版权说明:本文档由用户提供并上传,收益归属内容提供方,若内容存在侵权,请进行举报或认领
文档简介
UrinaryObstruction&Stasis
——《Smith’SGeneralUrology》,the15thedition
Becauseoftheirdamagingeffectonrenalfunction,obstructionandstasisofurinaryflowareamongthemostimportantofurologicdisorders.Eitherleadseventuallytohydronephrosis,apeculiartypeofatrophyofthekidneythatmayterminateinrenalinsufficiencyor,ifunilateral,completedestructionoftheorgan.Furthermore,obstructionleadstoinfection,whichcausesadditionaldamagetotheorgansin-
volved.
CIassification
Obstructionmaybeclassifiedaccordingtocause(congenitaloracquired),duration(acuteorchronic),degree(partialorcomplete),andlevel(upperorlowerurinarytract).
Etiology
Congenitalanomalies,morecommonintheurinarytractthaninanyotherorgansystem,aregenerallyobstructive.Inadultlife,manytypesofacquiredobstructioncanoccur.
A.Congenital:Thecomtllonsitesofcongenitalnarrowingaretheexternalmeatusinboys(meatalstenosis)orjustinsidetheexternalurinarymeatusingirls,thedistalurethra(stenosis),posteriorurethral
valves,ectopicureters,ureteroceles.andtheureterovesicalandureteropelviciunctions.Anothercongenitalcauseofurinarystasisisdamagetosacralroots2-4asseeninspinabifidaandmyelomeningocele.Vesicoureteralrefluxcausesbothvesicalandrenalstasis(seeChapter13)
B.Acquired:Acquiredobstructionsarenumerousandmaybeprimaryintheurinarytractorsecondarytoretroperitoneallesionsthatinvadeorcompresstheurinarypassages.Amongthecommoncausesare(1)urethralstricturesecondarytoinfectionorinjury;(2)benignprostatichyperplasiaorcanceroftheprostate;(3)vesicaltumorinvolving
thebladderneckoroneorbothureteralorifices;(4)localextensionofcanceroftheprostateorcervixintothebaseofthebladder,occludingtheureters;(5)compressionoftheuretersatthepelvicbrimbymetastaticnodesfromcanceroftheprostateorcervix;(6)ureteralstone;(7)retroperitonealfibrosisormalignanttumor;and(8)pregnancy.
Neurogenicdysfunctionaffectsprincipallythebladder.Theuppertractsaredamagedsecondarilybyureterovesicalobstructionorrefluxand,often,complicatinginfection.Severeconstipation,especiallyinchildren,cancausebilateralhydroureteronephrosisfromcompressionofthelowerureters.
Elongationandkinkingoftheuretersecondarytovesicoureteralrefluxcommonlyleadtoureteropelvicobstructionandhydronephrosis.Unlessavoidingcystourethrogramisobtainedinchildrenwiththislesion,theprimarycausemaybemissedandimpropertreatmentgiven.
Pathogenesis&Pathology
Obstructionandneuropathicvesicaldysfunctionhavethesameeffectsontheurinarytract.Thesechangescaubestbeunderstoodbyconsidering(1)theeffectsonthelowertract(distaltothebladderneck)ofsevereexternalurinarymeatalstricturcand(2)theeffectsonthemidtract(badder)anduppertract(ureterandkidney)ofbenignprostatichyperplasia.
A.LowerTract(e9,UrethralStricture):Hydrostaticpressureproximaltotheobstructioncausesdilationoftheurethra.Thewalloftheurethramaybecomethin,andadiverticulummayform.Iftheurinebecomesinfected,urinaryextravasationmayoccur,andperiurethralabscesscanresult.Theprostaticductsmaybecomewidelydilated.
B.MidTract(e9,ProstaticHyperplasia):Intheearlierstages(compensatoryphase),themuscleWallofmebladderbecomeshypertrophiedandthickened.Withdecompensation,itbecomeslesscontractileand,therefore,weakened.
1.Stageofcompensation-Inordertobalancetheincreasingurethralresistance,thebladdermusculaturehypertrophies.Itsthicknessmaydouortriple.Completeemptyingofthebladderisthusmadepossible.
Hypertrophiedmusclemaybeseenmicroscopically.Withsecondaryinfection,theeffectsofinfectionareoftensuperimposed.Theremaybeedemaofthesubmucose,whichmaybeinfiltratedwithplasmacells,lymphocytes,andpolymorphonuclearcells.
Atcystoscopy,surgery,orautopsy,thefollowingevidenceofthiscompensationmaybevisible(Figure12-1)
a.Trabeculationofthebladderwall-Thewallofthedistendedebladderisnormallyquitesmooth.Withhypertrophy,individualmusclebundlesbecometautandgiveacoarselyinterwovenappearancetothemucosalsurface.Thetrigonalmuscleslightlyraisedabovethesurroundingtissues,respondtoobstructionbyhypertrophyoftheirsmoothmusculature.Theridgethenbecomesprominent.Thistrigonallaypertroplaycausesincreasedresistancetourinetlowintheitravesicalureteralsegmentsowingtoaccentuateddownwardpullonthem.Itisthismechanismthatcausesrelativefunctionalobstructionoftheureteroveslcaljunctions,leadingtobackpressureonthekidneyandhydroureteronephrosis.Theobstructionincreasesinthepresenceofsignificantresidualurine,whichfurtherstretchestheureterotrigonalcomplex.(Aurethralcatheterrelievestheobstructionsomewhatbyeliminatingthetrigonalstretch.Definifiveprostatectomyleadstopermanentreleaseofstretchandgradualsofteningoftrigonalhypertrophywithreliefoftheobstruction.)
b.Cellules—Normalintravesicalpressureisabout30cmofwateratthebeginningofmicturition.Pressures2-4timesasgreatmaybereachedbythetrabeculated(hypertrophied)bladderinitsattemptto
forceurinepasttheobstruction.Thispressuretendstopushmucosabetweenthesupefficialmusclebundles,causingtheformationofsmallpockets.orcellules(Figure12-1).
c.Dirertieula-Ifcellulesforcetheirwayentirelythroughthemusculatureofthebladderwall,theybecomesaccules,thenactualdiverticula,whichmaybeembeddedinperivesicalfatorcoveredby
peritoneum,dependingontheirlocation.Diverticulahavenomusclewallandarethereforeunabletoexpeltheircontentsintothebladderefficientlyevenaftertheprimaryobstructionhasbeenremoved.When
secondaryinfectionoccurs,itisdifficulttoeradicate;surgicalremovalofthediverticulamayberequired.Ifadiverticulumpushesthroughthebladderwallontheanteriorsurfaceoftheureter,theureterovesicaljunctionwillbecomeincompetent(seeChapter13).
d.Mucosa-Inthepresenceofacuteinfection,themucosamaybereddenedandedematous.Thismayleadtotemporaryvesicoureteralrefluxinthepresenceofa“borderline”iunction.ThechronicallyinflamedmembranemaybethinnedandDale.Intheabsenceofinfection,themucosaappearsnormal.
2.Stageofdecompensation-Thecompensatorypowerofthebladdermusculaturevariesgreatly.Onepatientwithprostaticenlargementmayhaveonlymildsymptomsofprostatismbutalargeobstructingglandthatcanbepalpatedrectallyandobservedcystoscopically;anothermaysufferacuteretentionandyethaveaglandofnormalsizeonrectal
palpationandwhatappearstobeonlyamildobstructioncystoscopically.
Inthefaceofprogressiveurethralobstruction,possiblyaggravatedbyprostaticinfectionwithedemaorbycongestionfromlackofintercourse,decompensationofthedetrusormayOCCUr,resultinginthepresenceofresidualurineaftervoidin9.Theamountmayrangeupto500mLarmore.
C.UpperTraot:
1.Ureter-Intheearlystagesofobstruction,intravesicalpressureisnormalwhilethebladderfillsandisincreasedonlyduringvoidin9.Thepressureisnottransmittedtotheuretersandrenalpelvesbecauseofthecompetenceoftheureterovesical“valves.”(Atruevalvelsnotpresent;theureterotrigonalunit,byvirtueotitsintrinsicstructure。resiststheretrogradetlowoturinc。)However,owingtotrigonalhypertrophy(seethesectionTrabeculationofthebladderwall)andtotheresultantincreaseinresistancetourineflowacrosstheterminalureter,thereisprogressivebackpressureontheureterandkidney,resultinginureteraldilatationandhydronephrosis.Later,withthephaseofdecompensationaccompaniedbyresidualurine,theresanaddedstretcheffectonthealreadyhypertrophiedtrigonethatincreasesappreciablytheresistancetoflowatthelowerendoftheureterandinducesfurtherhydroureteronephrosis.Withdecompensationoftheureterotrigonalcomplex,thevalvelikeactionmaybelost,vesicoureteralrefluxoccurs,andtheincreasedintravesicalpressureistransmitteddirectlytotherenalpelvis,aggravatingthedegreeofhydroureteronephrosis.
Secondarytothebackpressureresultingfromrefluxorfromobstructionbythehypertrophiedandstretchedtrigoneorbyaureteralstone,theureteralmusculaturethickensinitsattempttopushtheurine
downwardbyincreasedperistalticactivity(stageofcompensation).Thiscauseselongationandsometortuosityoftheureter(Figure12-2).Attimes,thischangebecomesmarked,andbandsoffibroustissuedevelop.Oncontraction,thebandsfurtherangulaetheureter,causingsecondaryureteralobstmction.Underthesecircumstances,removaloftheobstmctionbelowmaynotpreventthekidneyfromundergoingprogressiveobstructionduetothesecondaryureteralobstruction.
Finally,becauseofincreasingpressure,theureteralwallbecomesattenuatedandthereforelosesitscontractilepower(stageofdecompensation).DilatationmaybesoextremethIattheureterresemblesaloopofbowel(Figures12-3and13-8,upperright).
2.Kidney-Thepressurewithintherenalpelvisisnormallyclosetozero.Whenthispressureincreasesbecauseofobstructionorreflux,thepelvisandcalycesdilate.Tlledegreeofhydronephrosisthatdevelopsdependsontheduration,degree,andsiteoftheobstruction(Figure12-4).Thehighertheobstruction,thegreatertheeffectonthekidney.Iftherenalpelvisisentirelyintrarenalandtheobstructionisattheureteropelvicjunction,allthepressurewillbeexertedontheparenchyma.Iftherenalpelvisisextrarenal,onlypartofthepressureproducedbyaureteropelvicstenosisisexertedontheparenchyma;thisisbecausetheextrarenalrenalpelvisisembeddedinfatanddilatesmorereadily,thus“decompressing”thecalyces(Figure12-2).
Inmyearlierstages,thepelvicmusculatureundergoescompensatoryhypertrophyinitsefforttoforceurineDasttheobstnlction.Later,however,themusclebecomesstretchedandatonic(anddecompensated)
Theprogressionofhydronephroticatrophyisasfollows:
(1)Theearliestchangesinthedevelopmentofhydronephrosisareseeninthecalyces.Theendofanormalcalyx(asseenonaurogram,Figure6-4)isconcavebecauseofthepapillathatprojectsintoit;withincreaseinintrapelvicpressure,thefornicesbecomebluntandrounded.Withpersistenceofincreasedintrapelvicpressure,thepapillabecomflattened,thenconvex(clubbed)asaresultofcompressionenhancedbyischemicatrophy(Figure12-5)
Theparenchymabetweenthecablcesisaffectedtoalesserextent.Thechangesintherenalparenchymaaredueto(1)compresstonatrophyfromincreaseinintrapelvicpressure(moreaccentuatedwithintrarenalpelves)and(2)ischemicatrophyfromhemodynamicchanges,mainlymanifestedinarcuatevesselsthatrunatthebaseofthepyramidsparalleltothekidneyoutlineandaremorevulnerabletocompressionbetweenthererialcapsuleandthecentrallyincreasingintrapelvicpressure.
Thisspottyatrophyiscausedbythenatureofthebloodsupplyofthekidney.Thearteriolesare“endarteries”;therefore,ischemiaismostmarkedintheareasfarthestfromtheinteflobulararteries.Asthebackpressureincreases,hydronepllroslsprogresses,withthecellsnearestthemainarteriesexhibitingthegreatestresistance.
Thisincreasedpressureistransmittedupthetubnles.Thetubulesbecomedilated,andtheircellsatrophyfromischemia.
Itshouldbepointedoutthatafewinstancesofdilatedrenalpelvesandcalycesarenotduetothepresenceofobstmction.Rarely,therenalcavitiesarecongenitallycapaciousandthussimulatehydronephrosis.Morecommonly,hydronephrosismayoccurinchildhoodowingtothebackpressureassociatedwithvesicoureteralreflux.Ifthevalvularincompetenceresolves(andthisiscommon),somedegreeofthehydronephroticchangesmaypersist.Thesepersistingchangesmaycausethephysiciantosuspectthepresenceofobstruction,whichmayleadtounnecessarysurgery.AnisotoperenogramortheWhitakertest(seep131)canbeperformedtodeterminewhetherorganicobstructionispresent.
(2)Onlyinunilateralhydronephrosisaretheadvancedstagesofhydronephroticatrophyseen.Eventuallythekidneyiscompletelydestroyedandappearsasathin-walledsacfilledwithclearfluid(waterandelectrolytes)orpus(Figure12-6).
Ifobstructionisunilateral,theincreasedintrarenalpressurecausessomesuppressionofrenalfunctiononthatside.Theclosertheintrapelvicpressureapproachestheglomerularfiltrationpressure(6-12mmHg),thelessurinecanbesecreted.Glomerularfiltrationrateandrenalplasmaflowarereduced,concentratingpowerisgraduallylost,andtheureacreatinineconcentrationratioofurinefromthehydronepkrotickidneyislowerthanthatofurinefromthenormalkidney.
Hydronephroticatrophyisanunusualtypeofpathologicchange.Othersecretoryorgans(eg,thesubmaxillarygland)ceasesecretingwhentheirductsareobstructed.Thiscausesprimary(disuse)atrophy,Thecompletelyobstructedkidney,however,continuestosecreteurine.(Ifthiswerenotso,hydronephrosiscouldnotoccur,sinceitdependsonincreasedintrarenalpressure.)Asurineisexcretedintotherenalpelvis,fluidand,particularly,solublesubstancesarereabsorbed.througheitherthetubulesorthelymphatics.Thishasbeendemonstratedbyinjectingphenolsulfonphthalein(PSP)intotheobstructedrenalpelvis.Itdisappears(isreabsorbes)inafewhoursandisexcretedbytheotherkidney.Iftheintrapelvicpressureinthehydronepkrotickidneyrapidlyincreasestoalevelapproachingfiltrationpressure(resultingincessationoffiltration),asafetymechanismisactivatedthatproducesabreakinthesurfaceliningofthecollectingstructureattheweakestpoint—thefornices.Thisleadstoescapeandextravasationofurinefromtherenalpelvisintotheparenchymalinterstitium(pyelointerstitialbackfiow).Theextravasatedfluidisabsorbedbytherenallymphatics,andthepressureintherenalpelvisdrops,allowingfurtherfiltrationofurine.Thisexplainstheprocessbywhichthemarkedlyhydronephrotickidneycontinuestofunction.Furtherevidenceoftheoccurrenceofextravasationandreabsorptionisthatthemarkedlyhydronephrotickidneydoesnotcontainurineinthetruesense;onlywaterandafewsaltsarepresent.
Functionalimpairmentinunilateralhydronephrosis,asmeasuredbyPSPtestsorexcretoryurograms,isgreaterandincreasesfasterthanthatseeninbilateralhydronephrotickidneysshowingcomparabledamageonurography.Asunilateralhydronephrosisprogresses,thenormalkidneyundergoescompensatoryhypertrophy(particularlyinchildren)ofitsnephrons(renalcounterbalance),therebyassumingthefunctionofthediseasedkidneyinordertomaintainnormaltotalrenalfunction.Forthisreason,successfulanatomicrepairoftheureteralobstructionofsuchakidneymayfailtoimproveitspowersofwasteelimination.
Ifbothkidneysareequallyhydronephrotic,astrongstimulusiscontinuallybeingexercedonbothhydronephroticsolitarykidney。Consequently,thereturnoffunctioninthesekidneysafterrepairoftheirobstructionsisattimesremarkable.
Experimentalstudieshaveshownrecoveryoffunctionafterreleaseofcompleteobstructionofupto4week’sduration.In2well-documentedhumancases,functionwasrecoveredafterobstructionof56and69days.However,irreversiblelossoffunctioncanbeginasearlyas7days,asevidencedbydilatationandnecrosisoftheproximaltubules,whichprogressivelyincreasewithtime.
Theextentofrecoveryafterpartialobstructionisdifficulttodeterminepreoperatively.RenalscanningwithDMSA(dimercaptosuccinicacid)ismosthelpful.Temporarydrainage,especiallybynephrostomy,followedbyteststoassessrenalfunctionisthebestmeasure.
PhysiologicExplanation
ofSymptomsofBladder
Neckobstruction
Thefollowinghypothesishasbeenproposedtoexplainthesyndromeknownas”prostatism,”whichoccurswithprogressivevesicalobstruction:
Thebladder,liketheheart,isahollowmuscularorganthatreceivesfluidandforcefullyexpelsit.
And,liketheheart,itreactstoanincreasingworkloadbygoingthroughthesuccessivephasesofcompensationandfinallydecompensation.
Normally,contractionofthedetrusormuscleandthetrigonepullsthebladderneckopensadformsafunnelthroughwhichtheurineisexpelled.Theintravesicalpressuregeneratedinthisinstancevariesbetween20and40cmofwater;thisforcefurtherwidensthebladderneck.
Withbladderneckobstruction,hypertrophyofthevesicalmusculaturedevelops,allowingmeintravesicalvoidingpressuretoriseto50-l00cmormoreofwaterinordertoovercometheincreasedoutletreststance.Despitethis,theencroachingprostateappearstointerferewiththemechanismsthatordinarilyopentheinternalorifice.Also,thecontractionphasemaynotlastlongenoughforalloftheurinetobeexpelled;“exhaustion”ofthemuscleoccursprematurely.Therefractoyphasethensetsin,andthedetrusoristemporarilyunabletorespondtofurtherstimuli.Afewminuteslater.voidingmaybeinitiatedagainandcompleted.
A.CompensationPhase:
1.Stageofirritability—Intheearlieststagesofobstructionofthebladderneck,thevesicalmusculaturebeginstohypertrophy。Theforceandsizeoftheurinarystreamremainnormalbecausethebalanceismaintainedbetweentheexpellingpowerofthebladderandurethralresistance.Duringthisphase,however,thebladderappearstobehypersensitive.Asthebladderisdistended,theneedtovoidisfeIt.Inpatientswithanormalbladder,theseearlyurgescanbeinhibited,andthebladderrelaxesanddistendstoreceivemoreurine.However,inpatientswithahypertrophieddetrusor,thecontractionofthedetrusorissostrongthatitvirtuallygoesintospasm,producingthesymptomsofanirritablebladder.Theearliestsymptomsofbladderneckobstruction.therefore.areurgency(eventothepointofincontinence)andfrequency,bothdayandnight.
2.Stageofcompensation—Astheobstructionincreases,furtherhypertrophyofthemusclefibersofthebladderoccurs,andthepowertoemptythebladdercompletelyistherebymaintained.Duringthisperiod,inadditiontourgencyandfrequency,thepatientnoticeshesitancyininitiatingurinationwhilethebladderdevelopscontractionsstrongenoughtoovercomeresistanceatthebladderneck.Theobstructioncausessomelossintheforceandsizeoftheurinarystream,andthestreambecomesslowerasvesicalemptyingnearscompletion(exhaustionofthedetrusorasitnearstheendofthecontractionphase).
B.DecompensationPhase:Ifvesicaltonebecomesimpairedorifurethralresistanceexceedsdetrusorpower,somedegreeofdecompensatlon(imbalance)occurs.Thecontractionphaseofthevesicalmusclebecomestooshorttocompletelyexpelthecontentsofthebladder,andsomeurineremainsinthebladder(residualurine).
1.Acutedecompensation-Thetoneofthecompensatedvesicalmusclecanbetemporarilyembarrassedbyrapidfillingofthebladder(highfluid
intake)orbyoverstretchingofthedetrusor(postponementofurinationthoughtheurgeisfelt).Thismaycausejncreaseddifficultyofurination,withmarkedhesitancyandtheneedforstrainingtoinitiateurination;averyweakandsmallstream;andterminationofthestreambeforethebladdercompletelyempties(residualurine).Acuteandsuddencomplete
urinaryretentionmayalsooccur.
2.Chronicdecompensation—Asthedegreeofobstructionincreases,aprogressiveimbalancebetweenthepowerofthebladdermusculatureandurethralresistancedevelops.Therefore.itbecomesincreasinglydifficulttoexpelalltheurincduringthecontractionphaseofthedetrusor.Thesymptomsofobstructionbecomemoremarked.Theamountofresidualurinegraduallyincreases,andthisdiminishesthefunctionalcapacityofthebladder.Progressivefrequencyofurinationisnoted.Onoccasion,asthebladderdecompensates,itbecomesoverstretchedandattenuated.Itmaycontain1000-3000mlofurine.Itlosesitspowerofcontraction.andoverflow(paradoxic)incontinenceresults.
ClinicalFindings
A.Symptoms:
1.Lowerandmidtract(urethraandbladder)—Symptomsofobstructionofthelowerandmidtractaretypifiedbythesymptomsofurethralstricture,benignprostatichyperplasia,neurogenicbladder,andtumorofthebladderinvolvingthevesicalneck.Theprincipalsymptomsarehesitancyinstartingurination,lessenedforceandsizeofthestream,andterminaldribbling;hematuria,whichmaybepartial,initially,withstrictureortotalwithprostaticobstructionorvesicaltumor;andburningonurination,cloudyurine(duetocomplicatinginfection),andoccasionallyacuteurinaryretention.
2.Uppertract(ureterandkidney)-Symptomsofobstructionoftheuppertractaretypifiedbythesymptomsofureteralstrictureorureteralorrenalstone.Theprincipalcomplaintsarepainintheflankradiatingalongthecourseoftheureter,grosstotalhematuria(fromstone),gastrointestinalsymptoms,chills,fever,burningonurination,andcloudyurinewithonsetofinfection.whichisthecommonsequeltoobstructionorvesicoureteralreflux.Nausea,vomiting,lossofweightandstrength,andpallorareduetouremiasecondarytobilateralhydronephrosis.Ahistoryofvesicoureteralrefluxinchildhoodmaybesignificant.Obstructionoftheuppertractmaybesilentevenwhenuremiasupervenes.
B.Signs:
1.Lowerandmidtract-Palpationoftheurethramayrevealindurationaboutastricture.Rectalexaminationmayshowatonyoftheanalsphincter(damagetothesacralnerveroots)orbenignormalignantenlargementoftheprostate。Vesicaldistentionmaybefound.
Althoughobservationoftheforceandcaliberoftheurinarystreamaffordsaroughestimateofmaximumflowrate,theratecallbemeasuredaccuratelywithaurineflowmeteror,evenmoresimply,bythefollowingtechnique:Havethepatientbegintovoid.Whenobservedmaximumflowhasbeenreached,interposeacontainertocollecttheurineandsimultaneouslystartastopwatch.Afterexactly5s,removethecontainer.Thetlowrateinmilliliterspersecondcaneasilybecalculated.Thenormalurineflowrateis20-25mL/sinmalesand25-30mL/sinfemales.Anyflowrateunder15mL/sshouldberegardedwithsuspicion.Aflowrateunder10mL/sisindicativeofobstructionorweakdetrusorfunction.Flowratesassociatedwithanatonicneurogenic(neuropathic)bladder(diminisheddetrusorpower),orwithurethralstrictureorprostaticobstruction(increasedurethralresistancelmaybeaslowas3-5mL/s。Acystometrogramcandifferentiatebetweenthese2causesofimpairedflowrate.Afterdefinitivetreatmentofmecause.theflowrateshouldreturntonormal.
Inthepresenceofavesicaldiverticulumorvesicoureteralreflux,althoughdetrusorpowerisnormal,theurinarystreammaybeimpairedbecauseofthediffllsionofintravesicalpressureintothediverticulumandvesicoureteraljunctionaswellasthetirethra.Excisionofthediverticulumorrepairofthevesicoureteraljunctionsleadstoefficientexpulsionofurineviatheurethra.
2.Uppertract-Anenlargedkidneymaybediscoveredbypalpationorpercussion.Renaltendernessmaybeelicitedifinfectionispresent.Cancerofthecervixmaybenoted;itmayinvadethebaseofthebladderandoccludeoneorbothureteralorifices.Oritsmetastasestotheiliaclymphnodesmaycompresstheureters.Alargepelvicmass(tumor,pregnancy)candisplaceandcompresstheureters.Childrenwithadvancedurinarytractobstruction(usuallyduetoposteriorurethralvalves)maydevelopascites.Ruptureoftherenalfornicesallowsleakageofurineretroperitoneally;withruptureofthebladder.urinemaypassintotheperitonealcavitythroughatearintheperitoneum.
C.LaboratoryFindings:Anemiamaybefoundsecondarytochronicinfectionorinadvancedbilateralhydronephrosis(stageofuremia).Leukocytosisistobeexpectedintheacutestageofinfection.Littleifanyelevationofthewhitebloodcountaccompaniesthechronicstage.
Largeamountsofproteinareusuallynotfoundintheobstructiveuropathies.Castsarenotcommonfromhydronephrotickidneys.Microscopichematuriamayindicaterenalorvesicalinfection,tumor,orstone.Puscellsandbacteriamayormaynotbepresent.
Inmepresenceofunilateralhydronephrosis,resultsofthePSPtestarenormalbecauseofthecontralateralrenalhypertrophy.SuppressionofPSPexcretionindicaresbilateralrenaldamage,residualurine(vesicalorbilateralureterorenal),orvesicoureteralreflux.
Inthepresenceofsignificantbilateralhydronephrosis,urineflowthroughtherenaltubulesisslowed.Thus,ureaissignificantlyreabsorbedbutcreatinineisnot.Bloodchemistrythereforerevealsa
urea-creatinineratiowellabovethenormal10:1.
D.X-RayFindings(Figure12-7):Aplainfilmoftheabdomenmayshowenlargementofrenalshadows,calcificbodiessuggestingureteralorrenalstone,ortumormetastasestothebonesofmespineorpelvis.Metastasesinthespinemaybethecauseofspinalcorddamage(neuropathicbladder);iftheyareosteoblastic,theyarealmostcertainlyfromcanceroftheprostate.
Excretoryurogramsrevealalmosttheentirestoryunlesstenalfunctionisseverelyimpaired.Theyaremoreinformativewhenobstructionispresentbecausetheradiopaquematerialisretained.Theseurogramsdemonstratethedegreeofdilatationofthepelves,calyces,andureters.Thepointofureteralstenosisisrevealed.Segmentaldilatationofthelowerendofaureterimpliesthepossibilityofvesicoureteralreflux(Figure12-7),whichcanberevealedbycystography.Thecystogrammayshowtrabeculationasanirregularityofthevesicaloutlineandmayshowdiverticula.Vesicaltumors,nonopaquestones,andlargeintravesicalprostaticlobesmaycauseradiolucentshadows.Afilmtakenimmediatelyaftervoidingwillshowresidualurine.Fewteststhatarcassimpleandinexpensivegivethephysiciansomuchinformation.
Retrogradecystographyshowschangesofthebladderwallcausedbydistalobstruction(trabeculation,diverticula)ordemonstratestheobstructivelesionitself(enlargedprostate,posteriorurethralvalves,cancerofthebladder).Iftheureterovesicalvalvesareincompetent,ureteropyelograrnsareobtainedbyreflux.
Retrogradeurogramsmayshowbetterdetailthantheexcretorytype,butcaremustbetakennottooverdistendthepassageswithtoomuchopaquefluid;sm
温馨提示
- 1. 本站所有资源如无特殊说明,都需要本地电脑安装OFFICE2007和PDF阅读器。图纸软件为CAD,CAXA,PROE,UG,SolidWorks等.压缩文件请下载最新的WinRAR软件解压。
- 2. 本站的文档不包含任何第三方提供的附件图纸等,如果需要附件,请联系上传者。文件的所有权益归上传用户所有。
- 3. 本站RAR压缩包中若带图纸,网页内容里面会有图纸预览,若没有图纸预览就没有图纸。
- 4. 未经权益所有人同意不得将文件中的内容挪作商业或盈利用途。
- 5. 人人文库网仅提供信息存储空间,仅对用户上传内容的表现方式做保护处理,对用户上传分享的文档内容本身不做任何修改或编辑,并不能对任何下载内容负责。
- 6. 下载文件中如有侵权或不适当内容,请与我们联系,我们立即纠正。
- 7. 本站不保证下载资源的准确性、安全性和完整性, 同时也不承担用户因使用这些下载资源对自己和他人造成任何形式的伤害或损失。
最新文档
- 2025版小程序SDK接入授权合同模板3篇
- 2025年度美容院加盟店品牌形象保护合同范本4篇
- 2025版国际合同授权委托书定制模板3篇
- 城市配送与物流配送环节的信息互联互通考核试卷
- 常州锂电池生产厂2025年度消防设备采购合同2篇
- 二零二五年度古法工艺木屋建造技艺传承合同4篇
- 物业设施设备维护2025年度合同3篇
- 设备租赁公司二零二五年度施工塔吊租赁合同
- 2025年代理销售分销链销售协议
- 2025年因施工责任赔偿协议
- 开展课外读物负面清单管理的具体实施举措方案
- 2025年云南中烟工业限责任公司招聘420人高频重点提升(共500题)附带答案详解
- 2025-2030年中国洗衣液市场未来发展趋势及前景调研分析报告
- 2024解析:第三章物态变化-基础练(解析版)
- 北京市房屋租赁合同自行成交版北京市房屋租赁合同自行成交版
- 《AM聚丙烯酰胺》课件
- 技术支持资料投标书
- 老年人意外事件与与预防
- 预防艾滋病、梅毒和乙肝母婴传播转介服务制度
- 《高速铁路客运安全与应急处理》课程标准
- 23J916-1:住宅排气道(一)
评论
0/150
提交评论