymaybefoundintheduralsinuses,portalvein,orhepaticvein.
Atautopsy,postmortem clots cansometimesbemistakenforvenousthrombi.However,theformeraregelatinousandbecauseofredcellsettlingtheyhaveadarkreddependentportionandayellow“chickenfat”upperportion;theyalsoareusuallynotattachedtotheunderlyingvesselwall.Bycontrast,redthrombitypicallyarefirm,focallyattachedtovesselwalls,andtheycontaingraystrandsofdepositedfibrin.
Thrombionheartvalvesarecalledvegetations. Bacterialorfungalbloodborneinfectionscancausevalvedamage,leadingtothedevelopmentoflargethromboticmasses(infective endocarditis) (Chapter11).Sterilevegetationsalsocandeveloponnoninfectedvalvesinhypercoagulablestates—thelesionsofso-called“nonbacterial thrombotic endocarditis” (Chapter11).Lesscommonly,sterile,verrucous endocarditis (Libman-Sacks endocarditis) canoccurinthesettingofsystemiclupuserythematosus(Chapter5).
(left side of photograph).
Fate of the Thrombus
If a patient survives an initial thrombotic event, during the ensuing days to weeks the thrombus evolves through some combination of the following four processes:
Propagation. The thrombus enlarges through the accretion of additional platelets and fibrin, increasing the odds of vascular occlusion or embolization.
Embolization. Part or all of the thrombus is dislodged and transported elsewhere in the vasculature.
Dissolution. If a thrombus is newly formed, activation of fibrinolytic factors may lead to its rapid shrinkage and complete dissolution. With older thrombi, extensive fibrin polymerization renders the thrombus substantially more resistant to plasmin-induced proteolysis, and lysis is ineffectual. This acquisition of resistance to lysis has clinical significance, as therapeutic administration of fibrinolytic agents (e.g., t-PA in the setting of acute coronary thrombosis) generally is not effective unless administered within a few hours of thrombus formation.
Organization and recanalization. Older thrombi become organized by the ingrowth of endothelial cells, smooth muscle cells, and fibroblasts (
Fig. 4.14 ). In time, capillary channels are formed that—to a limited extent—create conduits along the length of the thrombus, thereby reestablishing the continuity of the original lumen. Further recanalization can sometimes convert a thrombus into a http://ebooksmedicine.net