外科學(xué)專業(yè)課 泌尿系梗阻英文預(yù)習(xí)資料學(xué)習(xí)課件

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．a(chǎn)ndtheureterovesicalandureteropelviciunctions．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，F(xiàn)igure6-4)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．a(chǎn)reurgency(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．a(chǎn)ndoverflow(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