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of otolaryngology. This journal will enrich their knowledge base. Otolaryngologists can make use of the simple online submission system after registering as author to submit documents. This journal is available free of cost. It is free to access and free to publish. Frequency of publication: 12 Issues in a year
PEER REVIEW PROCESS All articles submitted will be triaged and sent for peer review before publication. 1. Articles should be submitted only by scholars in the field. 2. Only unpublished work will be considered for publication 3. Authors who indulge in plagiarism will be banned from future submissions. 4. Authors are encouraged to register at Researcher id inorder to secure an unique identity. This Id will add to their credibility.
ABOUT THE JOURNAL This Journal is a venture of drtbalu's otolaryngology online. Publisher: Dr T Balasubramanian Editor: Dr U. Venkatesan Assocaite Editor: Dr. R. Geetha
Contents: 1. Advanced anatomy of lateral nasal wall 2. Allergic rhinitis an overview 3. Anatomy of paranasal sinuses 4. Choanal atresia 5. Complications of sinusitis 6. Concept of unified airway 7. Dentigerous cyst 8. Drug induced gingival overgrowth 9. Epistaxis 10. Evaluation of lacrimal appratus 11. Intrinsic rhinitis 12. Local anesthesia of nose and sinuses 13. Reducing bleeding during endoscopic sinus surgery
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Authors
BalasubramanianThiagarajan
Fig.1:Figureshowingturbinatesinthelateral nasalwall
Theseturbinatesprojectfromthelateralwallofthenose.Outoftheseturbinatesthefollowingare presentinallindividuals:
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lateralwallofnoseafterremovalofturbinates
Thisprominenceisknownastheaggernasicell.Thisprominencevariesinsizeindifferent individuals.Theseaggernasicellsoverliethelacrimalsac,separatedfromitjustbyathinlayerof bone.Infactthisaggernasicellisconsideredtobearemnantofnasoturbinalbonesseeninanimals. Whentheanteriorattachmentoftheinferiorandmiddleturbinatesareremoved,thelacrimal drainagesystemandsinusdrainagesystemcanbeclearlyseen. Theinferiorturbinateisaseparatebonedevelopedembryologicallyfromthemaxilloturbinalbone. Theinferiormeatusispresentbetweentheinferiorturbianateandthelateralnasalwall.Thenasal openingofthenasolacrimalductopensintheanteriorthirdoftheinferiormeatus.Thisopeningis coveredbyamucosalvalveknownastheHassnersvalve.Thecourseofthenasolacrimalductfrom thelacrimalsaclieundertheaggernasicell. Themiddlemeatusliebetweenthemiddleturbinateandthelateralnasalwall.Themiddleturbinateis partoftheethmoidalcomplex.Thesinuseshavebeendividedintotheanteriorandposteriorgroups. Theanteriorgroupofsinusesarefrontal,maxillaryandanteriorethmoidalsinuses.Thesesinuses drainintothemiddlemeatus,i.e.underthemiddleturbinate.Themiddlemeatushostsfromanterior toposteriorthefollowingstructures: 1.Aggernasi 2.Uncinateprocess 3.Hiatussemilunaris 4.Ethmoidalbulla 5.Sinuslateralis 6.Posteriorfontanelle Uncinateprocess:actuallyformsthefirstlayerorlamellaofthemiddlemeatus.Thisisthemost stablelandmarkinthelateralnasalwall.Itisawingorboomerangshapedpieceofbone.Itattaches
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anteriorlytotheposterioredgeofthelacrimalbone,andinferiorlytothesuperioredgeoftheinferior turbinate6.Superiorattachmentoftheuncinateprocessishighlyvariable,maybeattachedtothe laminapalyracea,ortheroofoftheethmoidsinus,orsometimestothemiddleturbinate.The configurationoftheethmoidalinfundibulumanditsrelationshiptothefrontalrecessdependslargely onthebehavioroftheuncinateprocess.TheUncinateprocesscanbeclassifiedinto3types dependingonitssuperiorattachment. Theanteriorinsertionoftheuncinateprocesscannotbeidentifiedclearlybecauseitiscoveredwith mucosawhichiscontinuouswiththatofthelateralnasalwall.Sometimesasmallgrooveisvisible overtheareawheretheuncinateattachesitselftothelateralnasalwall.Theanteriorconvexpart formstheanteriorboundaryoftheostiomeatalcomplex.Itisherethemaxillary,anteriorethmoidal andfrontalsinusesdrain.Uncinateprocesscanbedisplacedmediallybythepresenceofpolypoidal tissue,orlaterallyagainsttheorbitin individualswithmaxillarysinushypoplasia7.Removingofthispieceofboneisthemostimportant stepinEndoscopicsinussurgery. TypeIuncinate:Heretheuncinateprocessbendslaterallyinitsuppermostportionandinsertsinto thelaminapapyracea.Heretheethmoidalinfundibulumisclosedsuperiorlybyablindpouchcalled therecessusterminalis(terminalrecess).Inthiscasetheethmoidalinfundibulumandthefrontal recessareseparatedfromeachothersothatthefrontalrecessopensintothemiddlemeatusmedial totheethmoidalinfundibulum,betweentheuncinateprocessandthemiddleturbinate.Therouteof drainageandventilationofthefrontalsinusrunmedialtotheethmoidalinfundibulum.
TypeIuncinateinsertion
TypeIIuncinateinsertion
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TypeIIIuncinateinsertion
Polypseenpushingtheuncinatemedially
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Hypoplasiaofmaxillarysinusseenpushingtheuncinatelaterally
Imageshowinguncinateprocess
Removalofuncinateprocessrevealsthenaturalostiumofthemaxillarysinus.Thisisanothervital landmarkinthelateralnasalcavity.Thesuperiorwallofthenaturalostiumofthemaxillarysinusisat thelevelofflooroftheorbit.Aggernasi:ThisisalatinwordforMound.Thisareareferstothemost superiorremnantofthefirstethmoturbinalwhichpresentsasamoundanteriorandsuperiortothe insertionofmiddleturbinate.Dependingonthepneumatizationofthisareamayreachuptothelevel oflacrimalfossatherebycausingnarrowingoffrontalsinusoutflowtract.Ethmoidalinfundibulum:isa cleftlikespace,whichisthreedimensionalinthelateralwallofthenose.Thisstructurebelongstothe anteriorethmoid.Thisspaceisboundedmediallybytheuncinateprocessandthemucosacovering it.Majorportionofitslateralwallisboundedbythelaminapapyracea,andthefrontalprocessof maxillatoalesserextent.Defectsinthemedialwalloftheinfundibulumiscoveredwithdense connectivetissueandperiosteum.Thesedefectsareknownasanteriorandpoteriorfontanelles. Anteriorlytheethmoidalinfundibulumendsblindlyinanacuteangle.
Figureshowinglargeaggernasiaircell
Bullaethmoidalis:ThisisderivedfromLatin.Bullameansahollowthinwalledbonyprominence.This isanotherlandmarksinceitisthelargestandnonvariantoftheaircellsbelongingtotheanterior
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ethmoidalcomplex.Thisaircellisformedbypneumatizationofbullalamella(secondethmoidbasal lamella).Thisaircellappearslikeablebsituatedinthelaminapapyracea.Someauthorsconsider thistobeamiddleethmoidcell.Ifbullaextendsuptotheroofofethmoiditcanformtheposteriorwall offrontalrecess.Ifitdoesnotreachuptothelevelofskullbasethenarecesscanbeformed betweenthebullaandskullbase.Thisrecessisknownassuprabullarrecess.Iftheposteriorwallof bullaisnotincontactwithbasallamellathenarecessisformedbetweenbullaandbasallamella. Thisrecessisknownasretrobullarrecess/sinuslateralis.Thisretrobullarrecessmaycommunicate withthesuprabullarrecess.Osteomeatalcomplex:Thistermisusedbythesurgeontoindicatethe areaboundedbythemiddleturbinatemedially,thelaminapapyracealaterally,andthebasallamella superiorlyandposteriorly.Theinferiorandanteriorbordersoftheosteomeatalcomplexareopen. Thecontentsofthisspacearetheaggernasi,nasofrontalrecess(frontalrecess),infundibulum,bulla ethmoidalisandtheanteriorgroupofethmoidalaircells.Thisisinfactanarrowanatomicalregion consistingof:1.Multiplebonystructures(Middleturbinate,uncinateprocess,Bullaethmoidalis)2.Air spaces(Frontalrecess,ethmoidalinfundibulum,middlemeatus)3.Ostiaofanteriorethmoidal, maxillaryandfrontalsinuses.Inthisarea,themucosalsurfacesareveryclose,sometimesevenin contactcausingsecretionstoaccumulate.Theciliabytheirsweepingmovementspushesthenasal secretions.Ifthemucosaliningthisareabecomesinflamedandswollenthemucociliaryclearanceis inhibited,eventuallyblockingthesinuses.Someauthorsdividethisosteomeatalcomplexintoanterior andposterior.Theclassicosteomeatalcomplexdescribedalreadyhasbeendescribedasthe anteriorosteomeatalcomplex,whilethespacebehindthebasallamellacontainingtheposterior ethmoidalcellsisreferredtoastheposteriorethmoidalcomplex,thusrecognisingtheimportanceof basallamellaasananatomicallandmarktotheposteriorethmoidalsystem.Hencetheanteriorand theposteriorosteomeatalcomplexhasseparatedrainagesystems.Sowhenthediseaseislimitedto theanteriorcompartmentoftheosteomeatalcomplex,theethmoidcellscanbeopenedanddiseased tissueremovedasfarasthebasallamella,leavingthebasallamellaundisturbedminimisingtherisk duringsurgery.Hiatussemilunaris:LiesbetweentheanteriorwalloftheBullaandthefreeposterior marginoftheuncinateprocess.Thisisinfactatwodimensionalspace.Throughthishiatusacleftlike spacecanbeentered.Thisisknownastheehtmoidalinfundibulum.Thisethmoidalinfundibulumis boundedmediallyalongitsentirelengthbytheuncinateprocessanditsliningmucosa.Thelateral wallisformedbythelaminapapyraceaoftheorbit,withparticipationfromthefrontalprocessofthe maxillaandthelacrimalbone.Theanteriorgroupofsinusesdrainintothisarea.Infactthisareaacts asacesspoolforallthesecretionsfromtheanteriorgroupofsinuses.
Osteomeatalcomplex
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CoronalCTshowingconchabullosa
References
1. OhnishiT,TachibanaT,KanekoY,etal.Highriskareasinendoscopicsinussurgeryand preventionofcomplications.Laryngoscope.1993103:1815 2. StoneyP,MacKayA,HawkeM.TheantrumofHighmoreorofdaVinci?JOtolaryngol.1991Dec 20(6):4568 3. BlantonPL,BiggsNL(1969)Eighteenhundredyearsofcontroversy:theparanasalsinuses.AmJ Anat124(2):13547. 4. GraneyDO,RiceDH,Paranasalsinusesanatomy.In:CummingsCW,FredricksonJM,HarkerLA etal(1998)OtolaryngologyHeadandNeckSurgery.Mosby,3rdedn. 5. BodinoC,JankowskiR,GrignonBetal(2004)Surgicalanatomyoftheturbinalwallofthe ethmoidallabyrinth.Rhinology42(2):7380. 6. BolgerWE,AnatomyoftheParanasalSinuses.In:KennedyDW,BolgerWE,ZinreichJ(2001) Diseasesofthesinuses,Diagnosisandmanagement.B.C.Decker 7. http://jorl.net/index.php/jorl/article/view/47 8. JoeJK,HoSY,YanagisawaE(2000)Documentationofvariationsinsinonasalanatomyby intraoperativenasalendoscopy.Laryngoscope110(2):22935.
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Authors
BalasubramanianThiagarajan Abstract: Rhinitisisclassicallydefinedasinflammationofnasalmucosacharacterisedbyasymptomcomplex whichincludessneezing,nasalcongestion,itchingandrhinorrhoea.Allergyhappenstobethemost commoncauseforrhinitisaffectingapproximately20%ofthepopulation.Eventhoughallergicrhinitis isnotalifethreateningdisorderitcausesafairdegreeofmorbidityandreductioninthequalityoflife. Thisalsohappenstobeoneofthecommoncausesofrhinosinusitis. Introduction: Rhinitisisdefinedasinflammationofnasalmucousmembranecharacterisedbysymptomcomplex whichincludessneezing,nasalcongestion,itichingandrhinorrhoea1.Thisconditionisrather commonaffectingnearly20%ofpopulation.Eventhoughthisisnotalifetheateningdisorderitcauses atremendousimpactonthequalityoflife2.TheclassicfeatureofallergicrhinitisisIgEmediatedType Ihypersensitivityreaction.Eveningestedfoodcancauseallergicreactioninthenasalmucous membraneduetothesimilariteswithinhalesallergens.Thesymptomcomplexwhicharefeaturesof allergicrhinitiscanbeclassifiedintonasalandnonnasalsymptoms3. Immunologicalmechanismsresponsibleforallergicrhinitis:
Nasalsymptoms
Allergicsensitizationofnasalmucosaoccursinaseriesofwellcaliberatedsteps4.
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StepI:Thisstepisalsoknownasantigenprocessingstage.Thisischaracterisedbyantigen processingbyantigenprocessingcells/macrophages.Antigenonenteringthenasalcavityis ingestedbythesecells(dendriticantigenprocessingcells/macrophages).Theingestedantigen undergoesaseriesofprocessingstageswithinthecell. StepII:ExposureofHLAClassIIreceptorsontheantigenprocessingcell.Successfulantigen processingwithintheantigenprocessingcell/macrophagesleadstoexposureofHLAclassII receptorsontheircellsurfaces. StepIII:InthissteptheactivatedantigenpresentingcellcomesintocontactwithHelperTcellsvia HLAClassIIreceptorspresentontheirsurface.TheseHelperTcellsbelongtoCD4+T H2THelper cellcategory.ThisinteractionactivatestheT H2HelperTcells. StepIV:ThisstepischaracterisedbyreleaseofcytokineslikeIL4andIL13whichstimulatesmore HelperTcellstorespondtotheantigenloadbyrecruitingthem.ThesecytokinesalsocausesB lymphocytestodifferentiateintoPlasmacells.TheseplasmacellssecreteIgEantibodiesspecificto theantigen. StepV:AttachmentofIgEantibodiestomastcells.Thisstagecausesreleaseofhistaminefromthe activatedmastcellsbyantigenspecificIgEantibodies.Mastcellsareknowntocontainpreformed immunemediatorslikehistamine,kininsandproteases. These5stagesconcludetheearlyphaseofallergicreaction.Thisresponseoccurswithinabout10 30minutesfollowingallergenexposure.Thedegranulatingmastcellspresentinthenasalmucosa increasesmembranepermeabilitycausingmucosaloedema,irritation,nasalpruritus,sneezing,and rhinorrhoea. Latephaseofallergicreaction: Thisphaseoccursbetween48hoursfollowingantigenexposure.Thisphaseiscausedueto: Chemotaxis Migrationofneutrophils,basophils,eosinophilsandmacrophagestothenasalsubmucosa Cytokinesandchemokinesreleasedfromthesecellsnotonlymaintainstheinflammatorystateof nasalmucosabutalsocausesirrepairabledamagetoit. Typeofallergicrhinitis: Allergicrhinitishasbeendivideintotwotypes: Seasonalallergicrhinitis Perennialallergicrhinitis Seasonalallergicrhinitis: ThisconditionisalsoknownasHayfever.Thisconditionoccursduringdifferentseasonsdepending upontheincitingallergen.TypicalallergenscausingHayfeveraccordingtoseasonsinclude:tree pollenduringspring,grasspolleninsummerandweedpollenduringfall.Historyisvirtually diagnostic.
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Clinicalfeatures: Mostofthesepatientsdevelopsymptomsbytheageof205. Familyhistoryofallergicrhinitisisveryimportant.Allergicrhinitishaspositivegeneticcomponent6. Symptomsinclude: Nasalblock Rhinorrhoea Wateryeyes Itchyeyes Repeatedepisodesofsneezing Intensenasalitchingwillcausethepatienttokeepstrokingthedorsumofnose.Thisisknownas AllergicSalute.Continuousstrokingofthedorsumofthenosewillcauseahorizontalskincreaseto develop.ThisisknownasDarriersline. Onclinicalexaminationnasalmucosamayappearaspaleandboggy.Someofthesepatientsmay evendevelopnasalpolyposis. Presenceofallergicshiners:Thisiscausedduetopersistentnasalcongestionleadingontolower eyelidoedema. DevelopmentofcreasesoverlowereyelidduetopersistentMullermusclespasm.Thisisknownas Denniesline. Posteriorpharyngealwallmucosawillshowcobblestoning.Someofthesepatientsmayalsohave prominentlateralpharyngealbands. Persistenceofnasalallergywillleadtoprolongedmucociliarymovementabnormalitycausing secondayrhinosinusitis. Management: Allergicrhinitisisbestmanagedmedically.Antihistaminesandnasaldecongestantsmayhelpduring acutephasesofthedisorder.Topicalcorticosteroidspraywillhelpinprolongedremission. LeukotreinereceptorantogonistlikeMontelukast7inhibitscysteinylleukotrienereceptorthereby preventingtheeffectsofleukotrienereleaedbymastcelldegranulationprocess.
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References
1. TogiasAG.Systemicimmunologicandinflammatoryaspectsofallergicrhinitis.JAllergyClin Immunol.Nov2000106(5Suppl):S24750 2. SummaryofhealthstatisticsforU.S.adults:nationalhealthinterviewsurvey,2002.Availableat: http://www.cdc.gov/nchs/fastats/allergies.htm.AccessedAugust1,2007. 3. DruceHM.Allergicandnonallergicrhinitis.In:MiddletonEMJr,ReedCE,EllisEF,AdkinsonNFJr, YungingerJW,BusseWW,eds.Allergy:PrinciplesandPractice.5Thed.St.Louis,Mo:MosbyYear Book1998:100516. 4. SkonerDP.Allergicrhinitis:definition,epidemiology,pathophysiology,detection,anddiagnosis.J AllergyClinImmunol.Jul2001108(1Suppl):S28 5. DykewiczMS,FinemanS,SkonerDP,NicklasR,LeeR,BlessingMooreJ.Diagnosisand managementofrhinitis:completeguidelinesoftheJointTaskForceonPracticeParametersin Allergy,AsthmaandImmunology.AmericanAcademyofAllergy,Asthma,andImmunology.Ann AllergyAsthmaImmunol.Nov199881(5Pt2):478518. 6. TorresBorregoJ,MolinaTeranAB,MontesMendozaC.Prevalenceandassociatedfactorsof allergicrhinitisandatopicdermatitisinchildren.AllergolImmunopathol(Madr).MarApr 200836(2):90100. 7. NayakA,LangdonRB.Montelukastinthetreatmentofallergicrhinitis:anevidencebasedreview. Drugs.200767(6):887901
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Authors
BalasubramanianThiagarajan
Abstract
Paranasalsinusesareairfilledhollowsacsseenaroundtheskullbone.Thesesacsprecisely surroundthenasalcavity.Therearefourpairedsinusessurroundingthenasalcavity.Thisarticle attemptstotracethehistoryofanatomyofparanasalsinusesfromearly16thcenturytilldate.The adventofnasalendoscopeshaveaddedanotherdimensiontotheanatomicalstudyofparanasal sinuses.Theentiresubjectofanatomyofparanasalsinuseshasbeenrewrittenafterendoscopes werestartedtobeusedcommonly. Introduction: Preciseunderstandingofanatomyofparanasalsinusesisanimportantprerequisiteinavoiding complicationsduringendoscopicsinussurgery.Commoncomplicationsfollowingendoscopicsinus surgeryarecausedbyinadequateunderstandingofthehighlycomplexandvariableanatomyof paranasalsinuses. History: Inancienttimesnasalsinuseswereconsideredtobeasystemofhollowspacesthroughwhich secretionsfrombraindrained1.LeonardoDavinciin1489wasthefirsttopreparedetailedanatomical drawingsofparanasalsinuseswhichisstillconsideredtobeaccuratetilldate2.Thisdrawingbecame accessibletothescientificcommunityonlyaslateas1901. Davincidescribedmaxillarysinusasthecavitywithinthebonethatsupportsthecheek.Thisisstillan undisputedfact.Thisdescriptioncomesfromaversatileartistcumscientist.Daviciniwasactuallyan uniquecombinationofanartistcumscientist.Hisscientificdescriptionswerebackedbyhisabilityto drawastoundingimages.
Fig.1:PortraitofDavinci
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descriptionofparanasalsinuses.Hewasalsoabletodemonstratethevariouspathologiesaffecting theseairfilledsacs.ItwasC.V.SchneiderofGermanywhosuggestedthatmucouswasnota productofbrainbutonthecontrarywassecretedbytheliningmucosaofparanasalsinuses.Inhis honorthenasalmucousmembraneisknownasschneiderianmembrane. TheadventofCTscanhasthrownalotoflightasfarasparanasalsinusanatomyisconcerned.It shouldalsobepointedoutevenaftertheadventofadvancedimagingtechniqueswehavenotadded muchtothedescriptionsalreadymadebyOnodi,GrunwaldandZuckerkandl.Thisisanapt testimonytotheabilityofourforefathers4. Definition: Paranasalsinusesareairfilledsacsfoundintheskullbone.Thesesacsinfactsurroundthenasal cavity.Thereare4pairedsinuses.Theyare: 1.Maxillarysinuses 2.Frontalsinuses 3.Ethmoidalsinuses 4.Sphenoidalsinuses Eachofthesesinusesarenamedaccordingtothefacialbones Maxillarysinus(AntrumofHighmore):Thesepairedsinuseslieunderthecheek.Itisthelargestof thegroupofparanasalsinuses.Thecapacityofthemaxillarysinusisroughly1fluidounze(30ml).It ismoreorlessshapedlikeapyramid.Thisisthefirstsinustodevelop Base(medialwall):Thebaseofthepyramidcorrespondstothelateralnasalwall.Thiswallhasits convexityfacingthesinus.Thecentralportionofthebaseisverythin,andinsomeareascouldeven bemembranous.Thenaturalostiumofthissinusispresentinthiswall.Itispresentmoretowardsthe roofofthesinuscavitythanitsbase. Anterior:Wallcorrespondstothefacialsurfaceofthesuperiormaxilla.Overthecaninefossaitisonly 2mminthickness.ItisthoughthiscaninefossaareathatmaxillayantrumisenteredduringCaldwell Lucsurgery.
Fig.2:Developmentofmaxillarysinus
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BoundariesofCaninefossa: Inferior:Boundedbythealveolarridge Laterally:Boundedbythecanineeminencewhichiscausedbythecaninetooth. Superior:Infraorbitalforamen Medial:Pyriformaperture.Thisdoesnotcontainbone,butislinedbymiddlemeatusmucosa,alayer ofconnectivetissueandthesinusmucosa6. Posteriorwall:ofmaxillarysinusisalsoknownastemporalsurface.Itisverythickandisformedby thebodyofthesuperiorportionofthemaxilla. Roof:ofthesinusisformedbyitsthinorbitalwallwhichistraversedbytheinfraorbitalforamen containingtheinfraorbitalvesselsandnerves.Thiswallisveryfragileandanydiseaseprocess involvingthemaxillaislikelytoaffecttheorbitthroughthiswall.Thiswallisfurtherthinnedoutwhere theinfraorbitalcanalispresent. Floor:isformedalveolarprocessofthemaxillaandthehardpalate.Therootsofthefirstandsecond molarreachuptothefloorofthemaxillarysinus.Inchildrenthefloorliesatthesamelevelasthatof thenasalcavity.Inadultsitlies510mmbelowthenasalcavity.Itisjustseparatedfromthefloorof thesinusbyathinlamellaofbone.Thislamellamaybedehiscentcommonly.Dentalinfections involvingthe1stand2ndmolarsmayinvolvethemaxillarysinusthroughthisthinlamellaofbone. Themostcommonanatomicalvariationisthepresenceofinfraorbitalcell(Hallercell).Theseare pneumatizedanteriorethmoidalcellsprojectingalongtheflooroftheorbit.Thesecellswheninfected cancompromisedrainageofmaxillarysinus.Ifthiscellispresentremovingitduringsurgerywillallow preciseidentificationofflooroftheorbitandtheposteriorwallofmaxillarysinus.Thisisratheruseful whenanatomyisratherdistortedduetodisease.
Fig.3:CTscanshowingHallercell
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Paranasalsinusesdevelopfromridgesandfurrowsinthelateralnasalwall.Thisdevelopmentbegins asearlyas8thweekofintrauterinelifeandproceedswellintoearlyadulthood5. Themaxillaysinushasbiphasicgrowth.Thefirstphaseofgrowthoccurduringthefirst3yearsoflife whilethesecondphaseoccurbetween718years. Ethmoidsinus: Theethmoidsinusisreferredtoasethmoidallabyrinthbecauseofthecomplexityofanatomy,its honeycombedappearanceandpresenceofintricatepathwaysandblindalleys.Itissituatedinthe anteriorskullbase.Itislocatedlateraltotheolfactorycleftandolfactoryfossa.Itismadeupof complexbonylabyrinthofthinwalledcells.Afewethmoidcellsmaybepresentatbirth.Thisnumber couldeasilygobeyond15inadults.Thecommoninfectionsaffectingthepediatricagegroupoccurin thissinuses.Inadults610ethmoidcellsmaybepresent.Itisthemostcompartmentalizedofall paranasalsinuses.Thewidthofethmoidincreasesfromanteriortoposteriorbecauseoftheconelike structureoforbit. Boundaries: Lateralwall:isformedbytheorbitalplateoftheethmoidotherwiseknownasthelaminapapyracea. Thisisathinlaminaofboneseparatingtheorbitfromtheethmoidalaircells.Thiswallcouldbe dehiscent(normalvariant).Infectionsinvolvingtheethmoidaircellsmayspreadtotheorbitthrough thiswall. Roof:isformedbythefrontalboneanteriorly,thisareaisknownasfoveaethmoidalis7,andbythe faceofsphenoidandorbitalprocessofpalatineboneposteriorly.Thefrontalbonecomponentofthe ethmoidalroofisverythick.Thetransitionofthisthickfoveatothethinportionofroofofethmoid mediallyisveryweak.Thisisinfacttheweakestportionofthisareaandisproneto injuriesduringsurgeryleadingontocsfleak.Theanteriorandposteriorethmoidalarteriesrunalong theroofoftheethmoidfromlateraltomedial.Thesearteriesarebranchesofopthalmicartery. Theethmoidalcellsincreaseinsizefromabovedownwards,andfrombeforebackwards. Thecellsoftheethmoidsinusaredividedintotwogroups,theanteriorandposteriorgroup.The anteriorethmoidalcellsdrainintotheinfundibulumofthemiddlemeatuswhiletheposteriorethmoid cellsdrainintothesuperiormeatus.Theanatomyoftheethmoidalcellsarehighlyvariable, sometimesthemiddleturbinatemaycontainanaircellknownastheconchabullosa.Anenlarged conchabullosamayimpededrainagefromthemiddlemeatus.Anothercommonanatomicalvariation isthepresenceofaggernasiaircell.Thisisalargeethmoidalaircellpresentjustanteriortothe anterosuperiorattachmentofthemiddleturbinate.Sincethesecellslieincloseproximitytothe frontalrecessarea,theycouldimpedeventilationanddrainageofthefrontalsinus.Theseaggernasi cellsarecommonlyinvolvedinthepathogenesisoftheformationoffrontalmucocele.
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Fig.4:Diagramshowingmaxillaryandethmoidsinuses
Obstructiontothefrontalsinusdrainagebythepresenceofalageaggernasicellmaycause secretionswithinthefrontalsinustobedammedinside.Accumulationofmucoidsecretionscause enlargementoffrontalsinus.Atfirstthefrontalsinusenlargesinsizebyexpansionofitsbonywalls. Atalaterstageboneerosioncanalsooccur.commonlytheposteriortableofthefrontalsinusis eroded.Theanteriortablealsocanbeerodedinrarecases. Hallercellsareethmoidalaircellsbelongingtotheanteriorethmoidalgroup.Thesecellsarealso knownastheinfraorbitalcells.Enlargementofthesecellscanimpedethemaxillarysinusdrainage. Anothervariationistheextensionoftheposteriorgroupofethmoidalaircellssuperolateraltothe sphenoidsinus.Thesecellsareknownasonodicells.Thesecellslieperilouslyclosetotheopticnerve makingthematriskduringfesssurgeries. Simplifiedanatomyofethmoidalsinus: Theentireanatomyofethmoidsinuscanbesimplifiedifitisconsideredtobe5obliquelyoriented parallellamellae.Theselamellaeareembryologicallyknowntobederivedfromtheridgesinthe lateralnasalwallofthefoetusknownasethmoturbinals.Theselamellaearerelativelyconstantand areeasytoidentifyduringsurgery. FirstLamella: Thisistheanteriormostlamella.Anatoimicallythiscorrespondstotheuncinateprocess. Embryologicallythisrepresentsthebasallamellaofthefirstethmoturbinal.Thislamellais encounteredbythesurgeonfirst.Itshouldberemovedbeforeotherportionsoftheethmoidsinus anditsdrainagesystembecomesvisible. SecondLamella: ThiscorrespondstoBullaethmoidalis.Thisisthelargestandmostconstantoftheanteriorethmoidal aircells8.ThiscellwasidentifiedbyZukerkandl.Thisisusuallyroundinshapewiththinwalls.It extendsfromthelaminapapyraealaterallyandbulgesintomiddlemeatusmedially.Rarelythisair cellisnotpneumatizedresultinginabonyprojectionarisingfromlaminapapyracea.Thisprojectionis knownastoruslateralis. ThirdLamella: Thisisthemostimportantofalllamella.Thishappenstobethegroundlamella/BasalLamellaof middleturbinate.Thislamellaseparatesanteriorethmoidalaircellsfromposteriorethmoidalones. Thisdivisionismandatoryforthesimplereasonthatanteriorethmoidaircellsdrainviathemiddle meatusandposteriorethmoidalaircellsdrainviasphenoethmoidalrecess.Fromsurgeonspointof viewitisthelimitforanteriorethmoidectomy.Thislamellastabilizesthemiddleturbinate. FourthLamella:
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Thishappenstobethebasallamellaofsuperiorturbinate. FifthLamella: Thisisthebasallamellaofsupremeturbinate. Anteriorethmoidalaircells: AggerNasi: Thisistheanteriormostofallethmoidalaircells.ThetermAggerinLatinmeansMound/Eminence. Endoscopicallythiscellisvisualisedasaprominenceanteriortotheinsertionofmiddleturbinate. Rarelythispneumatizationcaninvolvetheanterosuperiorportionofunicinateprocess. Embryologicallythiscellisapneumatizationofsuperiorremnantoffirstethmoturbinalwhorlpresent inthelateralwallofnasalcavity.Identificationofaggernasiholdsthekeytoaccesstofrontalrecess area.Pneumatizationofaggernasicanhaveanimpactonuncinateprocessinsertionandpatencyof frontalrecessarea.
Fig.5:Largeaggernasicell
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pneumatizationoforbitalplateoffrontalbone.Thisinassociationwithlargeaggernasican compromisefrontalsinusdrainagepathway.Duringsurgerythisaircellcanbemistakenasfrontal sinus.Ontransilluminationwithtelescopethelightwillbeseenintheinnercanthalareaascompared tothatofsupraorbtialareawhichwillbetransilluminatedbyfrontalsinus8. Middleturbinatepneumatization: Sometimesmiddleturbinatemaybepneumatized.Apneumatizedmiddleturbinateisknownas conchabullosa.Pneumatizationofconchabullosausuallyarisesfromfrontalrecessarea/aggernasi aircells.Thisshouldbeconsideredasanormalvariantanddoesnotrequiresurgery.Ofcourse extensivepneumatizationmaynarrowosteomeatalcompleximpedingsinusdrainage.Thiscondition requriessurgicalintervention7. InterlamellarcellofGrunwald: Thiscellispneumatizationofverticalportion/lamellaofmiddleturbinate.Thispneumatizationarises fromthesuperiormeatus.ThisaircellwasfirstdescribedbyGrunwald7. OnodiCell: Thiscellisalsoknownassphenoethmoidalcell.ThiscellischristenedafterAdolfOnodi9ofBudapest whostudiedtherelationshipofethmoidaircellsinrelationtoopticnerve.Thesecellsbelongto posteriorethmoidgroup.Onodicellsextendsuperiorlyandlaterallytothesphenoidsinus.Its pneumatizationcanreachuptotheclinoidprocess.Thiscellisrelatedtoopticnerveinitslateralwall. Ifthiscellislargecarotidarterycouldbeseenbulgingfromitsposteriorwall.Anyattempttoopenthe sphenoidsinusthroughthiscellisfraughtwithdangerouscomplicationslikeinjurytoopticnerve/ internalcarotidartery.PreopCTscanisthebestwaytoidentifythiscondition.Forewarnedis forearmed.
Fig.6:CTscanaxialcutshowingonodicell
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sinusishighlyvariable. Posteriorwall:correspondstotheanteriorwalloftheanteriorcranialfossa. Floor:isformedbytheupperpartoftheorbits. Frontalsinusappearverylateinlife.Infacttheyarenotseeninskullfilmsbeforetheageof6. Thesinusdrainsintotheanteriorpartofthemiddlemeatusthroughthefrontonasalduct. Frontaloutflowtractshowsconglomeratizationofaircells Typesoffrontalsinusaircellsinclude: ITypeIfrontalcell(asingleaircellaboveaggernasi) IITypeIIfrontalcell(aseriesofaircellsaboveaggernasibutbelowtheorbitalroof) IIITypeIIIfrontalcell(thiscellextendsintothefrontalsinusbutiscontiguouswithaggernasicell) IVTypeIVfrontalcellliescompletelywithinthefrontalsinus Sphenoidsinus: Islocatedintheskullbaseatthejunctionoftheanteriorandmiddlecranialfossa.Pnematisationof sphenoidstartsduringthe4thyearofchildhoodandgetscompletedbythe17thyear.Thesphnoid sinusesvaryinsizeandmaybeasymmetric.Eachofthesesinusesareseparatedbyanintersinus septumwhichmaynotbeinthemidline.Becauseofasymetrytheintersinusseptumcouldbe deviatedtooneside.Thisintersinusseptumcouldattachposteriorlytothebonycarotidcanal.Care shouldbetakenwhileremovingthisseptumwithoutinjuringcarotidarterycanal.Itisprudenttouse truecutforcepstoremovetheintersinusseptum.Pneumatizationofsphenoidsinuscanalsoinvolve anteriorclinoidprocess,posteriorclinoidprocessandposteriorendofnasalseptum. Theydrainthroughthesuperiormeatusviaasmallostiumabout4mmindiameterlocated disadvantageously20mmabovethesinusfloor. Thissinusisrelatedtoseveralimportantvitalstructures.Theyare: 1.Pituitaryglandliesabovethesphenoidsinus. 2.Opticnerveandinternalcarotidarteriestraverseitslateralwall. 3.Thenerveofpterygoidcanallieinthefloorofthesinus. Henceinfectionsofsphenoidsinusmayinvolvetheopticnerveifthecanaloftheopticnerveis dehiscent. Typesofsphenoidalsinusesdependingonextentofpneumatization: Conchaltype: Inthistypetheareabelowthesellaisasolidblockofbonewithoutanaircavity.Thistypeiscommon inchildrenundertheageof12becausepneumatizationbeginsonlyaftertheageof12.
Fig.7:Conchaltypepneumatizationofsphenoid
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Fig.8:Sellartypepneumatization
Fig.9:Postsellartypepneumatization
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Theroofofthesphenoid(planumsphenoidale)anteriorlyiscontinuouswiththeroofofethmoidal sinus.Atthejunctionoftheroofandposteriorwallofsphenoidtheboneisthickenedtoformthe tuberculumsella.Inferiortothetuberculumsellaontheposteriorwallisthesellaturcica.Itformsa bulgeinthemidline.Theboneoverthesellacouldbe0.51mmthick.Thismaygetthinner inferiorly.Itishenceeasytobreechthesellainthistinnestpart.Thisareacanbeeasilyidentifiedby abluishtingeofthedurawhichisvisiblethroughthethinbonycovering. Possiblevariationsofintersinusseptumareasfollows: 1.Asinglemidlineintersinusseptumextendingontotheanteriorwallofsella. 2.Multipleincompleteseptaemaybeseen 3.Accessoryseptamaybepresent.Thesecouldbeseenterminatingontothecarotidcanaloroptic nerve. Lateralwallofsphenoidsinus:isrelatedtothecavernoussinus.Thissinusisformedbysplittingof thedura.Itextendsfromtheorbitalapextotheposteriorclinoidprocess.Cavernoussinuscontains verydelicatevenouschannels,cavernouspartofinternalcarotidartery,3rd,4thand6thcranial nerves.Italsocontainssomeamountoffattytissue.
Fig.10:Endoscopicviewofinteriorofsphenoid sinus
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Theprominenceofinternalcarotidarteryistheposterolateralaspectofthelateralwallofsphenoid sinus.Thisprominencecanbewellidentifiedinpneumatizedsphenoidbones.Ontheanterosuperior aspectofthelateralwallofsphenoidsinusisseenthebulgeformedbytheunderlyingopticnerve. Thesetwoprominencesareseparatedbyasmalldimpleknownastheopticocarotidrecess.The opticnerveandinternalcarotidarteryisseparatedfromthesphenoidsinusbyaverythinpieceof bone.Bonedehiscenceisalsocommoninthisarea. Histology: Allthesesinusesarelinedbyrespiratorytypepseudostratifiedciliatedcolumnarepithelium.This epitheliumiscomposedof4majortypesofcells: Ciliatedcolumnarcells Nonciliatedcolumnarcells Gobletcells Basalcells Sincethemucosaliningtheparanasalsinusesareattachedtotheboneitisknownas mucoperiosteum.Themucoperiostealliningofthesinusisthinnerthanthemucosalliningofthe nasalcavity.Thisliningiscontinuouswiththemucosalliningofthenasalcavityviathesinusostium6. Theostiumisthoughwhichvarioussinuscavitiescommunicatewiththenasalcavity.Theconceptof muciliaryclearancemechanismpushingthesecretionsoutviathenaturalostiumistheconcept behindfunctionalendoscopicsinussurgery.
References
1. [ArticleinGerman]FeldmannH.HNOKlinik,UniversittMnster.Laryngorhinootologie.1998 Oct77(10):58795. 2. LeonardodaVinci.1977.AnatomicaldrawingsfromtheRoyalCollection.London:RoyalAcademy ofArts.P50. 3. BlantonPL,BiggsNL(1969)Eighteenhundredyearsofcontroversy:theparanasalsinuses.AmJ Anat124(2):13547 4. StammbergerH(1989)Historyofrhinology:anatomyoftheparanasalsinuses.Rhinology 27(3):197210. 5. BolgerWE,AnatomyoftheParanasalSinuses.In:KennedyDW,BolgerWE,ZinreichJ(2001) Diseasesofthesinuses,Diagnosisandmanagement.B.C.Decker. 6. VanCauwenbergeP,SysL,DeBelderTetal(2004)Anatomyandphysiologyofthenoseandthe paranasalsinuses.ImmunolAllergyClinNorthAm24(1):117 7. StammbergerHR,KennedyDW(1995)Paranasalsinuses:anatomicterminologyand nomenclature.TheAnatomicTerminologyGroup.AnnOtolRhinolLaryngolSupplOct167:716 8. PolavaramR,DevaiahAK,SakaiOetal(2004)Anatomicvariantsandpearlsfunctional endoscopicsinussurgery.OtolaryngolClinNorthAm37(2):22142. 9. KantarciM,KarasenRM,AlperFetal(2004)Remarkableanatomicvariationsinparanasalsinus
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regionandtheirclinicalimportance.EurJRadiol50(3):296302.
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Choanal atresia
August 30, 2012 Rhinology
Authors
BalasubramanianThiagarajan
Abstract:Choanaisalsoknownasposteriornasalaperture.Nasalairwaycontinueswiththatof posteriornares.Airfromnasalcavityfindsitswayintothelungsviathechoanalapertures.Insome childrenthechoanamaybecongenitallyclosed.Thiscauseseithertotal(bilateralchoanalatresia)or partial(unilateralchoanalatreisa)nasalobstruction.Childbeingobligatenasalbreathers,findit ratherdifficulttobreathewhenthereisbilateralchoanalatresia.Thisismoresoduringthefirst6 weeksoflife.Hencebilateralchoanalatresiashouldbeconsideredasanemergencyinpaediatric agegroup.Thisarticleattemptstodiscusstheetiopathologyandmanagementofthiscondition. Introduction: Choanalatresiaisactuallyadevelopmentalfailureofthenasalcavitytocommunicatewith nasopharynx..Thisconditionisratherrareoccurringinabout1in10000livebirths.Thisconditionis morecommoninfemalechildrentheratiobeing2:11.About50%ofofthesepatientshaveother associatedcongenitalanamolies.ThemostcommonlyassociatedcongenitalanomalyisCHARGE Syndrome. CHARGESyndromeinclude2: CColoboma HHeartdisease AChoanalatresia RMentalandgrowthretardation GGenitalhypoplasia EEardeformities Otheranomaliesassociatedwithchoanalatresiainclude3: 1.Polydactyly 2.Nasal/auriculardeformities 3.Palataldeformities 4.Downssyndrome 5.DiGeorgesyndrome 6.Meningocele 7.Menigoencephalocele
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8.TreacherCollinssyndrome 9.Midfacehypoplasia Typesofchoanalatresia: 1.Unilateral/Bilateral:Unilateralchoanalatresiaisanincidentalfindingandisverycommon(about 70%)4.Highdegreeofsuspicionisnecessarytoidentifythiscondition.An infantwithunilateralchoanalatresiawillhaveproblemssucklingmilkfromthebreastoppositetothe sideofatresia. 2.Bonyatresia90%,Membranousatresia6%,Combinedatreisa4%5. Anatomicdeformititesassociatedwithchoanalatresiainclude6: 1.Thebonyatreticplateissituatedinfrontoftheposteriorbonyseptum 2.Nasalcavityisnarrowinthesepatients 3.Lateralpterygoidplatesarefoundtobethickenedcompromisingthenasalairway 4.Mediallyvomeristhickened 5.Inbetweenlateralpterygoidandvomeristhemembranousplate 6.Higharchedpalateiscommoninthesepatients Historyofchoanalatresia: ThisconditionwasfirstdescribedbyJohannGeorgeRoedererin1755.Thiswaslatertermedasan anatomicalabnormalityofpalatinebonebyAdolfOttoin18547. CarlEmmerthasbeensuccessfullycreditedwiththefirstchoanalatresiarepairin18547. Embryologyofchoanalatresia: Developmentoffaceandcranialstructuresoccurduringthefirst12weeksofgestation.The developmentofchoanaetakesplacebetweenthe4thand11thweeksofgestation8.Cranial structuresdevelopfromneuralcrestcellmigration.Developmentofnosebeginsduringthe4thweek ofgestation.Thisisindicatedbytheformationofnasalpits.Duringthe5thweekofgestationthe nasalpitsbegintofoldinwardsintothemesenchymeformingnasalsacs.Theseprimitivenasalsacs areseparatedfromoralcavitybyoronasalmembranes.Duringthe8thweekofgestationthis oronasalmembranerupturescreatingnasalcavityandaprimitivechoanalocatedatthejunctionof nasalcavitiesandnasopharynx.Duringthisphaseofdevelopmentthereisgradualproliferationof neuralcrestcells.Thesecellscontributetotheformationofskullbaseandnasalvaults.Duringthe 10thweekofgestationthenasalseptumanddevelopingpalatefuse.The primitivechoanaegetspushedposteriorly.Thischoanaewhichformsduringthe10thweekof gestationisknownasSecondarychoanae.Innormalfoetusthesesecondarychoanaearepatent forafunctioningairwaybetweentheanteriornasalcavityandnasopharynx9. Theoriesofdevelopmentofchoanalatresia10: Fourtheoriesforthedevelopmentofchoanalatresia:
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1.Persistenceofabuccopharyngealmembranefromtheforegut. 2.PersistenceofthenasobuccalmembraneofHochstettermostcommonlyacceptedtheory. 3.Theabnormalpersistenceorlocationofmesodermaladhesionsinthechoanalregion. 4.Amisdirectionofmesodermalflowsecondarytolocalgeneticfactorsbetterexplainsthepopular theoryofpersistentnasobuccalmembrane Othertheoriesthatarenotsowidelyacceptedinclude: 1.Resorptionofthefloorofsecondarynasalfossa 2.Incompletedorsalextensionofnasalcavity 3.Migrationofdorsalpartoffrontonasalprocesstofusewiththepalatalshelves Studieshaverevealedthatcraniofacialanamolieswithmesenchymaldamageandcelldisruption werefoundinmotherswhoingestedhighdosesofvitaminAduringtheirperiodofpregnancy. Thishasbeenattributedtodisturbancesinmigrationpatternofneuralcrestcells,whichisalso followedbydisturbancesinmesodermdevelopmentinthecraniofacialarea11. Inpatientswithchoanalatresiatheatreticplatehasthefollowingboundaries: Superiorundersurfaceofbodyofsphenoid Lateralmedialpterygoidlamina Medialvomer Inferiorhorizontalplateofpalatinebone Thisanatomicalknowledgeofatrophicplateishighlyvaluablewhileperformingsurgeryonthese patients. Clinicalfeatures: Bilateralchoanalatresiaisconsideredtobeaneonatalemergency.Theseinfantspresentwith asphyxianeonatorum.Bilateralchoanalatresiaiscommonlyassociatedwith: 1.NursingdifficultiesSuckingdifficulties 2.RespiratorydistressCyclic.Whentheinfantfallsasleepitbecomesbreathlessasthenoseis blocked 3.Respiratoryinfectionscanoccurduetoaspiration 4.Recurrentnasalallergies 5.Cyanosiswhichgetsbetterwhenthechildcries. 6.Cryisnotnormal(Rhinolaliaclausa) 7.Bilateralchoanalatresiaisalsocommonlyassociatedwithotherbirthdefectslikeorofacial defects,cardiacdefectsandlimbdefects12. Teratogenicsyndromescausingbilateralchoanalatresiainclude:
13
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1.Methimazoleembryopathy13 2.Carbimazoleembryopathy14 Detaileddrugintakehistoryisamustindiagnosingembryopathies. Unilateralchoanalatresiaiscommonlymissed.Theseinfantsfinddifficultyinsuckingmilkfrombreast oppositetothesideofchoanalatresia.Thesechildrenhaveunilateralnasalobstructionwithnasal discharge.Astrongdegreeofsuspicionisamusttoidentifythiscondition. Teststoidentifychoanalatresia: 1.Attemptingtopass68sizedFrenchplasticcatheterthroughthenose.Ifthereisnoatresiathe catheterwilleffortlesslypassthroughthenasalcavityintothenasopharynx.Ifthereischoanalatresia thenatypicalsolidfeelingwouldbeencounteredatabout33.5cmsfromthealarrim.Ifobstruction isencounteredwithin12cmsfromtheanteriornares,thenitcouldbecausedduetotraumatic deflectionofnasalseptumduetotrauma. 2.Whenawispofcottonisplacedclosedtothenasalopeningthenitwouldmoveinthepresenceof airflow. 3.Whenmethylenedyeisinstilledintotheanteriornasalcavityitcanbeseenpassingthroughthe nasopharynx.Obstructionduetochoanalatresiawillpreventflowofmethylenedyeintothe nasopharynx. CTscanimagingisvirtuallydiagnostic: Ithastheuniqueadvantageofdifferentiatingmembranouschoanalatresiafrombonyones.In patientswithcombinedatresiaitwillalsorevealthecontributionofthesetwoelementstotheatretic plate.Actualstructuresinvolvedintheatreticplatewouldbeclearlyseen.Inallthesepatients vomerappearstobethickened,thelateralnasalwallbendsmediallytofusewithvomerthereby obstructingthenasalcavity. Management: Inbilateralchoanalatresiasecuringtheairwaytakesthetoppriority.Anoralairwaycanbe introducedtotideovertheimmediatecrisis. Roleofintraoralnipple: Anipplewithalargeopening(McGovern)Nipple15canbeintroducedintotheoralcavityoftheinfant totideoverthecrisis.Thisprovidesadequateairwaytotheinfant.Asmallinfantfeedingtubecanbe passedthroughanothersmallopeningpresentinthenippleoralongsidethenipplefor gavagefeeding.Thishelpstobuytimetillthechildhasgainedadequateweighttowithstand correctivesurgery. Tracheostomy: Thisshouldbeconsideredonlyonrarestofrareoccasionswhenthepatientisnotabletoadequately maintainoralairway. Timingofrepairinunilateralchoanalatresia: Choanalatresiarepairinunilateralatresiaisdelayedtillthechildreachesitsfirstbirthday.Thisallows
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thesurgerysitetoenlargetherebyreducingtheriskofpostopstenosis.Bleedingisalsoreducedif surgeryisdelayed.Olderinfantstoleratestentingbetterthanyoungones. Transnasalapproach: Transnasalapproach:(usingendoscopes):Thesurgeryisperformedundergeneralanesthesia.A selfretainingnasalspeculumisusedtoexposethenasalcavityandtheatreticplate.Iftheatresiais membranousinnatureasimpleperforationofthesameunderendoscopicguidancewouldsuffice. Thenasalcavityisdecongestedusing4%xylocainewithadrenalineintheconcentrationof1in 10,000concentration.Underendoscopicguidanceamucosalincisionismadeandthemucosalflaps areelevatedexposingtheposteriorvomerandlateralpterygoidlamina.Adiamondburronanangled handpieceisusedtodrilltheatreticbonyplate.Itisperforatedatthejunctionofthehardpalateand thevomer.Incidentallythisisthethinnestpartoftheatreticplate.Thisprocedurewasfirstdescribed byStankiewicz.Toimprovevisualisationtheinferiorturbinatecanbeoutfractured orevenbetrimmed.Afterdrillingcareistakentopreservethemucosalflaps.Asilasticstentisplaced intoeachnostrilpassingthroughthedrilledneochoana.Thishelpsinreducingtheincidenceof restenosis.Stentiskeptinplaceforatleast6weeks19. Openingmadeshouldbelargeenoughtoallowsmoothpassageofsuctioncatheter.34size Endotrachealtubecanbeusedasstenttopreventrestenosis.Thesizeshouldbechoosencarefully insuchawaythatitshouldbeadequatetopreventrestensosisandinadequatetocausenasal regurgitation. Caution: Whileperformingthisprocedurecautionmustbetakennottoinjurethesphenopalatinevessels behindthemiddleturbinate. Advantagesofthisprocedure: 1.Thisprocessisfasterandeasier 2.Bloodlossisminimal 3.Canbeperformedinchildrenofallageswhodonothaveassociatedexternalnasaldeformities 4.Childcanbeimmediatelybreastfed 5.Childcanbedischargedonthe3rddayitself Disadvantages: 1.Visionishighlylimitedespeciallyinthenewborn 2.Inabilitytoadequatelyremoveenoughoftheposteriorvomerineseptalboneandprevent restenosis 3.Longerstentingtime 4.Endoscopesdonotofferbinocularvision 5.Cannotbedonesafelyandwithgoodresultsonpatientswithmultiplenasalandnasopharyngeal anomalies.
18
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FirsttransnasalrepairofchoanalatresiawasperformedbyDehaen18in1985.Heusedmicroscope formagnificationandvisulizationoftheatreticplate. Endoscopictransnasalapproach16isfacilitatedbyadvancesininstrumentation,anesthesia,imaging etc.CTimagingrevealstheamountofcontributiontothestenoticsegmentbythelateralnasalwall.It isprudenttoavoiddrillingtoomuchintothelateralnasalwallasitcoulddamagethe sphenopalatinevessels17.Useofpoweredinstrumentationlikesofttissueshaversanddrillshave madethisprocedurealotsafer. UseofMitomycinC19topreventrestenosis: InadditiontoroutinestentingrestenosiscanbepreventedbytopicalapplicationofMitomycinC, whichisanantimetaboliteknowntoinhibitfibroblastformation. Complicationsofuseofstentsfollowingtransnasalrepairofchoanalatresia: 1.Formationofgranulationtissue 2.Crustformation 3.Septalperforation 4.Persistentnasaldischarge Transpalatalapproach: Thisapproachismoresuitableforbilateralchoanalatresia.Undergeneralanesthesiathepalateis exposedwithamouthgag.Palatalmucosaisinfiltratedwith2%xylocainewith1in100000 adrenaline.Thisinfiltrationservesthedualpurposeofhelpinginflapelevationandprovidingmuch neededhemostasisduringtheentiresurgicalprocedure.Acurvedincisionisgivenonthepalate startingfromjustbehindthemaxillarytuberosityononesideandiscarriedmediallyalong thealveolarridgeuptothecanineregion.Thesameincisioniscarriedoutevenontheoppositeside. AUshapedpalatalflapiselevated.Thisflapiselevateduptotheedgeofthehardpalate. Thegreaterpalatineneurovascularbundleispreservedatallcosts.Thesoftpalateisnowretracted posteriorlyandsuperiorlyexposingtheposterioredgeofhardpalate.Thisareaistheareafor dissection.Theposterioredgeofhardpalateistakendownusingkerrisonspunchordrill.The nasalmucosaisexposed.Thismucosalflapisliftedposteriorlytillthechoanaisreached.The posteriorportionofnasalseptumandlateralsuperiornasalwallisalsotakendown.Astentisplaced. Themucosalflapisthenredrapedinposition. Complicationsoftranseptalapproach: 1.Pressurenecrosisofcolumella 2.Pluggingofstent 3.Displacementofstent 4.Palataldehiscence 5.Maxillaryhypoplasiacausingmalocclusion 6.Granulationtissueformationaroundthestents.
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Endoscopicviewofchoanalatresia
CTscanshowingbilateralchoanalatresia
References
1. TheogarajSD,HoehnJG,HaganKF.Practicalmanagementofcongenitalchoanalatresia.Plast ReconstrSurg198372:63442. 2. BergstromL,OwensO.Posteriorchoanalatresia:asyndromaldisorder.Laryngoscope198494: 12736. 3. HarrisJ,RobertE,KallenB.Epidemiologyofchoanalatresiawithspecialreferencetothe
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CHARGEassociation.Pediatrics199799:3637. 4. DobrowskiJM,GrundfastKM,RosenbaumKN,ZajtchukJT.Otorhinolaryngicmanifestationsof CHARGEassociation.OtolaryngolHeadNeckSurg198593:798803. 5. BrownOE,PownellP,ManningSC.Choanalatresia:anewanatomicclassificationandclinical managementapplications.Laryngoscope1996106:97101. 6. HarnerSG,McDonaldTJ,ReeseDF.Theanatomyofcongenitalchoanalatresia.Otolaryngol HeadNeckSurg198189:79. 7. HengererAS,BrickmanTM,JeyakumarA.Choanalatresia:embryologicanalysisandevolutionof treatment,a30yearexperience.Laryngoscope.May2008118(5):862866. 8. DunhamME,MillerRP.Bilateralchoanalatresiaassociatedwithmalformationoftheanteriorskull base:embryogenesisandclinicalimplications.AnnOtolRhinolLaryngol.Nov1992101(11):916919. 9. JohnstonMC.Theneuralcrestinabnormalitiesofthefaceandbrain.BirthDefectsOrigArticSer. 197511(7):118. 10. http://www.drtbalu.co.in/choa_atre.html 11. MosseyPA,LittleJ,MungerRG,DixonMJ,ShawWC.Cleftlipandpalate.Lancet.Nov21 2009374(9703):17731785. 12. BurrowTA,SaalHM,deAlarconA,MartinLJ,CottonRT,HopkinRJ.Characterizationof congenitalanomaliesinindividualswithchoanalatresia.ArchOtolaryngolHeadNeckSurg.Jun 2009135(6):543547 13. ClementiM,DiGianantonioE,PeloE,MammiI,BasileRT,TenconiR.Methimazole embryopathy:delineationofthephenotype.AmJMedGenet.Mar5199983(1):4346. 14. WolfD,FouldsN,DayaH.Antenatalcarbimazoleandchoanalatresia:anewembryopathy.Arch OtolaryngolHeadNeckSurg.Sep2006132(9):10091011. 15. McGovern,FH.Associationofcongenitalchoanalatresiaandcongenitalheartdisease.Reprotof twocases.Ann.Otol.Rhinandlaryng195362:894895 16. McGovern,FH.Associationofcongenitalchoanalatresiaandcongenitalheartdisease.Reprotof twocases.Ann.Otol.Rhinandlaryng195362:894895 17. PasquiniE,SciarrettaV,SaggeseD,CantaroniC,MacriG,FarnetiG.Endoscopictreatmentof congenitalchoanalatresia.IntJPediatrOtorhinolaryngol200367:2716. 18. DehaenF,ClementPA(1985)Endonasalsurgicaltreatmentofbilateralchoanalatresiaunder opticcontrolintheinfant.JOtolaryngol14:9598. 19. SelikYK,BiesmanBS,RebeizEE(2000)TopicalapplicationofMitomycinCinendoscopic dacryocystorhinostomy.AmJRhinol14:205207.
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Complications of sinusitis
January 16, 2013 Rhinology
Authors
BalasubramanianThiagarajan
Abstract
Anatomicallyparanasalsinusesareincloseproximitytovitalstructureslikebrainandorbit.Lesions affectingnasalsinusescanaffecttheseareasaswell.Infectionsinvolvingmucosalliningofparanasal sinusescanalsospreadtotheseadjacentvitalareas.Thisarticleattemptstostudytheorbitaland intracranialcomplicationsofsinusitis.
Introduction: Anatomicallyparanasalsinusesarecloselyrelatedtoorbitandskullbase.Theysharecommonbony boundaries,andbloodsupply1.Complicationsattributedtosinusitisarecausedbyspreadof infectionstoadjacentareas2. Routesofspread: 1.Bacterialinfectionsfromthesinusescanspreadthroughnaturaldehiscencesandweaknessofthe bonybarriers.Inchronicinfectionsthesurroundingboneundergoessclerosis,whileinacutesinusitis massiveosteolysisiscommonlyseen. 2.Laminapapyraceaisapaperthinboneseparatingtheorbitfromtheethmoidalsinuses.Congenital dehiscencesofthisboneiscommonlyseenthroughwhichspreadofinfectioncanoccurfromthe ethmoidsintotheorbit.Inchildhoodthefrontalsinusesareunderdevelopedandorbitalcomplications arecausedcommonlybyacuteethmoiditis. 3.Floorofthefrontalsinusesformtheroofoftheorbit.Inolderchildrenandinadultsfrontalsinus infectionscanspreadintotheorbitcausingorbitalcomplications. 4.Infraorbitalcanalintheflooroftheorbitisaweakareathroughwhichinfectionsfromorbitmay enterintothemaxillarysinus. 5.Spreadofinfectioncanalsooccurviadiploicveinspresentinthefrontalbone.Theseveinsare knownastheveinsofBreschet.Thisisprecededbythrombophlebitis. 6.Venousconnectionsbetweenthesinusesandtheorbitdonothaveanyvalvesfacilitatingspreadof infectionfromthesinusestotheorbit3. 7.Therootsofthesecondpremolarandthefirstuppermolarareintimatelyrelatedtothefloorofthe maxillarysinus.Thisfacilitatesatwowayspreadofinfection.Incasesofisolatedmaxillarysinusitis dentalcausesmustbesuspected. Predisposingfactorsfordevelopementofcomplicationsfollowingsinusitis: 1.Immunocompromisedpatient(e.g.HIV)
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2.Diabetesmellitus 3.Irregulartreatmentforsinusinfections 4.Inappropriate/Inadequateantibiotictherapy Complicationsofsinusitisinclude: 1.Orbitalcomplications(Commonest) 2.Intracranialcomplications4(includingmeningitis,subduralempyema,intracerebralabscess, epiduralabscess,cavernoussinusthrombosis) 3.Mucocele 4.Pyocele 5.Osteomyelitis 6.Pyocele 7.Facialcellulitis 8.Subperiostealabscess Orbitalcomplicationsofsinusitis: Thisismorecommoninyoungerindividuals.Orbitalcomplicationsarefrequentlycausedby ethmoiditisbecauseethmoidalsinussharesitsborderwithorbit.Laminapapyracea(paperthinbone) isthelateralbarrierseparatingethmoidalsinusfromorbit.Thisbonecaneasilybebreachedduring activeinfections.Ethmoiditisasacausefororbitalcomplicationisrathercommoninyoungchildren, whereasinadultsfrontalsinusitishappenstobethemostcommoncausefororbitalcomplications.In adultssphenoidsinusitiscaninvolveopticnerveleadingontoblindness.Leftorbitis commonlyinvolvedthanrightone5.Theincidenceoforbitalcomplicationsfollowingsinusitisishighly variablei.e.Morethan20%.7 Hubertsclassificationoforbitalcomplicationsofsinusitis8: Hubertclassifiedorbitalcomplicationsarisingfromsinusitisintofivegroups: GroupI:Inflammatoryoedemaofeyelidswithorwithoutoedemaoforbitalcontents. GroupII:Subperiostealabscesswithoedemaoflidsorspreadofpustothelids. GroupIII:Abscessoforbitaltissues GroupIV:Mildtosevereorbitalcellulitiswithphlebitisofophthamicveins GroupV:Cavernoussinusthrombosis Smith&Spencerclassificationoforbitalcomplications: GroupI:PreseptalcellulitisCharacterisedbyoedemaofeyelidswithouttenderness,visuallossor limitationofocularmobility. GroupII:Orbitalcellulitiswithoutabscessformationcharacterisedbydiffuseoedemaofadipose tissuesoforbit. GroupIII:Orbitalcellulitiswithsubperiostealabscessformationwithdisplacementoftheglobe.May
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ormaynotbeassociatedwithvisualloss.Ocularmobilityisrestricted. GroupIV:Orbitalcellulitiswithintraperiostealabscess.Herethedisplacementofglobeisseverewith restrictionofocularmobility. GroupV:Cavernoussinusthrombosis. Routeofspreadtoorbit: 1.Throughbonydehiscence/defect(maybecongenitaloracquired) 2.Throughneurovascularforamen 3.Throughvenouschannels Chandlerclassifiedorbitalinfectioninto5stages9: StageI: Periorbitalcellulitis.Alsoknownaspreseptalcellulitis.Itshouldnotbeconfusedwithorbitalcellulitis whichoccursbehindtheorbitalseptum.Thisconditionisactuallyinflammationandinfectionofthe eyelidandportionsofskinaroundtheeye.Thesepatientsdonothaveproptosis,limitationofeye movement,painfuleyemovementandlossofvision.Thesefeaturesactuallyhelpindifferentiating preseptalcellulitisfromorbitalcellulitis.Eyelidsinthesepatientsappearswollenbutnottender.There isnochemosis. StageII: Orbitalcellulitis.Alsoknownaspostseptalcellulitis.Thisconditionischaracterizedbypronounced oedemaandinflammationoforbitalcontentswithoutabscessformation.Thesepatientshavevarying degreesofproptosis,restrictionofocularmovements,painfuleyemovementsandchemosis.Since lossofvisioncouldoccurinthesepatientsitismandatorytomonitortheirvisiononaregularbasis. StageIII: Subperiostealabscess.Abscessdevelopsinthesepatientsbetweenboneandperiosteum.Orbital contentsareinvariablydisplacedinaninferolateraldirectionduetomasseffectofaccumulatingpus. Chemosisandproptosisareinvariablypresent.Decreasedocularmobilityandlossofvisionmayalso occurinthesepatients. StageIV: Orbitalabscess.Thisinvolvescollectionofpuswithintheorbitalcontents.Thisiscauseddueto relentlessprogressionoforbitalcellulitisorruptureoforbitalabscess.Thesepatientshavesevere proptosis,completeopthalmoplegiaandcommonlylossofvisionalso. StageV: Cavernoussinusthrombosis.Developmentofbilateralocularsignsistheclassicfeatureofthisstage. Thisstagecarriesworseprognosis.Featuresofthisstageinclude10: 1.Fever 2.Headache 3.Photophobia
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References
1. BolgerWE,AnatomyoftheParanasalSinuses.In:KennedyDW,BolgerWE,ZinreichJ(2001) Diseasesofthesinuses,Diagnosisandmanagement.B.C.Decker. 2. BalasubramanianThiagarajan.AnatomyofParanasalsinuses[Internet].Version9.EntScholar. 2012Nov8.Availablefrom:http://entscholar.wordpress.com/article/anatomyofparanasalsinuses/. 3. YounisRT,LazarRH,AnandVK.Intracranialcomplicationsofsinusitis:a15yearreviewof39 cases.EarNoseThroatJ200281:63644. 4. BluestoneCD,SteinerRE,Intracranialcomplicationsofacutefrontalsinusitis.SouthMedJ1965 58:110. 5. GambleR.C(1933),Acuteinflammationoftheorbitinchildren.ArchivesofOphthalmology10, 483497. 6. Chandler.J.R,Langenbrunner.D.JStevens.E.R(1970).ThepathogenesisofOrbitalcomplications inacutesinusitisLaryngoscope80,14141428 7. Chandler.J.R,Langenbrunner.D.JStevens.E.R(1970).ThepathogenesisofOrbitalcomplications inacutesinusitisLaryngoscope80,14141428 8. LavaniaA,SharmaV,ReddyNS,BakshR.Orbitalcellulitis:AComplicationofsinusitis KathmanduUniversitymedicaljournal2005Jul3(3):292293 9. ChandlerJR,LangenbrunnerDJ,StevensER.Thepathogenesisoforbitalcomplicationsinacute sinusitis.Laryngoscope197080:141428. 10. YaringtonCT,Jr.Cavernoussinusthrombosisrevisited.ProcRoyalSocMed.197770:456459.
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Authors
BalasubramanianThiagarajan Abstract: AccordingtoEuropeanrhinologicalsocietyguidelineschronicrhinosinusitiswithnasalpolypiand chronicrhinosinusitiswithoutnasalpolypiaretwodifferententities.Thisarticleattemptstoreview publishedliteraturewhichattemptstostudylinkbetweennasalpolyposisandlowerairwaydisorders. Theconceptofunifiedairwayattemptspreciselytoexplainthislinkage.Developmentallyand functionallyitmakessensetocombinebothupperandlowerairwaysinstudyingpathophysiologyof variousairwaydisorders. Introduction: Anattempttodefinethefollowingterminologieswillnotbeoutofplace. Rhinosinusitis/Nasalpolyposis: Numberofauthorshaveattemptedtodefinethiscondition,majorityofthesedefinitionswerebased onsymptomatologyanddurationofthedisease.Tilldatethereisnouniversallyaccepteddefinitionof thiscondition1.Europeanrhinologicalsocietyhassteppedintodefinerhinosinusitisinunambiguous terms. Rhinosinusitis/Nasalpolyposisisdefinedas: Inflammationofmucosalliningofnoseandparanasalsinusescharacterisedbytwoormore symptoms,oneofwhichshouldbeeithernasalblock/nasalobstruction/nasaldischarge(anterior/ posteriordischarge): Presenceorabsenceoffacialpain/tenderness Reduction/Lossofsmell. And/either: Endoscopicsignsof: Polypi Mucopurulentdischarge/oedematousmucosaovermiddlemeatus And/either CTscanchangesshowingmucosaloedema/OMCobstruction Theseverityofthediseasecanbeclassifiedusingvisualanaloguescale: 1.MildVisualanaloguescore03 2.ModerateVisualanaloguescore37 3.SevereVisualanaloguescore710
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Visualanaloguescoreofmorethan5affectsqualityoflifeofthepatient. Durationofthedisease: Acute:<12weekswithcompleteresolutionofsymptoms Chronic:>12weekswithoutcompleteresolutionofsymptoms.Chronicrhinosinusitiscanshow periodsofacuteexacerbations. Studiesattempttodividechronicrhinosinusitiswith/withoutnasalpolyposisbasedoninflammatory markers2,3.Whynasalmucosaballoonsintopolypiincertainpatientswithchronicsinusitisisstillan enigma.Inthesepatientspolypitendtorecurevenafterapparantlycompletesurgicalremoval.Some studieshavedemonstratedpronouncedeosinophiliaandIL5expressioninpatientswithnasal polyposisthaninthosewithchronicsinusitiswithoutnasalpolypi.Samterinhisclassicdescription statesthepresenceofatriadinsomeofthesepatients.ThistriadgoesafterhisnameSamters Triad.PatientswithSamterstriadhaveasthma,aspirinhypersensitivityandnasalpolyposis. Majorityofpatientswithchronicrhinosinusitiswithnasalpolypolismanifestwithasthmaandbronchial hyperresponsiveness3.Theroleofmedicosurgicalmanagementofnasalpolyposisinmanaging patientswithassociatedlowerairwaysymptomatologyisstillnotclear.Somestudiesevengotothe extentofsuggestingthatsurgicalremovalofnasalpolypiinthesepatientsactuallyworsensbronchial asthmainthesepatients4.Vleming5inhisstudyhasreportedthatnasalpolypectomyactuallyhelped inalleviatingsymptomsduetobronchialasthmainthesepatients. Theoreticallylarynxisconsideredtobetheboundarybetweentheupperandlowerairwaysystem. Functionallyspeakingthemajorfunctionoftheupperairwayistoconductairandalsomakeitfitfor gasexchangeinthelowerairwaybyaddingmoisturetoinspiredair.Thelowerairwayplaysavital roleingasexchange.Currentlythetermunifiedairwayencompassesthefollowingstructures:middle earmucosa,nasalcavityandparanasalsinusmucosa,andtheentiretracheobronchialtree.Studies havedemonstratedthatpathologiesaffectingoneportionofthisunifiedairwayultimatelyprogresses toinvolvetheotherareasaswell. ItwasKellerin19206whonoticedthatcommonlypatientswithlowerrespiratorydiseasesalsohad complaintspertainingtotheupperairwayaswell.Kelleralsohypothesisedthatdecreasedabilityof upperairwaytohumidifyinspiredairleadstoworseningofbronchialasthma.
Conceptofunifiedairway
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Currentstatusisthatwheneveradiagnosisofrhinitisorasthmaisconsideredthentheentireairway shouldbe evaluated7.EvenGastrooesophagealreflux8diseasehasalsobeenimplicatedwithairway disorders.Hencenoinvestigationforasthma/upperairwaydisorderiscompletewithoutupperGI endoscopy. Criteriasupportingtheconceptofunifiedairway: 1.Patientswithupperairwaydiseaseslikerhinitisandrhinosinusitishaveincreasedprevalenceof lowerrespiratorydisorderslikebronchialasthma 2.Patientswithlowerairwaydisorderslikebronchialasthmahaveincreasedprevalenceof rhinosinusitis 3.Pathophysiologicalmechanismscausingbothupperandlowerairwaydisordersaremoreorless similar 4.Treatingonecomponentofunifiedairwaydisordershouldhavebeneficialeffectontheother componentsaswell. Correns9roleinstrengtheningtheconceptofunifiedairway: Correntinhisclassicalpaperclearlydemonstratedthecoexistanceofrhinitisinpatientswith bronchialasthma.Healsoobservedatemporalrelationshipbetweenbronchialasthmaandrhinitis. Hestatedthatattacksofbronchialasthmawasprecededbyanattackofrhinitis. AccordingtoGuerraetal10sufferersofallergicrhinitisarethreetimesmorelikelytodevelopasthma whencomparedtocontrolsintheirstudy. Startingfrom1991whenNatioalInstituteofHealth11classifiedasthmaasinflammatorydisease, therebyshiftingthefocusfrombronchospasmtoinflammation.Thiscausedamajorshiftinthe treatmentstratergy.Inflammationisthecommondenominatordefiningbothupperandlowerairway disorders.Itshouldalsobestressedatthispointthattheliningepitheliumofbothupperandlower airwayi.eciliatedcolumnarepitheliumfunctionallyaresimilar.Inresponsetochronicinflammationthe
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mucosalliningofbothupperandlowerairwaydemonstratesimilarhistopathologicalpatternsi.e. Inflammatorycellularinfiltrateandeventualthickeningofbasementmembrane.Eosinophilshave beenidentifiedasthecommoninflammatorycellcausingproblemsindisordersinvolvingbothupper andlowerairway.Otherinflammatorycellsthathavebeenimplicatedinunifiedairwaydisorders includeCD4TLymphocytesandmononuclearcells. Themostcompellingproofoftheconceptofunifiedairwaycomesfromthefactthattheinflammatory mediatorsreleasedstartingthecascadeofinflammationintheupperandlowerairwayarevirtually thesame.Inflammatorytriggersfromoneportionofairwayalsoaffectsotherportionsaswell. Hencebyviewingtheentireairwayasasingleunitpatientreapsthebenefitofunifiedtreatment protocol.Itisalwaysprudenttocontrolchronicsinusitisinadditiontomanagingasthmaby bronchodilators.Successfulmanagementofchronicrhinosinusitisresultsindecreasedasthma medication12inthesepatientswithtelltaleimprovementinpulmonaryfunction.Anadditionalbenefit beingreducednumberofexacerbations. Mechanismsresponsibleforunifiedairwaydisease: 1.Nasobronchialreflex 2.Lossofnasalprotectiontolowerairway 3.Sharedinflammationthroughouttherespiratorytract Nasobronchialreflex: ThisconceptwasfirstproposedbySluder13whostatedthatnasalirritationcancausebronchial irritationleadingontobronchospasm.Kaufmann14andWrightaddedfurtherprooftothisconcept.In theirstudytheyappliedsilicaparticlestothenasalmucosaofindividualswithoutbronchialasthma anddemonstratedthereisincreasedlowerairwayresistancefollowingthisapplication.Evenin individualsinwhomthisreflexisnotreadilydemonstrabledelayedchangeshavebeendemonstrated inthelungsstartingfrom30mins4hoursfollowingantigenicchallengeofnasalmucosa.This observationsuggeststhatothermechanismsinadditiontodirectreflexarc15couldberesponsiblefor interactionbetweenupperandlowerairwaystructures. Lossofnasalprotectiontonasalairway: ThisconceptwasfirstproposedbyShturmanEllesteinin197816.Intheirclassicexperiments performedonvolunteerstheywereabletodemonstratethatmouthbreathingworsened bronchospasm,whilenasalbreathingreducedlowerairwayresistance.Thisphenomenoncanbe explainedwhentheprimaryfunctionofthenosalairway(airconditioning)istakenintoconsideration. Lowerairwayrespondstounconditionedinspiredairbyincreasingtheirresistancetotheinspiredair. Thiscaninfactbeconsideredtobeaprotectivemechanism. Sharedinflammation: Thisconceptisalsocatchingupasoneoftheexplanationsforcommonpathologicalbasisofunified airwaydisorders.Thisconcepthasfounditsrootfromtheobservationthatinflammatorydisordersof variousportionsoftheunifiedairwayarecausedbyreleaseofsameimmune/inflammatory mediators.Braunstahletal17observedthatstimulationofoneportionoftheairwaymucosawith anigenresultsinasystemwideinflammatorychangeswithinhours. Conclusion:
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References
1. AnonJB,JacobsMR,PooleMD,AmbrosePG,BenningerMS,HadleyJA,etal.Antimicrobial treatmentguidelinesforacutebacterialrhinosinusitis.OtolaryngolHeadNeckSurg.2004Jan130(1 Suppl):145. 2. HedmanJ,KaprioJ,PoussaT,NieminenMM.Prevalenceofasthma,aspirinintolerance,nasal polyposisandchronicobstructivepulmonarydiseaseinapopulationbasedstudy.IntJEpidemiol. 199928(4):71722. 3. LarsenK.Theclinicalrelationshipofnasalpolypstoasthma.AllergyAsthmaProc.199617(5):243 9. 4. LawsonW.(1991)Theintranasalethmoidectomy:anexperiencewith1077procedures.101:367 371 5. VlemingM.,StoopA.E.,MiddelweerdR.J.,deVriesN.(1991)Resultsofendoscopicsinus surgeryfornasalpolyps.5:173176. 6. KellerI.Sinusdisease.Lancet192040:1334 7. BousquetJ,vanCauwenbergeP,KhaltaevN,etal.Allergicrhinitisanditsimpactonasthma (ARIA):executivesummaryoftheworkshopreport.Allergy200257:84155. 8. LoehrlTA,SmithTL.Chronicsinusitisandgastroesophagealreflux:aretheyrelated?CurrOpin OtolaryngolHeadNeckSurg200412:1820. 9. CorrenJ.Theconnectionbetweenallergicrhinitisandbronchialasthma.CurrOpinPulmMed 200713:138. 10. GuerraS,SherrillDL,MartinezFD,etal.Rhinitisasanindependentriskfactorforadultonset asthma.JAllergyClinImmunol200210941925. 11. NationalAsthmaEducationandPreventionProgram(NAEPP).Guidelinesforthediagnosisand managementofasthma.NationalHeart,Lung,andBloodInstitute.NationalAsthmaEducation Program.ExpertPanelReport.JAllergyClinImmunol199188:425534. 12. StelmachR,doPatrocinioT,NunesM,etal.Effectoftreatingallergicrhinitiswithcorticosteroids inpatientswithmildtomoderatepersistentasthma.Chest2005128:31407. 13. SluderG.Asthmaasanasalreflex.JAMA191973:58991. 14. KaufmanJ,WrightGW.Theeffectofnasalandnasopharyngealirritationonairwayresistancein man.AmRevRespirDis1969100:62630. 15. 15.AssanasenP,BaroodyFM,AbbottDJ,etal.Naturalandinducedallergicresponsesincrease theabilityofthenosetowarmandhumidifyair.JAllergyClinImmunol2000106:104552.
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Dentigerous cyst
From supernumerary teeth
October 3, 2012 Rhinology
Authors
BalasubramanianThiagarajan
Abstract
Dentigerouscystsarethemostcommondevelopmentalodontogeniccysts.Theyareusuallyderived fromtheepithelialremnantsoftoothformingorgans.Thesecystsincreaseinsizegradually.There mayalsobeassociatedboneresorption.Managingtheselesionscreatesproblemsin children.Itisalwaysbettertobeconservativeinmanagingthisprobleminchildrenbecausedentition isyettocompleteinthem.
Introduction: Dentigerouscystsarethemostcommondevelopmentalodontogeniccysts.Theyareusuallyderived fromtheepithelialremnantsoftoothformingorgans1.Dentigerouscystsareclassicallydefinedas cysticlesionsthatarecausedbyseparationoffolliclesfromaroundthecrownofuneruptedteeth. Mostcommonlydentigerouscystinvolveslower3rdmolar(mandibular)2.Dentigerouscystswere earliertermedasFollicularcystssinceitwasassumedthatthesecystswerederivedfromtooth folliclewhichisamesodermalstructure.Laterthistermwasabandonedasitwasconceivedonan erroneousperception.Dentigerouscystscanalsobecausedby: 1.Impactedteeth 2.SupernumeraryteethIsdefined8asteethinexcessofusualconfigurationof20deciduousand 32permanentteeth.Dentigerouscystsarisingfromsupernumeraryteethaccountsfornearly5%of allthesecysts. 3.Ectopicteeth(eruptionofateethinsitesotherthanthenaturalposition).Mostcommonlyseen ectopicallyeruptedteethinvolves3rdmolars 4.Rarelyatooth/rootofteethmaybefoundinthesinuscavity.Thisteethmayhavedentigerous cystassociatedwithit3. Theoriesofdentigerouscystformation: Usuallyalldentigerouscystsarisefromtheenamelorganaftercompletionofamelogenesis. Dentigerouscystarisesduetoaccumulationoffluidcausingseparationofenameloftheunerupted tooth.Thefluidpresentinsidethecystishyperosmolarduetothepresenceofalbumin, immunoglobulinandsquamousepithelialdebris.Thishyperosmolarfluidcausesinfluxofextracellular fluidintothecystcausinghugeexpansionofcysttooccur.Theepithelialliningofthecystsecretes collagenaseandosteoclastactivatingfactorwhichcauseslocalboneresorptioncausingfurther increaseinthesizeofthecyst.Thisenlargingcystenclosesthecrownoftheuneruptedteethandis
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attachedtoitscementoenameljunction. TheoriesexplaininggenesisofDentigerouscyst: 1.Theoryofstimulation 2.Theoryofinflammation4 Incidence: Studiesrevealthatdentigerouscystconstitutemorethanaquarterofalljawcysts.Itpredominates duringthe2nd3rddecadesoflife5.Thereisaveryslightmalepreponderance. Majorityofdentigerouscystsinvolvesthemandibularthirdmolarwhilemaxillarycanineisthenextin theorderofinvolvement.Veryrarelydentigerouscystcanoccurfromectopicallyeruptedtoothwithin themaxillarysinus6. Symptoms: Thesepatientsusuallypresentwithpainlessslowgrowingswellinginvolvingtheaffectedarea.This swellingisveryfrimonpalpationindicatingcorticalexpansion.Ifitispresentintheupperjawthenthe swellingcouldinvolvethehardpalatealso. Thesecystsareusuallypainlessanddormant.Theremaybesomedegreeofexpansionofcortical bone.Presenceofpainandrapidswellingdefinitlyindicatesinflammation.Fistulacanrarelyoccur whenthedentigerouscystispresentinthemaxillarysinus.Thesepatientsusuallypresentwith evidenceofsinusitis7.Whenthesecystsareaspiratedthenyellowishfluid9couldbeobserved.The swellingmayalsoreduceinsizefollowingaspirationonlytoincreaseinsizelater. Histology: Histopathologicalexaminationofthecystwallshowedthecysttobelinedbyreducedenamel epithelium.Connectivetissuestromawillshowfeaturesofprimitivetypeofectomesenchyme. Findingswoulddependonwhetherthereisinflammatorycomponenttothecystispresentornot.In noninfectedcyststheliningepitheliumis24layersthickformedbyprimitiveectomesenchyme. Theseliningcellsarelowcuboidaltocolumnar.Retepegscouldbeseenonlyincystswhichare infected.Theconnectivetissuestromaislooseandisrichinacidmucopolysaccharides.Whenthe dentigerouscystisinflamedthenitischaracterisedbythepresenceofhyperplasticreteridgesandthe cystwalldemonstratesinflammatoryinfiltrate. Theoriesofdentigerouscystformation: Intrafolliculartheory: Accordingtothistheorycystformationoccursduetofluidaccumulationbetweenthelayersofinner andouterenamelepitheliumaftercrownformation. Enamelhypoplasiatheory: Thistheorysuggeststhatdentigerouscystformationoccursduetodegenerationofstellatereticulum ataveryearlystageoftoothdevelopment.Thereisalsoassociatedenamelhypoplasia. Mainstheory: Thistheorysuggeststhatimpactedtoothexertspressureonthefolliclewithresultingobstructionof venousoutflow.Thisinducesrapidtransudationoffluidacrossthecapillarywalls.Thiscausesan
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increaseinthehydrostaticpressureexertedcausingseparationofcrownfromthefollicle.Thismay beassociatedwithreducedenamelepithelium. Radiographicfeatures: Inplainradiographsthesecystspresentasawelldefinedunilocularradiolucency.Oftenthereisa demarcatingscleroticborder.Sincethecystliningisderivedfromreducedenamelepitheliumthis radiolucencypreferentiallysurroundsthecrownoftheteeth.Alargedentigerouscystmayprovidean impressionasifitismultilocular.Thisappearanceisduetothepersistenceofbonytrabeculaewithin theradiolucency.Thesecystsareparticularyunilocularinnature. Radiographictypesofdentigerouscysts: 1.Centralvariety:Inthisvarietytheradiolucencysurroundsthecrownoftheuneruptedteeth.The crowncanclearlybeseenprojectingintothecystlumen. 2.Lateralvariety:Inthisvarietythecystdevelopslaterallyalongthetoothroot,partiallyencirclingthe crown 3.Circumferentialvariety:Thecystentirelysurroundstheuneruptedteeth.Radiologicallythe uneruptedteethcouldbeseenwithinthecystcavity.
Dentigerouscystshowinguneruptedteeth
CTscanshowingdentigerouscyst
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Dentigerouscyst
Uneruptedteethseeninsidedentigerouscyst
References
1. AminZA.,AmranM.,Khairudin.RemovalofextensivemaxillarydentigerouscystviaaCaldwell Lucprocedure.ArchOrofacSci20083(2):4851. 2. NevilleBW,DamDD,AllenCM,BouquetJE.OralandMaxillofacialPathology.2nded.Saunders c2001.768p
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Authors
BalasubramanianThiagarajan Abstract: Gingivalhyperplasia/hypertrophyisarathercommoncondition.Thisarticlereviewsliterature pertainingonlytogingivalovergrowthfollowingdrugingestion.Awiderangeofcauseshavebeen attributedtogingivalovergrowth.Druginducedovergrowthcommonlyoccursfollowingmedications prescribedfornondentalcauses.Pathogenesisofgingivalovergrowthfollowingingestionofcertain drugsisstillunsure.Certainhighriskcoexistantfactorslikepresenceofgingivitishasbeen implicated.Managementofthisconditionshouldtakeintoconsiderationtheconditionforwhichthe offendingdrughasbeenprescribed.Physiciansshouldbeawareofdrugsthatcouldcausegingival overgrowthinordertoidentifyandmanagethisproblem. Introduction: Alargenumberofdrugshavebeenimplicatedascauseforgingivalhypertrophy/hyperplasia.Useof thetermhypertrophy/hyperplasiaisrathercontroversial.Thesetermsdonotaccuratelyreflectthe currentunderstandingofthecurrenthistopathologicalscenario.Gingivalenlargementinthese patientsisnotduetoincreaseinthenumberofperiodontalcellsbutduetoanincreaseinthe extracellularvolume1.Thisincreaseintheextracellularvolumeiscausedbyhyperplasiainvolving fibroblasts. Gingivalovergrowthwasfirstdescribedindentalliteratureof1960s2whencasereportsstarted appearingaboutchildrenwhodevelopedenlargedgingivaduetotreatmentofepilepsyusing phenytoin.Thisconditionwasalsodescribedinchildrenbornofepilepticmotherswhowerebeing treatedwithsodiumvalproate.Thesechildrenwerebrandedtobesufferingfromfetalvalproate syndrome3.FetalvalproatesyndromewasfirstdescribedbyDiLibertiin19844.Thesechildrenalso hadneurodevelopmentalproblems.AssociatedcongenitaldefectsinthissyndromeincludeNeural tubedefects,congenitalheartdefects,orofacialclefts,andlimbdefects. Drugsinvolvedincausinggingivalenlargement: Threetypesofdrugcategories6havebeenimplicatedascausativefactorsofgingivalenlargement. Theyinclude: 1.AntiepilepticdrugsPhenytoin,Phenobarbitone,Valproicacid,Primidone,Vigabatrinand carbamazepine. 2.CalciumchannelblockersNifidepine,Verapamil,DiltiazemandAmlodepin 3.ImmunosuppresivedrugsCyclosporine Studiesrevealthatdruginducedgingivalovergrowthusuallyoccurswithinfirstthreemonthsof startingdrugtherapywiththeoffendingdrug.Thisusuallybeginsasanenlargementinvolving Interdentalpapillae. Prevalance:
7
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Reviewofliteratureshowsawidevariationinprevalancerates7.Ahighfigureof50%hasbeen quotedforthedrugphenytoin,whereasforcyclosporinitis30%andforcalciumchannelblockers 10%.Recentstudieshavedemonstratedthesynergisticeffectofcyclosporinwithcalciumchannel blockersincausinggingivalovergrowth8.Indianstatisticsarerathersketchyinthisaspect.Onestudy reportsthat57%ofepilepticchildrenintheagegroup813onphenytoindevelopedgingival overgrowthwithinthefirst3monthsofstartingthetreatment9. Etiology: Etiologyalthoughenoughpointersaretheretopointfingersatanoffendingdrug,isstillconsideredto bemultifactorial.Therelationshipbetweenthedrugdosage,durationoftherapyandsexprediliction isstillnotclear.Thereisstillaragingdebategoingonastowhetherdruginducedgingival hyperplasiacouldbecausedbyhyperplasiaofgumepitheliumorofsubcutaneousconnectivetissue orboth. Certainpredisposingriskfactorshavebeenindentifiedanddocumented.Theyinclude: Poororalhygiene:Presenceofdentalplaquecanprovideareservoirforaccumulationofdrugslike phenytoin/cyclosporin8. Inpatientswhohaveundergoneorthodonticproceduresthepresenceofnickelcouldpredisposeto formationofgingivalovergrowth Susceptibilityofsomesubpopulationoffibroblastsandkeratinocytestophenytoin,cyclosporinand otherdrugswhichcouldcausegingivalovergrowth Numberoflanghanscells10presentintheoralepitheliumisanotherriskfactor.Morethenumber worsetherisk.Thesedrugshaveatendencytoaccumulateinsidethesecellscausingprolonged effectonthegums. CytochromeP450genepolymorphism11cancauseindividualvariationsindrugmetabolism predisposingtogingivalovergrowth Inpatientsusingcalciumchannelblockersgingivalovergrowthcouldbecausedby: Defectivecollagenaseactivity Blockageofaldosteronesynthesisfromadrenalcortexfollowedbyfeedbackincreaseinthesecretion ofACTH Upregulationofkeratinocytesgrowthfactor Upregulationoftransforminggrowthfactoralpha412 Thetissueovergrowthisclassicallyofdensecollagentissueandotherconnectivetissueelements. Scatteredinflammatorycellscanalsobeseen.Classicallygingivaltissueadjacenttoanteriorteethis morecommonlyaffectedthantheposteriorones.Presenceofbacterialplaqueintheteethis essentialforgingivalovergrowthtooccur.Histologyofovergrowthrevealedhyperplasiaofconnctive tissue,epithelialacanthosisandelongatedreteridges.
Pictureshowinggingivalovergrowth
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References
1. DesaiP,SilverJG.Druginducedgingivalenlargement.JCanDentAssoc199864:2638. 2. KimbalOP.Thetreatmentofepilepsywithsodiumdiphenylhydantoinate.JAmMedAssoc1939 112:12445. 3. RodriguazVazquezM,CarrascosaRomeroMC,ParddalFernandozM,etal.Congenitalgingival hyperplasiainaneonatewithfoetalvalproatesyndromeNeuropediatrics200738:2512. 4. DiLibertiJH,FarndonPA,DennisNR,CurryCJ.Thefetalvalproatesyndrome.AmJMedGenet 198419:473481 5. PerlikF,KolinovaM,ZvarovaJ,etal.Phenytoinasariskfactoringingivalhyperplasia.Therap DrugMonitor199517:4458. 6. PerlikF,KolinovaM,ZvarovaJ,etal.Phenytoinasariskfactoringingivalhyperplasia.Therap DrugMonitor199517:4458. 7. 6.EllisJS,SeymourRA,SteeleJG,etal.Prevalenceofgingivalovergrowthinducedbycalcium channelblockers:acommunitybasedstudy.JPeriodontol.199970:637. 8. SprattH,BoomerS,IrwinCR,etal.Cyclosporinassociatedgingivalovergrowthinrenaltransplant recipients.OralDis19995:2731. 9. MejiaLM,LozadaNurF.Druginducedgingivalhyperplasia.Emedicins.Medscope.com2009 article/1076264
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Epistaxis
October 7, 2012 Rhinology
Authors
BalasubramanianThiagarajan Introduction: Epistaxisisdefinedasbleedingfromthenasalcavity.ItisactuallyaGreekwordfornosebleed.Itis actuallyaverycommonproblemandhenceitsincidenceisratherdifficulttoaccess.Crudeestimates oritsincidencerangesfrom514%1.Theincidenceofepistaxisalsoshowssignificantincrease duringwintermonths/hotdryclimateswithlowhumidity.Thisclimaticincreaseinincidenceof epistaxishasbeenattributedtoincreaseintheincidenceofupperrespiratorytractinfections. Forcefulblowingofinflammatednasalmucosaprovokesepistaxisinthesepatients2.Classically epistaxisisknowntomanifestbimodalincidencewithpeaksinagegroupsof210and6080.Only asmallpercentageofthispopulationseekOtolaryngologistintervention.Thisamountstoabout1%of allpatientswithnasalbleed3. History: Epistaxishasbeenacentreofallfolklores.SomeassociatedepistaxiswithLovewhileothers believedthatitforetolddeath/someformofsevereillness.Onthewholespiritswerebelievedto causeepistaxis.Luptonin1601suggestedthatthepatientsusetheirownbloodfromepistaxisto writethewordsconsummatumestontheforeheadinordertoavoidfurtherepisodes.Thesewords wereutteredbyJesusChristashewasdyingonthecross.Theexactmeaningofthesewordsmean Itsfinished.Moncriefin1716friedthepatientsownepistaxisbloodandappliedthesameassnuff astreatment.Hippocratesoneoftheearliestphysiciansappreciatedthatpressureonalaenasiin patientswithepistaxismanagedtostopthenasalbleed.AliIbnRabbanAlTabiri4aPersianHakim (850A.D.)wroteinhisclassictreatisethatepistaxiswasduetoswellingofvein(Retrocolumellar) anditseventualrupture.GiovanniBattisataMorgagnianItalianAnatomistobservedturgidblood vesselslocatedaboutafingersbreadthfromtheanteriornasalcavity.Heattributedepistaxisto bleedingfromthisarea. CarlMichel,JamesLawrenceLittleandKiesselbachidentifiedvenousplexusovertheanteriorpartof cartilagenousseptumasasourceofepistaxis.In1868Pilzperformedthefirstdocumentedcommon carotidarteryligationastreatmentofepistaxis.AlfredSeiffertin1928introducedtheconceptof ligationofinternalmaxillaryarteryviatransantralapproachasatreatmentmodalityforepistaxis.It wasHenryGoodyearin1937whofirstligatedanteriorethmoidalarterytotreatepistaxis. Vascularityofnasalmucosa: Nasalmucosaishighlyvascular.Thesubmucosalbloodvesselsofnasalcavityreceivebloodsupply frombothinteranalandexternalcarotidsystems.Thegeneralruleofthumbisthattheareaofnasal cavitybelowthelevelofmiddleturbinateissuppliedbyexternalcarotidbrancheswhilethearea abovethelevelofmiddleturbinate5issuppliedbyinternalcarotidartery.Anastomosisbetweenthese twosystemsareknowntooccurwithinthenasalcavity.Itshouldbeborneinmind thatthepressurelevelsattheinternalcarotidarteryishigherthanthatofexternalcarotidartery.
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Externalcarotidsystem:Bloodfromtheexternalcarotidsystemreachesthenasalcavityviathefacial andtheinternalmaxillaryarterieswhicharebranchesoftheexternalcarotidartery.Thearteryof epistaxisisthesphenopalatinebranchofinternalmaxillaryartery.Thisiscalledsobecausethis vesselssuppliesthemajorportionofthenasalcavity.Itentersthenasalcavityattheposteriorendof themiddleturbinatetosupplythelateralnasalwall,italsogivesoffaseptalbranchwhichsupplies thenasalseptum. Facialartery:thesuperiorlabialbranchofthefacialarteryisoneofitsterminalbranches.Itsupplies theanteriornasalfloorandanteriorportionofthenasalseptumthroughitsseptalbranch. Internalmaxillaryartery:afterenteringintothepterygopalatinefossathisvesselgivesriseto6 branches.Thesebranchesareposteriorsuperioraleveolarartery,descendingpalatineartery,infra orbitalartery,sphenopalatineartery,pterygoidartery,andpharyngealartery.Thedescending palatinearteryentersthenasalcavitythroughthegreaterpalatinecanaltosupplythelateralwallof thenose,italsocontributesbloodsupplytothenasalseptumthroughitsseptalbranch. Internalcarotidsystem:theinternalcarotidarterysuppliesthenasalcavityviaitsophthalmicartery.It enterstheorbitviathesuperiororbitalfissureanddividesintomanybranches.Theposteriorethmoid arteryoneofthebranchesofophthalmicarteryexitstheorbitviatheposteriorethmoidalforamen located29mmanteriortotheopticcanal.Theanteriorethmoidalarterywhichislargerleavesthe orbitthroughtheanteriorethmoidalforamen.Boththesevesselscrosstheroofoftheethmoidand descendsintothenasalcavitythroughthecribriformplate.Itisherethatthesevesselsdivideinto lateralandseptalbranchestosupplythenose.
Bloodsupplyoflateralnasalwall
Littlesarea:Thisareaislocatedintheanteriorpartofthecartilagenousportionofthenasalseptum. Herethereisextensivesubmucousanastomosisofbloodvesselsbothfromtheexternalandthe internalcarotidsystems.Bleedingcommonlyoccursfromthisareasinceitishighlyvascularand isalsoexposedtotheexterior.Anastomosisoccurbetweentheseptalbranchesofsphenopalatine artery,greaterpalatineartery,superiorlabialarteryandtheanteriorethmoidalartery.Thisplexusis alsoknownasKeisselbachsplexus.Bleedingfromthisareaiscommonbecausemucosaldrying occurscommonlyhereandthisareaiseasilyaccessibletonosepicking.Amongthevesselstaking partintheanastomosistheanteriorethmoidalarteryisfromtheinternalcarotidsystemwhilethe othervesselsarefromtheexternalcarotidsystem.Bleedingfromthisareaisclearlyseenandeasily accessibleandflowsthroughtheanteriornasalcavityhenceitisknownasanteriorbleed.
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Twoareashavebeenimplicatedinepistaxis.Littlesareahasbeenimplicatedinanteriorepistaxis andWoodruffsplexusinposteriorepistaxis.Anteriorepistaxisiscommoninchildrenwhileposterior epistaxisiscommoninadults. Woodruffsplexus:isresponsibleforposteriorbleeds.Thisareaislocatedovertheposteriorendof themiddleturbinate.Theanastomosishereismadeupofbranchesfromtheinternalmaxillaryartery namelyitssphenopalatineandascendingpharyngealbranches.Themaxillarysinusostiumformsthe dividinglinebetweentheanteriorandposteriornasalbleeds.Posteriornasalbleedsaredifficultto treatbecausebleedingareaisnoteasilyaccessible.BleedingfromWoodruffsplexuscommonly occurinpatientswithextremelyhighbloodpressure.Infactthisplexusactsasasafetyvalvein reducingthebloodpressureinthesepatients,lesttheywillbleedintracraniallycausingmore problems.Inpatientswithposteriorbleedsitisdifficulttoaccesstheamountofbloodlossbecause mostofthebloodisswallowedbythepatient.
Littlesarea
Woodruffin1949reportedagroupoflargebloodvesselsinthelateralwallofinferiormeatus posteriorly.Hewasabletovisualizethesebloodvesselsusingarigidnasopharyngoscope.Hecoined thetermNasonasopharyngealplexustodescribethesevessels.Hesuspectedtheassociation betweenthepresenceofthesedilatedbloodvesselsandposteriorepistaxis.Hewasnotsure whetherthesevesselsareveinsorarteries. Microdissectionstudiesrevealedasuperficialcollectionoffragilefairlylargecalibrebloodvessels lyingjustbeneaththesurfacemucosa7.Therewasverylittleinterveningconnectivetissue. Histologicalstudiesrevealedthattheepitheliumoverlyingtheposteriorinferiormeatuswastypical respiratoryepithelium.Thebloodvesselsinthisareaweresinuslikewithverylittlemuscleorfibrous tissuewithintheirwalls.Theaveragebloodvesseldiameterinthisareais12mm. ShaheendescribedWoodruffsplexusasanarterialplexusformedbyanastomosisbetween pharyngeal,posteriornasal,sphenopalatineandposteriorseptalarteries.Microdissectionand histologicalstudieshaveprovedWoodruffsplexustobevenousinorigin. BleedingfromthebloodvesselsofWoodruffsplexuscouldresultinaslowbutprolongedooze.Since thesebloodvesselshavenomusclewalls,hemostasisispoor.Postnasalpackingwillhavetobe resortedtoinrarecasestostopbleeding. Etiology:Theetiologyofepistaxisisnotjustsimpleorstraightforward.Itiscommonlymultifactorial, needingcarefulhistorytakingandphysicalexaminationskilltoidentifythecause.Forpurposesof
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clearunderstandingtheetiologyofepistaxiscanbeclassifiedundertwobroadheads,i.e.localand systemiccauses7. Localfactorscausingepistaxis:includevascularanamolies,infectionsandinflammatorystatesofthe nasalcavity,trauma,iatrogenicinjuries,neoplasmsandforeignbodies.Amongthesecausesthe commonestlocalfactorsinvolvedinepistaxisisinfectionandinflammation.Infectionsand inflammationofthenasalmucousmembranemaydamagethemucosaleadingontobleedingfrom theunderlyingexposedplexusofbloodvessels.Chronicgranulomatouslesionslikerhinosporidiosis cancauseextensiveepistaxis. Aneurysmsinvolvingtheinternalcarotidarterymayoccurfollowingheadinjury,injurysustained duringsurgicalprocedures.Theseextraduralaneurymsandaneurysmsinvolvingthecavernous sinusmayextendintothesphenoidsinuswaitfortheopportunemomenttorupture.Itcancause suddenfatalepistaxis,orblindness.Urgentembolisationisthepreferredmodeofmanagementof thiscondition. Traumaisoneofthecommonlocalcausesofepistaxis.Itiscommonlycausedbytheactofnose pickingintheLittlesareaofthenose.Thisiscommonlyseeninyoungchildren.Acutefacialtrauma mayalsoleadtoepistaxis.Patientsundergoingnasalsurgeriesmayhavetemporaryepisodesof epistaxis. Irritationofthenasalmucousmembrane:anydisruptionofnormalnasalphysiologycancause intensedryingandirritationtothenasalmucosacausingepistaxis.Theseepisodesarecommon duringextremesoftemperaturewhenthenasalmucosaisstressedtoperformitsairconditioningrole oftheinspiredair.Intheseconditionsthereisextensivedryingofnasalmucosacausesoedemaof thenasalmucousmembrane.Thisoedemaiscausedduetovenousstasis.Ultimatelythemucosa breachesexposingtheunderlyingplexusofbloodvesselscasuingepistaxis. Anatomicalabnormalities:Commonanatomicalabnormalitycausingepistaxisisgrossseptal deviation.Grossdeviationsofnasalseptumcausesdisruptiontothenormalnasalairflow.This disruptionleadstodessication/dryingofthelocalmucosa.Thedrymucosacracksandbleeds. Septalperforations:Chronicnonhealingseptalperforationscancausebleedingfromthegranulation tissuearoundtheperforation. Neoplasms:involvingthenoseandparanasalsinusescancauseepistaxis.Neoplasmsincludebenign vasculartumorslikehemangioma,juvenilenasopharyngealangiofibroma,andmalignant neoplasmslikesquamouscellcarcinoma.Ifepistaxisoccursalongwithsecretoryotitismediathen nasopharyngealcarcinomashouldbetheprimesuspect. Systemiccausesforepistaxis: Hypertensionisoneofthecommonsystemiccausesofepistaxis.Accumulationofatheroscerotic plaquesinthebloodvesselsofthesepatientsreplacesthemuscularwall.Thisreplacementof muscularwallreducestheabilityofthebloodvesselstoconstrictfacilitatingepistaxis.Thisisoneof thecommoncausesofposteriornasalbleeds.ItcommonlyarisesfromtheWoodruffsplexusfound closetheposteriorendofthemiddleturbinate.Beranetalconcludedthathypertensionhadno significantimpactasetiologicalfactorforepistaxis8. HereditaryhemarrhagictelengectasiaalsoknownasOslerRenduWeberdiseaseisanother systemicdisorderknowntoaffectthebloodvesselsofthenose.Thisisanautosomaldominantnon
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sexlinkeddisorder.Thisdiseasecauseslossofcontractileelementswithinthebloodvesselscausing dilatedvenules,capillariesandsmallarteriovenousmalformationsknownastelengectasia.These changescanoccurintheskin,mucosalliningthewholeoftherespiratorypassageandurogenital passage.Bleedingfromthesetelengectasiaisdifficulttocontrol.Bleedinginvariablystartswhenthe patientreachespuberty.Commoncauseofmortalityinthesepatientsisgastrointestinalbleed. Thisconditionismorecommoninwomen5:1.Seriousepistaxisisknowntooccurinnearly80%of thesepatientsbytheageof3010.Dependingontheamountofbloodlossdecisionontransfusionis made.Nasalpackingandcauterizationisadvocatedformildtomoderatebleedinginthesepatients. Treatmentofthisconditionisratherpalliativesincetheunderlyingdiseaseisnotcurable9.Laser coagulationofbleedershavebeentriedoutwithreasonabledegreeofsuccessinthesepatients. Topicaloestrogentherapyfollowinglasercauterizationofbleedershelpinsquamousmetaplasiaof nasalepitheliumtherebyreducingtheincidenceofbleeding10.Inveryretractablecasesnasal obliterationtoohasbeenattempted(Youngsprocedure). Systemicdiseaseslikesyphilis,tuberculosis&wegnersgranulomatosiscauseepistaxisbecauseof theirpropensitytocauseulcerationofthenasalmucousmembrane.Viralinfectionslikedengueand haemorrhagicfevercauseepistaxisduetoreducedplateletcount. Blooddyscrasiascanalsocauseepistaxis.Alowplateletcountisonecommoncauseofnasalbleed inthiscategory.Inthrombocytopeniatheplateletcountislessthan1lakh.Epistaxiscanstartwhen theplateletcountreducesto50,000.Plateletdeficiencycanbecausedbyingestionofdrugslike aspirin,indomethacinetc.Hyperspenismcancausethrombocytopeniainidiopathicthrombocytopenic purpura.Thesepatientsneedtobetransfusedfreshbloodinadequatequantities.Onlywhenthee plateletcountincreaseswillthenasalbleedstop. Incidence:Theincidenceofepistaxisisknowntobeslightlyhigherinmales.Italsohasabimodal distributionaffectingyoungchildrenandoldpeople. Evaluation:Whileevaluatingapatientwithepistaxisitisabsolutelynecessarytoassessthequantum ofbloodloss.Thebloodpressureandpulserateofthesepatientsmustbeconstantlymonitored. Thesepatientswillhavetachycardia.Infusionoffluidmustbestartedimmediatly. Initiallyringerlactatesolutionwillsuffice.Ifthepatienthassufferedbloodlossofmorethan30%of theirbloodvolume(about1.5liters)thenbloodtransfusionbecomesamust.Furtherexamination shouldbestartedonlyafterthepatientsgeneralconditionstabilises. History:Carefulhistorytakingisamust.Historytakingshouldcoverthefollowingpoints: 1.Historyregardingthefreqency,severityandsideofthenasalbleed. 2.Aggravatingandrelievingfactorsmustbecarefullysought. 3.Historyofdrugintakenmustbesought. 4.Historyofsystemicdisorderslikehypertensionanddiabetesmellitusmustbesought. Physicalexamination: Thenasalpackifanymustberemoved.Anteriornasalexaminationshouldbedone,firstattempted withouttheuseofnasaldecongestants.Ifvisualisationisdifficultduetooedemaofthenasalmucosa thennasaldecongestantscanbeusedtoshrinkthenasalmucosa.Thesolutionusedfor anesthetisingthedecongestingthenoseisamixtureof4%xylocaineandxylometazoline.
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Nasalendoscopycanbeperformedunderlocalanesthesiatolocaliseposteriorbleeds. Investigations: Ifbleedingisminimalnoinvestigationisnecessary. Ifbleedingismorethenacompletebloodworkuptoruleoutblooddyscrasiasisamust.Itincludes bleedingtime,clottingtime,plateletcountandpartialthromboplastintime. ImagingstudieslikeCTscanoftheparanasalsinusesmustbedonetoruleoutlocalnasalconditions ofepistaxis.Imagingmustbedoneonlyafter24hoursofremovingthenasalpacking.Scansdone withthenasalpackorimmediatlyafterremovingthenasalpackmaynotbeinformative. Indiffiucultandintractablecasesangiographycanbedoneandtheinternalmaxillaryarterycanbe embolisedinthesamesitting.Thisprocedureshouldbereservedonlyforcasesofintractablenasal bleeding. Classificationofetiologicalfactorsofepistaxis: Forbetterunderstandingetiologicalfactorsofepistaxishasbeenclassifiedundertwoheads: 1.Localcauses 2.Systemiccauses
Localcauseofepistaxis
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Septalperforation
CTscanshowingseptalperforation
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Invertedpapilloma
Tumors: BenignInvertedpapilloma,JNA,Septalangioma
Nasalmass
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JNAmass
JNAmassseeninthenasopharynx Malignanttumormaxilla
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Atrophicrhinitis
Rhinosporidialmass
Systemiccauses
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Midlinegranuloma CTscannoseshowingrhinolith
Intoxicants: Cobalt Phosphorous Arsenic Lead Vascularcauses: Hypertension Atherosclerosis HereditaryHaemorrhagicTelengiectasia Management: Generalassessment: 1.Assessmentofairway 2.Vitalstobechecked 3.Bloodgroupingandcrossmatching Pinchingthenose:
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Noseclip
Managementofanteriornasalbleed: IfthebleedingarisesfromLittlesarea/retrocolumellarveinareathencauterizationmayberesorted to.Bipolarcauteryisideal.Inoutpatientsetupchemicalcautery(Chromicacid,aceticacid)canalso betriedout.Silvernitrateeventhoughcommonlyusedisnoteffectiveduringactivebleeds.Studies showthat30secondsofexposuretochemicalagentcauses1mmpenetrationoftissue13. Cauterizationshouldbeprecise.Randomcauterizationshouldbeavoidedatallcostsasthiscould leadtotroublesomeseptalperforation.Aftereffectivecauterizationofthebleedingpointpatientis advisedtousesalinenasalspraytopreventexcessivedryingofnasalmucosa. Useofnasalcream: Inchildrenthemostcommoncauseofbleedingisfromenlargedretrocolumellarvein.Constantnose pickingcouldcausebleedingfromthisarea.ThisarealiesslightlyanteriortotheLittlesarea. Applicationofantisepticcream13inthisareawouldreducetheincidenceofnasalpickinginthese children.
Bipolarcautery
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4.Providestemplateformaintainanceofendogenouscoagulation TypesofTopicalHaemostats: 1.Collagenbased 2.Gelatinbased 3.Cellulosebased 4.Albuminderived 5.Inorganichaemostats 6.Fibrinbased 7.Polymerichaemostats Collagenbased: Thesehaemostatswerefirstintroducedin1970.Thesesubstancespossessmicrofibrillarstructure comprisingofcollagenmoleculeswithnoncovalentlyboundhydrochloricacid.Themolecular structureandthelargesurfaceareaitprovidesareimportantforachievinghaemostasis15.Contact withthebleedingareaattractsplateletswhichgetsentangledwithinthemicrofibrillarstructureand degranulatestherebypromotingcoagulation. Gelatinbased: Themechanismofactionofgelatinbasedtopicalhaemostasisisnotclearlyunderstood.Itpromotes coagulationbecauseofitssurfaceeffects.Thismayalsobeusedaloneorincombinationwith procoagulants.Flosealisacharacteristicexample.Itcontainsgelatinbasedtopicalhaemostaticand aprocoagulant. Cellulosebased: Thesehavebeeninuseformorethandecades.Mechanismofactioninclude: 1.Absorptionofblood 2.Surfaceinteractionswithproteinsandplatelets 3.Activationofbothintrinsicandextrinsicpathways16 Albuminderived: Classicexampleofdrugbelongingtothiscategoryisgelatinresorcinolformaldehyde.Ithasbeen abandonednowduetotoxicreactionscausedbyformaldehyde.Anotherhaemostatofthiscategory whichiscommonlyusedisBioglue.Inbioglueformaldehydeisreplacedbylesstoxicgluteraldehyde. Advantageofthiscategoryoftopicalhaemostatsincludeitsabilitytocausecoagulationoutsideboth extrinsicandintrinsicpathways. Ionicbased: Thisisactuallyarecentadditiontothehaemostatarmamentorium.MostcommonlyusedisQuickclot. Thisisbasedonzeolite.Themodeofactionisabsorptionofwaterfromthebleedingsitecausingan increaseintheconcentrationofplateletsandcoagulationfactors.
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Sitesofactionoflocalhaemostats
Fibrinbased:Fibrinbasedtissueadhesiveshasbeeninusesince1970s.Theyhaveboth hameostaticandadhesivepropertiesandcanbeusedtodeliverantibioticstothewoundsite.They havebeenreportedtoreduceadhesionformationandenhancewoundhealing. UseofGelfoam/Surgicel: AbsorbablehaemostaticmateriallikeGelfoam/surgicelcanbeusedtopackthenasalcavity.Thisis veryusefulinmanagingpatientswithcoagulopathy.Sincethispackneednotberemovedmucosal traumaduringremovalcanbeavoidedinthesepatients. GelfoamisactuallyasterilehaemostaticspongepreparedfrompurifiedPorcineskingelatine.Thisis actuallywaterinsoluble.Ithasthecapacitytoabsorb45timesitsweightofblood17.Henceits absorptivecapacityisdirectlyproportionaltoitssize17.Themechanismofhaemostaticactionof gelfoamissupportiveandmechanicalinnature.Whenappliedtobleedingsurfacesthesesubstances arrestbleedingbyformingartificialclotstherebyprovidingthemechanicalmatrixthatfacilitates clottingmechanism19.ClottingeffectsofgelfoamisduetoreleaseofthromboplastinbyPlatletsthat comeintocontactwithgelfoam20.Gelfoampackwhenappliedtonasalcavitycompletelyliquifies within25days. Conventionalnasalpacking: Thisisindicatedinpatientswherecauterizationisnotpossible/fails.Conventionalnasalpackingare oftwotypes:Anteriornasalpackingandpostnasalpacking. Materialsusedfornasalpacking: 1.Rollergauzeimpregnatedwithantibioticandlubricantlikeliquidparaffin 2.Merocel 3.Tampoons 4.Foleyscatheterforpostnasalpacking
Merocel
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Anteriornasalpacking
Merocel
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ThenewerpacksliketheBIPP(BismuthIodineparaffinpaste)packscanbeleftsafelyinplacefor morethanaweek. Tomanagepostnasalbleedapostnasalpackisamust.Postnasalpackingcanbedonein2ways: Postnasalpacking(conventional):Agauzerollaboutthesizeofthepatientsnasopharynxisused here.Threesilkthreadsmustbetiedtothegauzeroll.Oneateachendandtheotheroneatthe middle.Thepatientshouldbeinarecumbentposition.Afteranesthetisingthenasalcavitywith4% xylocainethemouthisheldopen.Twonasalcathetersarepassedthroughthenasalcavitiestillthey reachjustbelowthesoftpalate.Theselowerendsofthecathetersaregraspedwithforcepsand pulledoutthroughthemouth.Thesilktiedtotheendsofthegauzeistiedtothenasalcatheters.The postnasalpackisintroducedthroughthemouthandgraduallypushedintothenasopharynx,atthe sametimethenasalcathetersonbothsidesofthenosemustbepulledout.Whenthepacksnugly sitsinsidethenasopharynx,thetwosilkthreadstiedtoitsendwouldhavereachedtheanaterior naresalongwiththefreeendofthenasalsuctioncatheter.
Postnasalpack
Thetwosilkthreadstiedtothesuctioncathetersareuntied.Thecathetersareremovedfromthe nose.Thesilkthreadisusedtosecurethepackinplacebytyingboththeendstothecolumellaof thenose.Thesilktiedtothemiddleportionofthegauzepackisdeliveredoutthroughtheoralcavity andtapedtotheangleofthecheek.Thismiddleportionsilkwillhelpinremovalofthenasalpack.In additiontothepostnasalpackanteriornasalpackingmustalsobedoneinthesepatients. Postnasalpackusingbalooncatheters:Speciallydesignedbalooncathetersareavailable.Thiscan beusedtoperformthepostnasalpack.Foleyscathetercanbeusedtopackthepostnasalspace. Foleyscatheterisintroducedthroughthenoseandsliduptothenasopharynx.Thebulbofthe catheterisinflatedusingairthroughthesideportalofthecatheter.Airisusedtoinflatethebulb becauseevenifthebulbrupturesaccidentallythereisabsolutelynodangerofaspirationintothe lungs.Afterthefoleyscatheterisinflatedthefreeendisknottedandanchoredatthelevelofthe anteriornares.
Foleyscatheter
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Nasalballoons
Newerpackingmaterials:Newerpackingmaterialsmadeofsiliconeareavailable.Theadvantagesof thesematerialarethattheyarenotirritating,patientcanbreaththroughthenosewiththepackon throughtheventprovided,thesepackscanberetainedinsidethenasalcavityformorethan2weeks. TheycanberemovedandrepositionedifnecessaryTheonlydisadvantageisthattheyareexpensive. Surgicalmanagement: Endoscopiccauterisationcanbetriedifthebleedersarelocalisedandaccessible.Ifnotaccessible, ligationoftheinternalmaxillaryarterycanbedonethroughcaldwellucapproach.Spenopalatine arteryclippingcanbedoneendoscopically.Itisaccessibleclosetotheposteriorendofthemiddle turbinate.Inrarecasesexternalcarotidarteryligationattheneckcanberesortedto.Externalcarotid arteryisdifferentiatedfromtheinternalcarotidintheneckbythefactthatinternalcarotidarterydoes notgiverisetobranchesintheneck,whiletheexternalcarotidarterydoesso. Ethmoidalarteryligation:Ifepistaxisoccurhighinthenasalvault,anteriorandposteriorethmoidal arteriesmaybeligatedusingligaclips.Thesearteriescanbeaccessedusinganexternal ethmoidectomyincision.Theanteriorethmoidalarteryisusuallyfound22mmfromtheanterior lacrimalcrest.Ifligationoftheanteriorethmoidalarterydoesnotstopbleedingthenposterior ethmoidalarteryshouldalsobeligated.Theposteriorethmoidalarterycanbefound12mmposterior totheanteriorethmoidalvessel. TESPAL: Tespal:(Transnasalendoscopicsphenopalatinearteryligation) History:ThisprocedurewasfirstreportedbyBudrovichandSaettiin1992. ThisprocedurecansafelybeperformedunderGA./L.A. Indication: Epistaxisnotrespondingtoconventionalconservativemanagement. Posteriorepistaxis Procedure:
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Thenoseshouldfirstbeadequatelydecongestedtopicallyusing4%xylocainemixedwith1in50,000 unitsadrenaline. A4mm0degreenasalendoscopeisintroducedintothenasalcavity.Theposteriorportionofthe middleturbinateis visualized.2%xylocainewith1in1lakhunitsadrenalineisinjectedintothisareatofurtherreduce bleeding. Incision:Anincisionrangingbetween1020mmismadeverticallyabout5mmanteriortothe attachmentofthemiddleturbinate.Themucosalflapisgentlyretractedposteriorlytillthecrista ethmoidalisisvisualized.Thecristaethmoidalisisareliablelandmarkforthesphenopalatineartery. Thearteryentersthenosejustposterior tothecrista.ThecristacaninfactberemovedusingaKerrisonspunchforbettervisualizationofthe artery. Thesphenopalatinearteryisclippedusingligacliporcauterizedasitentersthenasalcavity.Thisis doneasclosetothelateralnasalwallaspossible,thiswouldensurethattheposteriorbranchesmay alsobereliableincluded. Followingsuccessfulligation/cauterization,theareaisexploredposteriorlyfor23mmtoensure thatnomore vesselsremainuncauterized. Nasalpackingisnotneeded. ComplicationsofTESPAL: 1.Palatalnumbness 2.Sinusitis 3.Decreasedlacrimation 4.Septalperforation 5.Inferiorturbinatenecrosis Thisprocedureincombinationwithtransnasalanteriorethmoidalarteryligationensuresthatepistaxis iscontrolledreliably.
References
1. CordesS.EpistaxisUTMBDepartmentofOtolaryngologyGrandRounds1996 2. IjaduolaG.T.A.,OkeowoP.A.Patternofepistaxisinthetropics.CentrAfrJMed.198329(4):77 80 3. MichaelS.Benninger,andBradleyF.Marple.MinorrecurrentepistaxisPrevalenceandanew methodformanagement.JournalofOtolaryngologyHeadandNeckSurgery.ZwischenbergerJB, BrunstonRLJr,SwannJR,ContiVR. 4. http://en.wikipedia.org/wiki/Ali_ibn_Sahl_Rabban_alTabari
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5. http://www.drtbalu.co.in/epistaxis.html 6. Woodruff'splexusTWChiu,JShawDunnetalTheJournalofLaryngology&Otology/Volume122/ Issue10/October2008,pp 7. Comparisonoftwotopicalcollagenbasedhemostaticspongesduringcardiothoracicprocedures.J InvestSurg199912:101106.2004,131:317320 8. Beran,M,B.Petruson.Occurrenceofepistaxisinhabitualnosebleedersandanalysisofsome etiologicalfactors.ORLJOtorhinolaryngolRelatSpec.198648:297303. 9. Lennox,P.A.,Harries,M.,Lund,V.J.,andHoward,D.J.Aretrospectivestudyoftheroleofthe argonlaserinthemanagementofepistaxissecondarytohereditaryhaemorrhagictelangiectasia.J LaryngolOtol1997111:3437. 10. LundVJ,HowardDJ.Atreatmentalgorithmforthemanagemenbtofepistaxisinhereditary hemorrhagictelangiectasia.AmJRhinol.199913:319322. 11. HitchingsAE,LennoxPA,LundVJ,HowardDJ.Theeffectoftreatmentforepistaxissecondaryto hereditaryhemorrhagictelangiectasia.AmJRhinol.200519:7578. 12. http://entscholar.wordpress.com/article/rhinosporidiosis/ 13. MurthyP,NilssenEL,RaoS,McClymontLG.Arandomizedclinicaltrialofantisepticnasalcarrier creamandsilvernitratecauteryinthetreatmentofrecurrentanteriorepistaxis.ClinOtolaryngolAllied Sci.199924:228231. 14. VaghelaHM.UsingaswimmersnoseclipinthetreatmentofepistaxisintheA&Edepartment. AccidEmergNurs.200529. 15. ZwischenbergerJB,BrunstonRLJr,SwannJR,ContiVR.Comparisonoftwotopicalcollagen basedhemostaticspongesduringcardiothoracicprocedures.JInvestSurg199912:101106. 16. KankoM,LimanT,TopcuS.Alowcostandsimplemethodtostopintraoperativeleakagetype bleeding:useofthevancomycinoxidizedregeneratedcellulose(ORC)sandwich.JInvestSurg2006 19:323327 17. CouncilonPharmacyandChemistry:AbsorbableGelatinspongenewandnonofficial remedies.JAMA1947135:921
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Authors
BalasubramanianThiagarajan
Abstract
Currentlyotolaryngologistshavestarteddoingdacryocystorhinostomyusingnasalendoscopes.This proceduredonebyanotolaryngologisthasitsownobviousadvantages.Thefirstandforemostbeing theneedforexternalincisionhasbeendispensedwith.Ontheflipsideotolaryngologistisnot conversantwiththeexaminationtechniquesinvolvingthisarea.Eventhestandardtextbooksof otolaryngologyarewoefullyinadequateindetailsregardingthissubject.Thisebookdiscussesthe examinationtechniquesandinvestigationspertainingtorhinolacrimalsystem
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GreekterminologymeaningDownpour. Thisisdefinedasexcessivewateringofeye.Thisisinvariablycausedbyobstructiontotear drainage.Causesofepiphorainclude: Congenital:Congenitalnasolacrimalductobstruction.Incidencevariesbetween16%4.Itis beleivedthatmassageofentirenasolacrimalsystemreleivesobstructioninmorethan90%5of cases.Majorityoftheseobstructionresolveduringthefirstyearoflifehenceurgentsurgical managementisnotnecessary6.Probingisalsoknowntobebeneficialinthesepatients.Thetime ofprobingiscontroversial.Probingisadviseduptotheageof5inthesepatients7. Acquired: 1.Primaryacquirednasolacrimalductobstructions 2.Dacryocystolithiasis 3.Orbital/lacrimaltrauma 4.Canalicularlacerations 5.ActinomyceswithinthecanaliculiActinomycesareanaerobicgrampositivebacilliresembling fungi.Theseorganismarenormalcommensaloforopharynx.Theseorganismarecapableof causingcastformingcanaliculitis9leadingontolacrimaltractobstruction. 6.Canalicularinfectionsfollowingherpesinfections/ectropionViralinfectionsconstituteawell recognisedcommoncauseofacquiredcanalicularobstruction8.Thesepatientsgivehistoryofan episodeofblepharokeratoconjunctivitisbeforeepiphora.Antivirals(idoxuridine)whichare prescribedforthisconditiontooaddtothewoesbycausingmorelacrimalobstruction.Naso lacrimalobstructioncausedbyantiviralsaretransientanddisappearafterthedrugisdiscontinued. Herpessimplexviralinfectionsareknowntocausepunctalchanges. Clinicalexaminationgoalinthesepatientsistodistinguishbetweenepiphoraandlacrimation. Whileepiphoraneedstobesurgicallymanagedmedically.Thefocusshouldbeindifferentiating anatomicalobstructionfromfunctionaldisorders. Anatomicalobstruction: Obstructiontothelacrimaldrainagesystemisthefeaturetolookforinthiscondition.Pathological changescouldbeseeninvolvingthelacrimalsac,irregularitiesinlacrimaldrainagesystem (canalicularstenosis,canalicularblockage,obstructiontonasolacrimalduct,diverticulousformation etc.)Lacrimalpathwayscanbeobstructedduetointernalderangementslikeinflammationofthe epitheliallinining.Thisisknownasintrinsicobstruction.Iflacrimalpathwaysareaffectedby
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Fig.1:Gradesofepiphora
Fig.2:Anatomyoflacrimalsytem
ThejunctionbetweenthecommoncanaliculusandthelacrimalsacisguardedbytheRosenmuller valve.Thisvalvepreventstearreflux.Thenasalendofthenasolacrimalductatthelevelofinferior
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Suprasaccalobstruction
Saccalobstruction
Subsaccalobstruction:
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Inthiscategorytheobstructionliesbelowtheleveloflacrimalsac.Thisconditioncommonlyrequires endoscopicdacryocystorhinostomy.Thisobstructionismorecommonthantherest.
Subsaccalincompleteobstruction
Completesubsaccalobstruction
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shouldbeusedonlytoindicateanatomicalobstructiononly. DiagnosisofepiphorathePhylosophybehindit: Theoreticallyspeakingexcessivetearingmaybecausedby Hypersecretion Epiphora Combinationofboth Diagnosticevaluationshouldinclude: 1.Quantificationoftearproduction 2.Assessmentofnasolacrimalsystempatency 3.Differentiatingepiphorafromlacrimation 4.Definingthepathologicalprocessofepiphora 5.Differentiatinganatomicalfromfunctionalobstruction 6.Attemptingtolocatetheobstructioninordertodefinetheoptimalsurgicalapproach ClassificationofTestsforlacrimaldrainagepathway: Anatomicaltests Functionaltests Secretorytests Anatomicaltests: Thesetestsareperformedtolocatetheprobableareaoflacrimaltractobstruction.Thesetests include: Palpationoflacrimalsac Syringing/irrigation Diagnosticprobing Dacryocystography Nasalexamination CT/MRI Functionaltests: Theseareperformedtoaccessthefunctionoflacrimalapparatusunderphysiologicconditions. Thistestisperformedifthereisnoobstructionasevdencedbynegativeanatomicaltests. Thesetestsinclude: Flouresceindyedisappearancetest
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Scintigraphy JonesdyetestI Sacharintest Testsofsecretion: Thesetestsareperformedtoaccesssecretoryfunctionofthelacrimalapparatus.Thesetestsare performedinexaminingdryeyes.Thesetestsinclude: Schrimerstest BengalRosetest Tearfilmbreakup Tearlysozyme Knowledgeofvariouscausesoflacrimationandepiphorareallyhelpsinclinicalexaminationof thesepatients. Excesslacrimation: SupranuclearcausesPsychogenic/emotions StimulationofVcranialnerve(Reflextearing) Lidcauses(Blepharitis/Trichiaris) Conjunctivaldiseases Cornealdiseases Neuralgia Ocularinflammation Infranuclearcausesfacialpalsy,abberantinnervation,crocodiletears Lacrimalglandstimulation OthersBrightlights,sneezing Epiphora: Functionalinsufficiency Incorrectlidclosure Lidmalposition Punctaleversion Punctalmedialization Anatomicalobstruction Combinedlacrimation/epiphoraAcombinationoftheabovetwocategories
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FacialnervepalsyCornealirritationandpumpdefects LowerlidectropionConjunctivalirritation,ineffectivepumpmechanism ThyroiddiseasesCornealirritation,defectivecanalicularfunction Clinicalhistory: Thisisaveryimportantaspectoflacrimalapparatusexamination.Thiswillprovidevitalcluesto thepresenceofcanaliculardisorders12.Historyshouldincludepatientspresentandpast ophthalmologicalproblems,nasalsymptoms,medicalandinterventionalrelevantproceduresalso. Unilateraltearingusuallyindicateobstructivepathologywhereasbilateraltearingcouldbe physiological.Achildwithahistoryoftearingsincebirthshouldarousesuspicionofmembranous obstructiontonasolacrimalduct.Nasaldisorderslikenasalpolyposis/sinusitiscanalsocause unilateralepiphora. Inspectionandpalpationshouldinvolvethefollowingareas: 1.Eyelids 2.Medialcanthus 3.Palpationoflacrimalsac Eyelidexamination: Lookoutforlowereyelidlaxity Ectropion Punctaleversion Trichiasis Blepharitis SnapbacktestThistestisperformedbypullingthelowereyeliddownandawayfromtheglobe andheldforseveralseconds.Onreleasethelowerlidresumesitsnormalposition.Thetimetakenfor resumptionofnormalpositionisnoted.Thepatientshouldnotblinkduringthetest.Thistestprovides anassessmentoflaxityoflowerlid.Thelongerittakesforthelowerlidtospringbackto positionthemorelaxitis.Thistestisgradedonascaleof4startingfrom0.0=normaland4=lax lowerlid. Medialcanthallaxity Lateralcanthallaxity Orbicularisoculimuscletonecheck PinchtestThistesthelpstoassessorbicularisoculimuscletension. Examinationofmedialcanthus: Lacrimalsacenlargementwillbeseenasmassbelowmedialcanthaltendon. Enlargementabovemedialcanthaltendonindicatesneoplasm.
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Swellingabovemedialcanthus
Painandtendernessoverthisareaindicatesacutedacryocystitis.
Sacbeingsqueezedoffitssecretions
Sacswelling
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Inperformingthistestonedropof1%fluoresceinisinstilledintothelowerfornixofeachconjunctival sac.After5mins,thethicknessoffluoresceinofthetearmeniscusismeasuredusingcobaltblue filter.Studiesrevealthatittakes5minsfortearstonormallydrainthroughthesystem. Thistestcansafelybeperformedininfantsandchildren13. Presenceoffluoresceingivesnoinformationonthelocalisationofobstruction.Presenceofresidual fluoresceinisanindicationforprobingandsyringing.Whenperformingthistestininfantsthechild shouldbeheldinaverticalposition. Dyetestgrading: 0=Nofluoresceinintheconjunctivalsac 1=Thinflurescingmarginalteardroppersists 2=Morefluoresceinpersistssomewherebetween1and3grades 3=Widebrightlyfluoresceintearstrip Amongthesegrades0and1areconsiderednormal Falsenegativescanoccurin: 1.Largelacrimalsac 2.Mucocele 3.Distalnasolacrimalductblock Breakuptimetest: Thistestisperformedbyplacingadropoffluoresceinintheexternalcanthusinthelowereyelid. Itstransportcanbeobservedfromlateraltomedialacrosstheeyelidandintoeachpunctum.Holesin thetearfilmcanbeobserved.Thisisbreakuptimetest. Jonesdyetests:Thisgroupoftestsareusedtodistinguishbetweenfunctionalandanatomicoutflow problems.Theprimarytestisperformedbyplacingtopicalanestheticandfluresceindyeintothe conjunctivalsac.Topical4%xylocaineandoxymetazolinenasalspraysmaybeusedtoanesthetize andvasoconstricttheinferiormeatusofthenose.Acottontippedapplicatorisplacedbeneaththe
Jonesdyetest
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inferiorturbinateneartheopeningofthenasolacrimalduct.Recoveryoffluoresceindyeinthenose indicatesafunctionallyandantomicallypatentsystem.Nonrecoveryofthedye(negativeresult) suggestsafunctionaloranatomicblockage. Intheeventofnegativedyetest,secondarydyetestshouldbeperformed.Thistestisperformed afterremovalofresidualfluoresceinfromtheconjunctivalsac.Clearsalinesolutionisplacedintothe inferiorcanaliculususingasyringe/cannula.Theirrigantisretreivedfromthenasalcavitybytilting thepatientsheadforwardoverabasin.Iffluoreseindyeispresentintheirrigant(positive result)thenitisassumedthattheupperlacrimalsystemisfunctionalwhilethelowersystemis partiallyopenandisnotfunctional.Recoveryofaclearirrigant(negativeresult)indicatesafunctional problemwiththeuppersystem. Caution:Thistestisuselessinpatientswithtotallacrimaltractobstruction.Thistestshouldbe performedonlyifthelacrimalsystemispatentforsyringing. Saccharintest: Thistestismoreorlesssimilartofluoresceindyetest.Thistestisalsohencephysiological.Adropof saccharinisplacedintoanesthetizedandthetimetakenforthepatienttotastesaccharinis measured.Approximatetimeisabout3.5mins.Theflipsideinthistestisthatthepatientshould havenormaltastesensation. Diagnosticprobingandlacrimalsyringing: Theseareinvasivetests.Theyprovidevaluableinformationonlocationofobstruction.Theyestablish diagnosisofanatomicalobstructioninthelacrimalsystem.Thistestisvirtuallyuselessinfunctional obstruction14.Syringing/irrigationoflacrimalsystemisnotaphysiologicaltestsincethepressures usedismorethanthenormalpressureoflacrimalsyste.Hencethistestshouldbe interpretedwithfluoresceindyetestandclinicalexamination. Procedure: 1.Topical4%xylocainedropsappliedtotheconjunctiva
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2.Punctumdilatorisusedtodilatethepunctumandampulla 3.Abluntcannulaisplacedintheinferiorcanaliculus.Thelowereyelidispulleddowntostraighten theinferiorcanaliculus.Superiorcanaliculusisgentlystretchedlaterallypriortoirrigation 4.Tipoftheirrigatorisplacedintheinferiorcanaliculus,firstverticallyandthenhorizontally withtheeyelidonstretch.Thetipisadvanced37mmintothecanaliculusandsterilesaline isinjected. 5.Itisimportanttoavoidforcedirrigationtoavoiddamagetothecanaliculi Interpretation:Regurgitationofirrigatedsalinethroughtheoppositepunctumindicatesanobstruction inthecommoncanaliculusormoredistalstructures.Regurgitationoffluidviathesamecanaliculus indicatespunctalobstructionandsyringingshouldberepeatedviatheoppositecanaliculus.Irrigation intothenoseindicatesnormaldrainagefunction.Itdoesnotruleoutfunctionalobstruction. Probing(Diagnostic): Thistestshouldbeperformedifsyringingtestindicateobstructionandthelocationoftheobstruction istobeascertained.Obstructioncanbelocatedinthecanaliculiandtheirassessmentisvitalin decidingthemangementmodalityinthesepatients.Ifirrigatedfluidregurgitatesthrough oppositepunctumobstructionofcommoncanaliculusormoredistallyispossible.Theexactsitein thisscenariocouldbeascertainedbycarefulprobingoftheentiresystem.Probingcanbeperformed usingbluntBowmansprobewhichcomeinvarioussizes. Procedure: Afterinstillingtopicalanestheticdropsintotheconjunctivathepunctumisdilatedusinglacrimal
Fig.3:Hardstop
Softstop
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probe.Theprobeisthenpassedverticallyandthenhorizontallywiththeeyelidinstretchtillthe lacrimalboneisencounteredorsoftobstructionisreached.Iftheprobeencounterslacrimalbone thenitisknownashardstop.Thisisactuallynormal.Iftheprobeencountersobstructionthenitis knownassoftstop.Ifirrigationshowedrefluxthroughtheoppositepunctumandtheprobe encountershardstopthenobstructioncouldbeattheleveloflacrimalsacornasolacrimalduct. Radiologicalevaluation: Include: Dacryocystography Nuclearlacrimalscintigraphy CT MRI Dacryocystography: Thisisananatomicalinvestigation.Thisisindicatedwhenthereisblockinthelacrimalsystemas indicatedbysyringingtest.Ithelpsincreatinganinternalimageoftheentirelacrimalsystem.In thistestradioopaquewatersolubledyeisinjectedeitherintoupper/lowercanaliculusand magnifiedimagesaretaken.Usingdigitalsubtractiontechniquesexcellentimagesoftheentire lacrimalsystemcanbeensured. Radiologiccriteriaoflacrimalpathology15: 1.Regurgitationofradioopaquefluidintotheconjunctivalsac 2.Absenceoffluidinthenose 3.Fluctuationoflumenoflacrimalsystem 4.Irregularityincontrast 5.Deformationinvolvinglacrimalsac
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Nuclearlacrimalscintigraphy: Thisisanoninvasivephysiologicaltest.Thistestutilizesradiotracertechnitium99Mpertechnitate. Thiscanbeanalysedusingagamacamera.Thisisusefulonlyinpatientswhoselacrimalsystemis patentonsyringingdespiteepiphora.Thisisfoundtobeusefulindifficultcases andincompleteobstruction. Thistestisperformedwithoutinstillingtopicalanesthesia.Adropoftechnetium99misinstilledinto eachconjunctivalsacofapatientsittinginfrontofagammacamera.Normalblinkingofeyesare allowed.Patientstaresatadistanttargetduringa20minstestperiodwhileimagesarebeing recordedwithagammacamera. CTscan/MRIscan: Helpfulinidentifyingtumorsinvolvingsac,oradjacentareas.
Rhinosporidiosisoflacrimalsac
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Schrimerstest
withtheeyesclosed.Producedtearswillwetthefilterpaper.Thelengthofthefilterpaperwhich becomeswetisassessedattheendof5minutes.Normaltestresultisbetween10mmand30mmof wetfilterpaper.Normallyitshouldnotexceed30mm.Avalueofmorethan30mmisconsideredto beepiphora.Avalueoflessthan10mmisconsideredtobedryeye(hyposecretion). Breakuptimetest: Thistestindicatesfunctionofmucinlayer/reflexhypersecretionofaquouscomponentofthetears. Onedropoffluoresceinisinstilledintotheexternalcanthusofalowerlidandthepatientisinstructed toblinkonceandthentokeephiseyesopen.Theholesdevelopedinthetearfilmareobservedat thecorneathroughaslitlampwithilluminationthroughthecobaltfilter.Thenormal breakuptimeshouldbeapproximately1530s.Abreakuptimeoflessthan10sindicatesa deficiencyandtheepiphorashouldbetreatedwithlibricatingeyedrops. BengalRosetest: ThistestisalsosimilartothatofBreakuptimetest.OnedropofBengalRosedyeisplacedinthe conjunctivaandthepatientisinstructedtoblinkseveraltimeswithinaminute.Interpalpebral stainingisseeninpatientswithdryeye. Lysozymelysistest: Theamountofalysozymeactivityandconcentrationisdecreasedinhypersecretionandin hyposecretion,anditusuallyprecedesclinicalsymptoms.Alysozymeactivity(andconcentration) isestimatedonthebasisoftheinhibitionofthegrowthofthebacteriumMicrococcuslysodicticus.
References
1. OnerciM.Dacryocystorhinostomy.Diagnosisandtreatmentofnasolacrimalcanalobstructions. Rhinology200240:4965. 2. CokkeserY,ErH.Comparativeexternalvesusendoscpicodacryocystorhinostomy.Otolaryngol
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HeadandNeckSurg2000123:48891 3. HurwitzJJ(1996)Thelacrimalsystem.LippincottRavenPublishers,Philadelphia 4. GuerryD,KendigEL.Congenitalimpotencyofthenasolacrimalduct.ArchOphthalmol1948,39: 193204. 5. PriceHW.Dacryostenosis.JPediatr1947,30:302305 6. BallardEA.Excessivetearingininfancyandearlychildhood:theroleandtreatmentofcongenital nasolacrimalductobstruction.PostgradMed2000107:14954 7. KashkouliMB,KassaeeA,TabatabaeeZ.InitialNasolacrimalDuctProbinginChildrenunderAge 5:CureRateandFactorsAffectingSuccess.JAAPOS20026:3603 8. Bouzas,A.(1965).Canalicularinflammationinophthalmiccasesofherpeszosterandherpes simplex.AmericanJournalofOphthalmology,60,713716. 9. SahlinS,RoseGE.(2001)Lacrimaldrainagecapacityandsymptomaticimprovementafter dacryocystorhinostomyinadultspresentingwithpatentlacrimaldrainagesystems.Orbit,20:173179. 10. http://www.drtbalu.com/Endo_dcr.html 11. MeyerDR,AntonelloA,LinbergJV(1990)Assessmentofteardrainageaftercanalicular obstructionusingfluoresceindyedisappearance.Ophthalmology97:370374 12. HurwitzJJ(1996)Thelacrimalsystem.LippincottRavenPublishers,Philadelphia 13. LloydGAS,WelhamRAN(1974)Subtractionmacrodacryocystography.BrJRadiol47:379382 14. SahlinS,ChenE(1996)Evaluationofthelacrimaldrainagefunctionbythedroptest.AmJ Ophthalmol122:701708 15. WaltherEK,KsterO,StraehlerPohlHJ(1989)Dakryozystographieindigilater Subtraktionstechnik.LaryngolRhinolOtol68:396400
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Intrinsic Rhinitis
December 20, 2012 Rhinology
Authors
BalasubramanianThiagarajan
Abstract
Intrinsicrhinitisisdefinedasanoninfectiveandnonallergicconditioncharacterisedbynasalblock, rhinorrhoeaandhyposmia.Thisispurelyamedicalcondition.Awarenessofthisconditionwillhelpus toavoidunnecessarysurgicalproceduresonpatientssufferingfromthisdisorder.Surgeryshouldbe reservedonlyforcasesthatareintractabletomedicalmanagement.Thisarticlediscussesthe completegamutofthisdisorder.
Intrinsic Rhinitis
Introduction: Rhinitisisinflammationofnasalmucosacharacterizedbynasaldischarge,itchingandcongestion.It affects20%ofthepopulation1. Intrinsicrhinitisisdefinedasanoninfectiveandnonallergicconditioncharacterizedbynasalblock, rhinorrhoeaandhyposmia.Thisispurelyamedicalcondition. Intrinsicrhinitisencompassestwoseparatediseaseentities2.Theseentitiesshow: 1.inferiorturbinatehypertrophy 2.nasalpolypformation. symptoms Symptomsofintrinsicrhinitis Symptom Eosinophilic Non eosinophilic Obstruction Moderate/ Mild severe Rhinorrhoea Mild/ Severe Moderate Sneezing/ Minimal Minimal Pruritis Hyposmia Usual Rare Mucosal Marked Mild swelling Inferior Marked Mild turbinate enlargement Polypi common Never
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Common
Rare
Clinicalpresentation: Rhinitisisgenerallycharacterisedby6mainsymptoms:Theyare 1.Congestion 2.Sneezing 3.nasalitching 4.rhinorrhoea 5.hyposmia 6.postnasaldischarge Amongthesemainsymptomsnasalitchingandsneezingarefeaturesofallergicrhinitisandhence arenotseeninintrinsicrhinitis.Alltheothersymptomsaremanifestedinintrinsicrhinitis. Seebohmidentifiedtwogroupsofpatientsamongstthosesufferingfromperenialrhinitis.Onegroup hadeosinophilsintheirnasalsecretionswhiletheotherdidnothaveanyeosinophilsintheirnasal secretions.Accordinglyheclassifiedintrinsic/perenialrhinitisintoeosinophilicandnoneosinophilic types. Eosinophilicgroup:Thisgroupischaracterisedbymarkednasalcongestion,profuserhinorrhoea, hyposmia,inferiorturbinatehypertrophyandmucoidnasalsecretion.Nasalpolyposisfrequently occurredinthisgroupofpatients. Noneosinophilicgroup:Inthesepatientsnasalobstructionisverymild,rhinorrhoeaisverysevere. Theydonothavesignificantmucosalswelling.Inferiorturbinatehypertrophyisnotsignificant. Tendencyofnasalpolypformationisrareinthisgroup. Aetiologyofintrinsicrhinitis: Theoriesregardingaetiologyofintrinsicrhinitisare: 1.Autonomicimbalance 2.Airwayhyperreactivity 3.Allergicreactiontounidentifiedallergen 4.DisturbancesofBetareceptorfunction MechanismsofBetareceptordysfunction: 1.Downregulationcausedbyexcessendogenousnoradrenalinestimualtion. 2.Downregulationanduncouplingofadenylatecyclaseproducedbytheinflammatorymediator inducedactivationofproteinkinase. 3.TheactionofBetareceptorinhibitoryfactorpresumedtobeanantibetareceptorautoantibody. 4.DysfunctionofBetareceptorkinasecausingshorttermdesensitisationofbetareceptorsafter
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exposuretobetaagonists. Roleofautonomicnervoussystemincausingintrinsicrhinitis: Theautonomicnervoussystemexertsitseffectsbysecretingneurotransmittersartheirnerve endings.Theneurotransmitterssecretedareadrenaline,noradrenaline,vasoactiveintestinal polypeptide,acetylcholineandneuropeptideY. Thenasalresistancetoairflowiscontrolledbysympatheticsystem,whereasthenasalglandsare innervatedbyparasympatheticnerves.Increasedparasympatheticoutflowcausesglandular hypersecretion.Vasoactiveintestinalpolypeptidehasbeenknowntocausethiseffect.The vasodilatationcausedduetotheeffectsofvasoactiveintestinalpolypeptideisresistanttotheeffects ofatropine. Management: Majorityofpatientswithintrinsicrhinitisbenefitfrommedicalmanagement.Onlyafewrequire Medicalmanagementofintrinsicrhinitis: Topicalisotonicsalinespraycanbeusedforbothformsofintrinsicrhinitis.Salinespraycausesa reductionofpostnasaldrip,sneezingandnasalcongestion3. TopicalintranasaladministrationofCapsaicin(derivedfrompepper).Thisirritantchemical desensitizesthesensorynerveendingsofthenasalmucosatherebyreducingnasalhyperactivity4. Eosinophilictype: SteroidsTopicale.g.fluticasone,budesonide.Ashortcourseofsystemicsteriodscanbe administered. AlphareceptoragonistsSystemice.g.pseudoephidrineTopicale.g.xylometazoline(shortcourse) MastcellstabilisersTopicalcromoglycatesolution. Noneosinophlictype: AnticholinergicTopicale.g.ipratropiumHyosineadministeredorallyorasapatch. Anticholinergic/sympathomimeticImipramineorally,chlorpheniramineorally. SurgicalManagement SurgicalmanagementofIntrinsicrhinitis Symptom Nasal obstruction Rhinorrohea Aim Turbinate reduction Turbinate resectionVidian neurectomy Surgery Submucosal diathermy CryosurgeryLaser surgeryPartial resectionSubmucosal turbinectomyRadical turbinectomyExcision ofvidian nerveEndoscopic vidianneurectomy
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References
1. PoweDG,HuskinssonRS,CarneyAS,etal.Evidenceforaninflammatorypathophysiologyin idiopathicrhinitis.ClinExpAllergy200131:8649. 2. SettipaneRA,SettipaneGA.Nonallergicrhinitis.In:KalinerMA,ed.CurrentReviewofAllergic Diseases.Philadelphia:CurrentMedicine,1999. 3. BronskyEA,DruceH,FindlaySR,HampelFC.Aclinicaltrialofipratropiumbromidenasalsprayin patientswithperennialnonallergicrhinitis.JAllergyClinImmunol199595:11171122. 4. StjrneP,LundbladL,nggardA,etal.Localcapsaicintreatmentofthenasalmucosareduces symptomsinpatientswithnonallergicnasalhyperreactivity.AmJRhinology19915:145151.
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Authors
BalasubramanianThiagarajan Introduction: Anaesthesiaofnoseandnasalcavityareindicatedforvariousdiagnosticandsurgicalprocedures involvingthenose.Someoftheseindicationsinclude: 1.InsertionofRylestube 2.Diagnosticnasalendoscopy 3.Repairoffracturenasalbone1 4.Nasalpackingforepistaxis 5.Foreignbodyremoval 6.Abscessdrainage/Septalhematomadrainage 7.Nasotrachealintubation12 Typesofanaesthesia: 1.Topicalanaesthesiausing4%topicalxylocaine/10%typicalxylocainespray3 2.Infiltrationanaesthesiausing2%xylocaine 3.Regionalblocks 4.Combinationofthese Innervationofnose: Foreffectiveadmininstrationoflocalanaesthesiaacompleteunderstandingofsensoryinnervationof noseandnasalcavityisamust.Innervationofnosecanbedividedinto: 1.Innervationofmucosawithinthenasalcavity 2.Innervationofexternalnoseanditsskincovering Sensoryinnervationofexternalnose: Externalnoseanditsskinliningisinnervatedbyophthalmicandmaxillarydivisionsoftrigeminal nerve. SuperioraspectofthenoseissuppliedbySupratrochlearandInfratrochlearnerves(branchesof trigeminalnerve)andexternalnasalbranchofanteriorethmoidalnerve. Inferiorandlateralpartsofthenoseissuppliedbyinfraorbitalnerve.
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Fig.1:SensoryInnervationofExternalNose
Sensoryinnervationofinteriorofnasalcavity: 1.Superiorinneraspectofthelateralnasalwallissuppliedbyanteriorandposteriorethmoidnerves 2.Sphenopalatineganglionpresentattheposteriorendofmiddleturbinateinnervatestheposterior nasalcavity 3.Nasalseptumissuppliedbyanteriorandposteriorethmoidalnerves.Sphenopalatineganglionalso contributestothesensorysupplytothenasalseptumviaitsnasopalatinebranch. 4.Cribriformplatesuperiorlyholdstheolfactoryspecialsensationfibers. Mucosalsurfaceanaesthesiacanbeachievedby: 1.Using10%xylocainenasalsprayTopicalsurfaceanaesthesiajustlastsforabout45mins.This typeofanaesthesiaispreferredwhileperformingdiagnosticnasalendoscopy/minorprocedures involvingthenasalcavitylikenasalpacking. 2.Nasalpackingusingcottonoids/pledgetssoakedin4%xylocainemixedwith1in10000adrenaline isusefulforperformingminorsurgicalproceduresinsidethenasalcavity.Cottonoidsare comparativelybetterthancottonpledgets.Eachnasalcavityshouldbepackedwith3packs.Oneis placedinthefloorofthenasalcavity,thenextoneisplacedoverittoencroachintothemiddle meatusandthelastoneisplacedabovethesecondonetoanaesthetizethefrontalrecessarea. Presenceofadrenalineinthemixtureshrinksthenasalmucosaandprolongesthedurationoftopical anaesthesia. 3.Infiltrationanaesthesiaispreferredwhileperformingsurgeriesinsidethenasalcavity.2%xylocaine mixedwith1in10000adrenalineisusedforinfiltration.Infiltrationcanbeusedtoanaesthetizethe anteriorethmoidalnerve,infraorbitalnerveviathecaninefossa.Thisisveryusefulduringreduction offracturenasalbone.
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Sensoryinnervationofnasalmucosa
References
1. WaldronJ,MitchellDB,FordG.Reductionoffracturednasalboneslocalversusgeneral anaesthesia.ClinOtolaryngolAlliedSci.Aug198914(4):3579 2. TechanivateA,LeelanukromR,PrapongsenaP,TerachindaD.Effectivenessofmouthpiece nebulizationandnasalswabstickpackingfortopicalanesthesiainawakefiberopticnasotracheal intubation.JMedAssocThai.Oct200790(10):2063 71 3. Stolz,D.,etal.,Nebulizedlidocaineforflexiblebronchoscopy:arandomized,doubleblind, placebocontrolledtrial.Chest,2005.128(3):p.175660.
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Authors
BalasubramanianThiagarajan
Abstract
Thisarticlediscussestheimportanceofanesthesiainendoscopicsinussurgery.Majoraimof anesthetistinFESSshouldbetoreducebloodpressuretosuchalevelthatbleedingisminimized.It alsodiscussesthevariousstepsthatshouldbefollowedbysurgeonstoreducedintraoperative bleedingduringtheprocedure. Introduction: Bleedingisonecomplicationthatcouldincreasetheriskofcomplicationduringendoscopicsinus surgery. Considerableamountofattentionshouldbepaidtoreducebleedingonthetableduringthesurgical procedure.Drysurgicalfieldnotonlyimprovesvisibilityduringendoscopicsinussurgery,italso shortensthe durationofsurgery.Inthisregardbothanesthesiologistandtheoperatingsurgeonhaveavitalroleto play. Endoscopebecomesratheruselesswhentheoperatingfieldbleeds.Bleedingismorecommonif surgeryis performedonallergic/inflamednasalmucosa.Thisiswhereoperatingsurgeonshouldtakeextra precaution inpreparingthepatient.Reductionofnasalallergyandinflammationisalsoknownasmucosal preparation priortosurgery.Thisisdonebyadministeringacourseofantibiotic,antihistamineandtopicalsteroid spray1. Ideallypatientshouldbeprescribedthesemedicationsatleast1weekpriortosurgery. Bleedingismorecommonclosetolargevessels.Stamberger2hasincluded4areaswhichare responsiblefor extensivebleedingduringendoscopicsinussurgery. 1.Anteriorethmoidalarterylocatedinanosseouschannelclosetoethmoidroof 2.Branchofsphenopalatinearteryclosetotheposteriorendofmiddleturbinate.Thisismoreprone for injuryinpatientswithwellpneumatizedmiddleturbinate(conchabullosa) 3.Damagetosphenopalatinearterywhileattemptingtowidenthesphenoidalostium
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Classificationofsurgicalbleedingduringendoscopicsinussurgery: SurgicalbleedingduringFESShasbeenclassifiedinto: Arterial Venous Capillary Outofthesethreetypesofbleedingitisthecapillarybleedthatcausesthemosttroubleduring FESS3. Capillarybleedingcanbereducedconsiderablybycarefulpackingofthenasalcavitywithcotton pledgets/ neuropattiessoakedin4%xylocainemixedwith1in10000adrenaline.Thisconcentrationisbeing usedby theauthorwithgreatdegreeofsuccess.Theconcentrationofadrenalineisthesourceofraging controversy. Oneaspectshouldbeclearlyborneinmind,neverexceed7mlof4%xylocainewhilepacking.Any volume about7mlshouldprovetobetoxictothepatient. Positionofthetable: Thisplaysavitalroleinreducingcapillarybleed.Ifthesurgicalfieldiskeptabovethelevelofthe heartblood flowtotheheartisconsiderablyreduced.Thisisalsoknownasposturalischemia.Systolicpressure has beenestimatedtoreduceby2mmofmercuryforevery2.5cmsofheadelevation4.Ideallyduring endoscopicsinussurgeryistheheadofthepatientisinanelevatedpositioncapillarybleedingwillbe reduced alot. Maintainingnormalbodytemperature5: Duringsurgicalproceduremaintainingnormalbodytemperatureisveryimportant.Significantlevels ofhypo/ hyperthermiacanaffectplateletfunctioncausingincreasedbleedduringtheprocedure. Roleofanesthesiologist: Anesthesiologistplayavitalroleinreducingbloodlossduringsurgery.Bleedingisdirectly proportionaltothe meanarterialpressure.Aslongasthemeanarterialpressureisheldwithinalowrangebleedingwill be minimal.UseofintravenousanestheticagentslikePropofolcanreducebleedingwhencomparedto
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thatof conventionalinhalationalagents.Propofolisknowntoreducebrainmetabolismanditscirculation. Maximum bleedingduringFessoccursfromcentralvessels.Thusitplaysavitalroleinreducingbleeding.Use of propofolwithfentanylsupplementationactuallyservesthepurpose.Evensevoflurane6isknownto increase bleedingduringFess. UseofNitroglycerineinfusion: Nitroglycerineinfusionduringsurgerycausesprolongedhypotension.OnlyflipsidetotheuseofNTG dripis compensatorytachycardiawhichcanpushupthebloodpressure.Thistendencyofcompensatory tachycardiaiscommonlyseeninyoungindividuals.Thiscanbeobviatedbyputtingthepatienton preoperativenightdoseofbetablockers.Captoprilcanbeusedonthetabletoreducethehearrate that couldoccurduetoNTGdrip. Ifthepatientisunderprolongedhypotension,theirstatusshouldbemeticulouslymonitored.
References
1. Preoperativetreatmentwithtopicalcorticoidsandbleedingduringprimaryendoscopicsinus surgery.AlbuS,GoceaA,MitreI.OtolaryngolHeadNeckSurg.2010Oct143(4):573 8. 2. StammbergerH.Functionalendoscopicsinussurgery:themesserklingertechnique.Philadelphia: BCDecker1991 3. JacobiKE,BohmBE,RickauerAJ,JacobiC,HemmerlingTM.Moderatecontrolledhypotension withsodiumnitroprussidedoesnotimprovesurgicalconditionsordecreasebloodlossinendoscopic sinussurgery.ClinAnesth 4. EnderbyGE.Pharmacologicalblockade.PostgradMedJ197450:572 5 5. SchmiedH,KurzA.Mildhypothermiaincreasebloodlossandtransfusionrequirementsduring totalhiparthroplasty.Lancet1995347(8997):289 2.
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