infarction.docx
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infarction.docx
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infarction
8infarction
Tissuenecrosisresultingfromreductionorlossofbloodsupplyistermedinfarctionandthedeadtissueiscalledaninfarct.Itisusuallycausedbyobstructionofoneormorearteriesbythrombsisorembolism.Theblockageofevenamajorarterysupplyingtheskeletalmusclesandintegumentofthebodydoesnotusuallyresultininfarctionbecauseanastomosiswithotherarteries,beyondthepointofobstruction,issufficienttomaintainthecirculation.Intheinternalorgans,however,anastomosisislessadequate,andblockageofasinglearteryiscommonlyfollowedbyinfarction.Sucharteriesaretermedendarteries.Insometissues,infarctionmayalsoresultfromarterialnarrowingwithoutcompleteocclusion.
Generalfeatures.Thesizeofaninfarctdependsupontheamountoftissuerenderedischaemic,theseverityanddurationoftheischaemic,andthesusceptibilityofthecompinentcellsofthetissuetoischaemicinjury.Apartfromwhetheritisredorpale,theappearancesofaninfarctdependonthenatureofthesubsequentchangesinthedeadtissueandinparticularonwhetheritundergoescoagulativeorcolliquativenecrosis.Inthedaysfollowinginfarction,thevesselsinthesurvivingtissuearoundtheinfarctarecongestedandproductsofthedeadcellsdiffuseoutandpromoteanacuteinflammatoryreactionatthemargin,withinflammatoryoedemaandaccumulationofpolymorpsandmacrophages,whichmigrateintotheedadtissue.Theacutereactionsoonsubsides,andtheinfarctisreplacedbytheprocessoforganisationmacrophagescontinuetomigrateintoanddigestthedeadtissue,followedbycapillarieswhichsproutfromtheadjacentvessels,andbyproliferatingfibroblastswhichlaydowncollagenfibrils.Alayerofgranulationtissuethusformsatthemarginandgraduallyreplacestheinfart.Asitages,thegranulationtissuematuresintodenserfibroustissueandeventuallythesiteoftheinfarctismarkedbyafibrousscar.
Thesefeaturesareillusratedbythefollowingexamplesofinfarction.
Myocardialinfarctionisextermelyimportantbecauseitisaverycommoncauseofdisabilityanddeathfromheartfailure.Itusuallyresultsfromocclusivethrombosissuperveningonatheromaofamajorcoronaryarteryandinvolvesapatchofventricularmyocardium.Thedeadmyocardiumundergoescoagulativenecrosisandgraduallybecomespale,butoftenwithscatteredhaemorrhages.Thesizeandsiteoftheinfarctdependonwhicharteryisoccludedandonthedegreeofcollateralcirculationforomothercoronaryarterialbranches.Polymorphsinfiltratethemarginoftheinfarctandbydigestingthedeadtissuemayincreasetheriskofruptureofthewalloftheventricle.Inpatientswhosurvive,granulationtissuegraduallygrowsintoreplacethedeadtissueandeventurllyafibrousscarisformed.Lesscommonly,infarctioninvolvestheinnerpartsofthewalloftheleftventriclethroughoutitswholecircumferene,thisiscommonlyassociatedwithseverenarrowingofthelumenofbothcoronaryarteriesortheirmajorbranchesbyatheroma,butwihtoutsuperaddedocclusivethrombosis.Myocardialinfarctionmaycausedeathfromventricularfibrillation,orheartfailuremayensuefromlosssofpartofthemyocardium,andissometimesaggravatedbyarrhythmisa.
Cerebralinfarction.Bloodsupplytomostpartsofthebrainisdependentonendarteries,occlusionofanyoneofwhichresultsininfarction.Suchocclusionusuallyresultsfromthrombosisoveranatheromatouspatchorfromembolismandaffectstheterritorysuppliedbytheoccludedartery,butthereissomecollateralcirculationbetweenthemajorarteriesandthesizeoftheinfarctvariesdependingonthestateoftheotherarteries,andinparticularwhethertheyarenarrowedbyathermoa.Thebraintissueisremarkablysusceptibletoischaemiaandpartsofit,termedboundaryzones,lieatthejunctionofterritoriessuppliedbythemajorarteries.Thesezonesareparticularlysusceptibletoamoregeneralreductioninbloodflowtothebrain,foeexampleinaseverehypotensiveepisode,asinshock.Severereductionofflowbylesionsproximaltothecircleofwillis,usuallybyacombinationofatheromaandocclusivethrombosisofthevertebralaninternalcarotidarteries,canalsocauseinfarctionintheboundaryzones.
Generalinfarctsmaybepaleorhaemorrhagic.Thedeadtissueundergoesautolyticdigestionandbreaksdowntoformasoftpulpymasswhichhaspopularisedtheterm‘softening’forabraininfarct.Incontrasttoothertissues,theinfarctisnotremovedbyorganisation:
thedebrisisgradualytakenupbymacrophages,leavingacavitywhicheventuallycomestocontainclearfluid.Aroundtheinfarctthereisazoneofbraintissueinwhichpartialischaemiaatthetimeofinfarctioncausesnecrosisofthehighlysusceptibleneurons,whiletheglialcellssurviveandtheastrocytesapparentlyincreaseinnumberandproxidealayerof‘gliosis’which,togetherwithalittlefibroustissue,formsaroundthecavity.Theeffectsofcerebralinfarctiondependonthepartofthebraininvolved.Atfirsttheremaybemarkedoedemaaroundtheinfarct,anddisabilityoftendiminishesasthissubsides.Thecommonestsitesofinfarctionarewithinthetissuesuppliedbythemiddlecerebralartery;theinternalcapsuleisofteninvolved,causinghemiplegia.
Infarctsofthelungaretypicallywedgeshaped,withthebaseprojectingslightlyonthepleuralsurface.Theyarefirmandhaemorrhagic.Insomeinstances,pulmonaryarterialocclusionresultsinawedge-shapedhaemorrhagicpatchwithoutnecrosisandresolutionmaythenoccur.Whenthereisnecrosis,i.e.infarction,organisationfollows,leavingadepressedscarinthosewohosurviveformorethanafewweeks.Blockageofevenamajorpulmonaryartery,whichisusuallycausedbythrombo-embolusfromthelegveins,isnotfollowedbyinfarctionproviedethegeneralpulmonarycirculationisnormal,andpulmonaryinfarctionoccursparticularlyinsubjectswithpulmoanryhypertensionorheartfailure.Thefactorsinvolvedare,however,complex.
Whenaninfarctextendstoacoelomicsurface,e.g.thepericardium,pleuraofspleniccapsule,thereisoftendepositionofafinelayeroffibrinonthesurfaceadescaprofclearofslightlyturbidfluidexudatefromit.Thefibrindepositmaygiverisetopainanda‘frictionrub’maybeheardonauscrltationwhentheaffectedorganslidesovertheparietalcoelomicsurface,e.g.durigbeatingoftheheartorthepulmonarymovementofrespiration.
Splenicinfarction.lthrombosisofthesplenicarteryisuncommonandleadstovirtualycompletesplenicinfarction.Morecommonlyabranchofthesp;enicarteryisoccludedbyanembolusandawedge-shapedinfarctresults.Atfirsttheinfarctstissueisdarkredfromcongestion,butitsoonchangestopaleyellow,andisslowlyorganisedtoleaveadepressedscar.
Renalinfarction.Unlessthereisanadditionalaverrantartery,thrombosisoftherenalarteryleadstoalmostcompleteischaemicnecrosisofthekidney.Occlusionofabranchoftherenalarteryresultsinawedge-shapedinfarctthesizeofwhichdependsonthearteryoccluded.Themarginoftheinfarctishaemorrhagicandthecentralpartisusuallypale.
Infarctionoftheintestinemayresultfromocclusionofamajorartery,usuallythesuperiormesenteric,orfrommechanicalobstructionofthebloodsupplybytwistingofaloopofthegutorimpactioninahernialsac.Theinfarctedintestineceasestocontractandtheeffectisthesameasmechanicalobstruction.
Thenecroticwalliscongested,oedematousandhaemorrhagic.Micro-organismsinthelumenproliferateandinvadethedeadtissueandbacterialtoxinsdiffusethroughit,causingseveretoxaemia.Finally,thenecroticwallislikelytoruptureanditscontentsescape.Theeonditionisusuallyfatalfromthesevariouseffectsunlesstheinfarctedlengthofgutisremovedsurgicallywithoutunduedelay.
Intheliver,obstructionofabranchoftheportalveinisnotfollowedbyinfarction,owingtothesupplyofbolldfromthehepaticartery.Theobstructiondoes,however,reducethebolldflowsufficientlytocauseatrophyandlossofhepaticparenchymalcells,andthesinusoidsbecomedilated,sothatthelesionappearsdarkredandshrunkenandissometimestermeda‘redinfarct’.Obstructionofthehepaticarteryofofitsbranchesmayresultininfarctionoftheliver.
Thesusceptiblityoftissuestoischaemia.Theextentofinfarctionisuwuallylessthanthatofthetissuesuppliedbytheoccludedartery,collateralcirculationsupplyingthetissueattheperipheryofthearea.Thesizeoftheinfarctresultingfromocclusionofaparticulararterymaythusvarygreatly,dependingonwhetherthecollateralarteriesarehealthyandcapableofdilatation.Theextentofnecrosisisdeterminedslaobythecapacityofthetissuetowithstandischaemia.Asageneralrule,theparenchymalcellsoftheinternalorgans,whichoperateatahighmetabolicrate,arerelativelysusceptibletoischaemis,whereasthesupportingtissues—fibrousandfattytissueandbone,aremuchlesssusceptible.Theneuronsofthecentralnerboussystemareperhapsthemostsusceptiblecellsofall,andcannotwithstanddeprivationofbloodsupplyformorethanaveryfewminutes.Glialcellsaresomewhatlessdemandingintheirrequirements,andsccordinglyatthemarginofabraininfarctthereisazoneinwhichpartialischaemiaisfollowedbyrestorationofthecirculationbycollaterals;thisresultsindeathoftheneurons,whiletheglialcessspersistandundergoreactiveproliferation.Hepaticparenchymalcellsarealsohaghlysusceptibletoischaemiaand,asdescribedabove,thrombosisofaportalvenousbranchiscomm
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