Fig.4.17A ).Extravasatedredcellsinhemorrhagicinfarctsarephagocytosedbymacrophages,andthehemeironisconvertedtointracellularhemosiderin.Smallamountsdonotimpartanyappreciablecolortothetissue,butextensivehemorrhagesleaveafirm,brownresidue.
Inmosttissues,themainhistologicfindingassociatedwithinfarctsisischemic coagulative necrosis (Chapter2).Aninflammatoryresponsebeginstodevelopalongthemarginsofinfarctswithinafewhoursandusuallyiswelldefinedwithin1to2days.Eventually,inflammationisfollowedbyrepair,beginninginthepreservedmargins(Chapter3).Insometissues,parenchymalregenerationcanoccurattheperipheryoftheinfarct,wheretheunderlyingstromalarchitecturehasbeenspared.Mostinfarcts,however,areultimatelyreplacedbyscar(
Fig.4.18 ).Thebrainisanexceptiontothesegeneralizations;ischemictissueinjuryinthecentralnervoussystemresultsinliquefactive necrosis (Chapter2).
Septic infarctis occurwheninfectedcardiacvalvevegetationsembolize,orwhenmicrobesseednecrotictissue. Inthesecasestheinfarctisconvertedintoanabscess,withacorrespondinglygreaterinflammatoryresponseandhealingbyorganizationandfibrosis(Chapter3).
Fig. 4.18 Remotekidneyinfarct,nowreplacedbyalargefibroticscar.
The effects of vascular occlusion range from inconsequential to tissue necrosis leading to organ dysfunction and sometimes death. The range of outcomes is influenced by the following three variables:
Anatomy of the vascular supply. The presence or absence of an alternative blood supply is the most important factor in determining whether occlusion of an individual vessel causes damage. The dual supply of the lung by the pulmonary and bronchial arteries means that obstruction of the pulmonary arterioles does not cause lung infarction unless the bronchial circulation also is compromised. Similarly, the liver, which receives blood from the hepatic artery and the portal vein, and the hand and forearm, with its parallel radial and ulnar arterial supply, are resistant to infarction. By contrast, the kidney and the spleen both have end-arterial circulations, and arterial obstruction generally leads to infarction in these tissues.
Rate of occlusion. Slowly developing occlusions are less likely to cause infarction because they allow time for the development of collateral blood supplies. For example, small interarteriolar anastomoses, which normally carry minimal blood flow, interconnect the three major coronary arteries. If one coronary artery is slowly occluded (e.g., by encroaching atherosclerotic plaque), flow in this collateral circulation may increase sufficiently to prevent infarction—even if the original artery becomes completely occluded.
Tissue vulnerability to hypoxia. Neurons undergo irreversible damage when deprived of their blood supply for only 3 to 4 minutes. Myocardial cells, although hardier than neurons, still die after only 20 to 30 minutes of ischemia. By contrast, fibroblasts within myocardium remain viable after many hours of ischemia.
Infarctsareareasofischemicnecrosismostcommonlycausedbyarterialocclusion(typicallyresultingfromthrombosisorembolization);venousoutflowobstructionisalessfrequentcause.
Infarctscausedbyvenousocclusionoroccurringinspongytissuestypicallyarehemorrhagic(red);thosecausedbyarterialocclusionincompacttissuestypicallyarepale(white).
Whetherornotvascularocclusioncausestissueinfarctionisinfluencedbycollateralbloodsupplies,therateatwhichanobstructiondevelops,intrinsictissuesusceptibilitytoischemicinjury,andbloodoxygenation.