Basic otorhinolaryngology

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  • 1. Basic Otorhinolaryngology A Step-By-Step Learning Guide Rudolf Probst Gerhard Grevers Heinrich Iro
  • 2. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 3. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 4. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. kroY weN ´ tragttutS galreV emeihT groeG selbat 45 ,snoitartsulli 663 tdlohsyE hcirlU ikswonasoR knarF yb snoitubirtnoc htiW ynamreG ,negnalrE latipsoH ytisrevinU rednaxelA hcirdeirF ygolognyralonihrotO fo tnemtrapeD rosseforP .D .M ,orI hcirnieH ynamreG ,grebnratS rosseforP .D .M ,sreverG drahreG dnalreztiwS ,elsaB elsaB latipsoH ytisrevinU ygolognyralonihrotO fo tnemtrapeD rosseforP .D .M ,tsborP floduR ediuG gninraeL petS-yb-petS A ygolognyral -onihrotO cisaB
  • 5. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 654321 )YNT( 0-733-09885-1 NBSI )VTG( 4-144231-31-3 NBSI gnidmeW ,lppA yb ynamreG ni detnirP trufsnilletnehcriK ,rellüM dnu relgeiZ :yb gnittesepyT eppurgsgalreV emeihT :ngised revoC .egarots dna gnissecorp atad cinortcele dna ,smliforcim fo noit -araperp ,gnihpargoemim ,gniypoc ,noitcudorper tats -otohp ot ralucitrap ni seilppa sihT .noitucesorp ot elbail dna lagelli si ,tnesnoc srehsilbup eht tuohtiw ,noital -sigel thgirypoc yb tes stimil worran eht edistuo noitaz -ilaicremmoc ro ,noitatiolpxe ,esu ynA .thgirypoc yb de -tcetorp yllagel si ,foereht strap lla gnidulcni ,koob sihT .niamod cilbup eht ni si ti taht rehsilbup eht yb noitatneserper a sa deurtsnoc eb ot ton si yrateirporp sa noitangised tuohtiw eman a fo ecnaraeppa eht ,erof -erehT .txet eht ni edam syawla ton si tcaf siht ot ecne -refer cificeps hguoht neve seman yrateirporp ro skram -edart deretsiger tcaf ni era koob siht ni ot derrefer sngis -ed deretsiger dna ,stnetap ,seman tcudorp eht fo emoS .egap noitpircsed tcu -dorp eht no moc.emeiht.www ta detsop eb lliw atarre ,noitacilbup retfa dnuof era krow siht ni srorre fI .decit -on seicaruccani ro seicnapercsid yna srehsilbup eht ot troper ot resu yreve tseuqer srehsilbup dna srohtua ehT .ytilibisnopser dna ksir nwo sresu eht ta yleritne si desu noitacilppa fo mrof yreve ro eludehcs egasod yre -vE .tekram eht no desaeler ylwen neeb evah ro desu yl -erar rehtie era taht sgurd htiw tnatropmi ylralucitrap si noitanimaxe hcuS .koob tneserp eht ni edam stnemetats eht morf reffid srerutcafunam eht yb detats snoitacidni -artnoc eht ro niereht denoitnem seludehcs egasod eht rehtehw ,tsilaiceps ro naicisyhp a htiw noitatlusnoc ni yrassecen fi ,kcehc ot dna gurd hcae gniynapmocca stel -fael srerutcafunam eht ylluferac enimaxe ot detseuq -er si resu yrevE .koob eht ni detats snoitacilppa fo smrof dna snoitcurtsni egasod yna ot tcepser ni srehsil -bup eht fo trap eht no ytilibisnopser ro eetnaraug yna sserpxe ro ,ylpmi ,evlovni ton seod siht ,sselehtreveN .koob eht fo noitcudorp fo emit eht ta egdelwonk fo etats eht htiw ecnadrocca ni era secnerefer hcus taht erusne ot trof -fe yreve edam evah srehsilbup dna ,srotide ,srohtua eht taht derussa tser yam sredaer ,noitacilppa ro egasod yna snoitnem koob siht sa rafosnI .ypareht gurd dna tnemtaert reporp fo egdelwonk ruo ralucitrap ni ,egde -lwonk ruo gnidnapxe yllaunitnoc era ecneirepxe lac -inilc dna hcraeseR .tnempoleved launitnoc gniogrednu ecneics gnignahc-reve na si enicideM :eton tnatropmI moc.emeiht.www//:ptth ASU 10001 YN ,kroY weN ,eunevA htneveS 333 ,kroY weN emeihT ed.emeiht.www//:ptth ynamreG ,tragttutS 96407 ,41 essartsregidüR ,galreV emeihT groeG 6002  pirtlA ,muaB niraK :rotartsullI ASU ,saxeT ,ocaW ,regleT yrreT :rotalsnarT ynamreG ,negnalrE latipsoH ytisrevinU rednaxelA hcirdeirF ygoloiduA cirtaideP dna yrtainohP fo noisiviD ygolognyralonihrotO fo tnemtrapeD rosseforP .D .M ,ikswonasoR knarF ynamreG ,negnalrE latipsoH ytisrevinU rednaxelA hcirdeirF ygoloiduA cirtaideP dna yrtainohP fo noisiviD ygolognyralonihrotO fo tnemtrapeD rosseforP .D .M ,tdlohsyE hcirlU srotubirtnoC 0002 noitide namreG ts1 .ednuklieH nerhO-nesaN-slaH :noitide namreG eht fo eltiT .ynamreG ,tragttutS ,galreV emeihT groeG yb 4002 dethgirypoc dna dehsilbup noitide namreG dn2 eht fo noitalsnart desiver dna dezirohtua na si koob sihT 8456105002 22cd±1©5.716 5002 31996P.64FR .eltiT .III )hcirnieH( .H ,orI .II .drahreG ,sreverG .I ]5002 h269P 041 VW .sesaesiD cigolognyralonihrotO .1 :MLND[ .ygolognyralotO .1 )repap .kla( 0-733-09885-1 NBSI ± )repap .kla( 4-144231-31-3 NBSI .4002  , emeihT groeG : tragttutS .de dn2 .ednuklieH nerhO-nesaN-slaH :fo noitalsnart desiver dna dezirohtuA .mc ; .p .]regleT yrreT ,rotalsnart[ ; reuarB samohT ,tdlohsyE hcirlU ,ikswonasoR knarF ,yb snoitubirtnoc htiw ; orI hcirnieH ,sreverG drahreG ,tsborP floduR / ygolognyralonihroto fo koobtxeT ]hsilgnE .ednuklieH nerhO-nesaN-slaH[ .D .M ,floduR ,tsborP ataD noitacilbuP-ni-gnigolataC ssergnoC fo yrarbiL VI
  • 6. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. tsborP floduR raE lanretxE 01 702 raE elddiM 11 722 sredrosiD raelhcocorteR dna raE rennI 21 552 sredrosiD ralubitseV 31 172 evreN laicaF 41 982 esaB llukS laretaL 51 792 tsborP floduR tsborP floduR tsborP floduR tsborP floduR tsborP floduR tsborP floduR raE eht fo ygoloisyhP dna ymotanA 7 351 )stseT gniraeH( ygoloiduA 8 561 ygoloiduA cirtaideP ,sredrosiD gniraeH cirtaideP 9 791 tsborP floduR tsborP floduR raE III serusaeM yramirP dna seicnegremE 704 secruoS 014 xednI 314 rerhafdlaW knarF htiw ,orI hcirnieH tsborP floduR 131 sdnalG yravilaS ehT 6 sreverG drahreG ytivaC larO dna spiL 4 96 sugahposE dna xnyrahP 5 79 sreverG drahreG xnyrahP dna ytivaC larO II xidneppA tdlohsyE hcirlU ,ikswonasoR knarF sreverG drahreG 72 ecaF dna ,sesuniS lasanaraP ,esoN eht fo sesaesiD 3 ecaF dna ,sesuniS lasanaraP ,esoN I kceN VI ecaF dna ,sesuniS lasanaraP ,esoN eht fo ygolonummI dna ,ygoloisyhP ,ymotanA 1 kceN lanretxE 61 113 aehcarT dna xnyraL 71 733 sredrosiD ecioV 81 583 sredrosiD egaugnaL dna hceepS 91 793 tdlohsyE hcirlU ,ikswonasoR knarF sreverG drahreG 51 rerhafdlaW knarF htiw ,orI hcirnieH rerhafdlaW knarF htiw ,orI hcirnieH sesuniS lasanaraP dna esoN eht fo noitaulavE citsongaiD 2 sreverG drahreG 1 stnetnoC V
  • 7. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .selbat dna ,serugif ,txet niam eht ni deniatnoc si cipot a fo gnidnatsrednu cis -ab eht rof dedeen si taht noitamrofni niam llA .yregrus kcen dna daeh dna ygolognyralonihroto ni stnempolev -ed tsetal eht ot smrofnoc koobtxet sihT :rettam tcejbuS History, observation, methods of examination Treatment, further management Signs and Symptoms Starting situation Diagnosis, differential diagnosis strahcwolf rof edoc roloC 1 .giF .smynonys sa deton era smret desu ylnommoc ssel ro redlo elihw ,txet eht ni desu era smret etad-ot-pu tsom ehT .ygolognyralonihroto fo saera suoi -rav ni erutalcnemon lanoitanretni dradnats a hsilbatse ot sraey tnecer ni edam neeb evah stroffE :ygolonimreT .tinu eht ni era uoy erehw swohs ogol deroloc-der ehT .tinu yduts tnerruc eht ni deniatnoc era taht stes egap -gnicaf fo rebmun eht setacidni )xis ot eno morf( sogol fo rebmun eht :egap dnah-thgir eht fo renroc mottob eht ta nwohs era sogol ºkoob-nepoª ,ytiralc roF .segap gnicaf no detneserp era tinu yduts hcae ni scipot ehT .yrammus a ton si retrats ehT .stinu yduts rehto ot detaler si lairetam eht dna ,deton era stniop laic -epS .emehcs llarevo eht otni tif yeht hcihw ni yaw eht dna tinu eht ni derevoc era taht scipot eht setats sihT .epyt ecafdlob ni retrats a htiw snigeb tinu yduts hcaE .erutcurts lanoitidart a htiw sretpahc otni etaroprocni ot tluciffid erom neeb evah dluow dna skoobtxet ni dnuof ton yllausu era taht sthgilhgih citam -eht tneserp ot elbissop ti sekam snoitrop elbaeganam otni stnetnoc eht gnidividbuS .tinu gninrael evisehoc a tneserper hcihw ,) ( stinu yduts feirb otni nwod nekorb si lairetam eht hcihw ni koobtxet fo dnik wen a si tlus -er ehT .tamrof yldneirf-resu ,nrael-ot-ysae na ni lairet -am eht tneserp ot saw slaog niam eht fo enO :erutcurtS hcaorppA 1 .koob -txet elbadroffa tey ,evitcartta yllacihparg ,gnillepmoc yllanoitacude na gnitaerc fo laog eht htiw desu neeb evah ygolonhcet noitcudorp latigid fo seitilibapac ehT .weiver maxe na naht erom eb ot seripsa koob siht ,esnes siht nI .stcepsa gnitan -icsaf sti dna lairetam eht fo tnemyojne yevnoc dluohs ti dna ,gnitseretni eb osla dluohs gninraeL .spihsnoitaler -retni xelpmoc yllaitnetop dna stpecnoc cisab gnidnats -rednu si gninrael fo trap laitnesse nA .gninialpxe snaem gnihcaet os dna ,gnidnatsrednu snaem gninrael eurT .gniniart rehtruf ni trap gnikat esoht yllaicepse ,snaicisyhp rof nettirw osla si tub ,stned -uts rof yliramirp dednetni si tI .krow ecnerefer a dna koobtxet a htob si koob sihT ?rof nettirw koob eht si ohW .txet niam eht ni lairetam eht dnatsrednu llits dna sexob htped-ni eht piks nac uoy ,yrruh a ni era uoy fI .)ygolo -yrbme ni ,.g.e( yduts reilrae morf snoititeper ro ,noitamrof -ni lacirotsih ,snoitpircsed esac evitartsulli ,seuqinhcet gnita -repo edulcni yam sihT .gnidnatsrednu cisab a dnoyeb seog taht noitamrofni edivorp lobmys siht htiw dekram sexoB .stniop yek ot noitnetta tcerid ot evres dna º,eton ekatª ro ºnoituacª etacidni ot tnaem era sisahpme fo stnioP htped ni egdelwonK ?ºmaet koobtxetª eht fo srebmem eht era ohW ?nrael ot reisae meht ekam ot detneserp stnetnoc eht era woh ,.e.iÐdesu si taht hcaorppa gnihcaet eht si tahW ?koob siht morf tsom tifeneb nac ohW :koobtxet siht no noitamrofni dnuorgkcab emos htiw uoy edivorp ot smia ecaferp sihT ecaferP IV
  • 8. IIV Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .dnalreztiwS ,elsaB latipsoH ytisrevinU eht ta ygolognyralonihrotO fo .tpeD eht fo namriahc eht si tsborP .R .forP dna ;ynamreG ,grebnratS ni tsigologny -ralonihroto gnicitcarp a si sreverG .G .forP ;ynamreG ,negnal -rE ni latipsoH ytisrevinU rednaxelA hcirdeirF ta ygolognyralon -ihrotO fo .tpeD eht fo namriahc eht si orI .H .forP :thgir ot tfeL orI .H sreverG .G tsborP .R .koob siht htiw sseccus yreve dna tnemyojne hcum uoy hsiw eW .noitide txen eht ni ees ot ekil dluow uoy taht segnahc yna gnidrager srehsilbup eht ro su tcatnoc ot uoy rof dethgiled eb erofereht dluow eW .siht dehsilpmoc -ca evah ew rehtehw egduj nac ,redaer eht ,uoy ylnO .sdeen sredaer teem ot koob siht roliat ot saw laog ruO ?evorpmI eW naC tahW srotide ehT 2 .giF rerhafdlaW knarF .rD orI .H .forP fo eugaelloC hcinuM fo ytisrevinU ,latipsoH retneC ytiC ,ygoloidaR citsongaiD fo etutitsnI ,seimiezS ekirlU .rD segap retpahc laitini rof segami TC lanoisnemid-eerht deraperP ejhtüL negrüJ .rD noitide namreG ,tnempoleved tpecnoc dna gninnalp margorp lacideM hcilttiforP enomiS rethciR neraK-ejtnA noitide namreG ,tnemeganam tcejorP yrnnoK nahpetS noitide hsilgnE ,tnemeganam tcejorP regleT yrreT rotalsnarT remmahllöhcS dirgnI regürK treG noitcudorP muaB niraK scihparG scirtainohp .D .M ,tdlohsyE hcirlU .forP no sretpahc eht fo rohtuA .D .M ,ikswonasoR knarF .forP srebmem maeT sksaT .D .M ,orI hcirnieH .forP .D .M ,sreverG drahreG .forP .D .M ,tsborP floduR .forP 2 .giF .s ,srotide dna srohtuA .edivorp nac ylimaf a ylno taht tnemegaruocne eht htiw koob eht no krow yhtgnel ruo detroppus yeht ,os nevE .tcejorp siht gniraperp tneps saw meht ot degnoleb evah yllaer dluohs taht emit fo laed taerg A .seilimaf ruo ot dewo si edutitarg laicepS .krowtra luflliks reh rof muaB .sM ot og osla sknaht ruO .tnempoleved sti gniretsof dna tcejorp eht gnitomorp rof ,emeihT ,srehsilbup eht ot luf -etarg osla era eW .noisrev hsilgnE eht rof edutitarg ruo nrae yeht ,noisrev namreG eht rof rethciR .sM sa hcum sa tsuJ .ssecorp a hcus fo stcepsa larutluc eritne eht tub egaugnal eht ylno ton dnim ni gnipeek ,ssecorp noital -snart eht deganam eH .noisrev hsilgnE eht rof lanoitan -retnI emeihT ta rotide tcejorp ruo saw yrnnoK nahpetS .noitacifiralc fo deen ni stniop niaga dna emit delaev -er eh ,slliks suodnemert dna msilanoisseforp lausu sih htiw tcejorp siht gnihcaorppa morf trapA .noital -snart hsilgnE eht deraperp ,saxeT ,ocaW fo regleT yrreT .edutitarg erecnis ruo denrae sah ehs dna ,sruo sa llew sa krow reh si koob eht ,tluser a sA .dettimo eb dluoc taht segassap sa llew sa ,noitacifiralc dedeen taht saera tuo detniop ehs ,niaga dna emiT .stpircsunam ruo gniti -de ni stroffe sselerit dna msaisuhtne reh hguorht emoc -tuo siht ot noitubirtnoc laitnatsbus a edam ,koob siht fo noisrev namreG lanigiro eht rof srehsilbuP lacideM emeihT ta rotide tcejorp ruo ,rethciR .sM .snoitubirtnoc laudividni srohtua eht fo mus eht naht retaerg si taht txet a ni detluser sah ti no noitaroballoc ruo dna ,koob siht no rehtegot gnikrow deyojne hcum yrev evah eW maet koobtxet ehT 1 elbaT stnemgdelwonkcA ecaferP
  • 9. 1 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 10. I 1 2 3 Nose, Paranasal Sinuses, and Face Diagnostic Evaluation of the Nose and Paranasal Sinuses Diseases of the Nose, Paranasal Sinuses, and Face Anatomy, Physiology, and Immunology of the Nose, Paranasal Sinuses, and Face 1.1 Basic Anatomy of the Nose, Paranasal Sinuses, and Face 2 Facial Skin and Soft Tissues 2 The Facial Skeleton 2 External Nose 2 Nasal Cavities 3 Paranasal Sinuses 4 Vascular Supply 6 Nerve Supply 6 Functional Anatomy of the Ostiomeatal Unit 7 1.2 Morphology of the Nasal Mucosa 8 Respiratory Mucosa 8 Olfactory Mucosa 8 1.3 Basic Physiology and Immunology of the Nose 10 Physical Principles of Nasal Airflow 10 Conditioning of the Inspired Air 10 Protective Functions of the Nasal Mucosa Speech Production 12 Olfaction 12 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 11
  • 11. 2 I Nose, Paranasal Sinuses, and Face 1.1 Basic Anatomy of the Nose, Paranasal Sinuses, and Face The shape and appearance of the external nose affect not only the overall appearance of the face, but also the functional processes that take place inside the nose. The structural anatomy of the nose is important for both aesthetic and functional reasons, since the nose, as the gateway to the respiratory tract, performs a variety of physiologic functions. Facial Skin and Soft Tissues Fig.1.1 For the effective surgical treatment of soft-tissue defects in the face, whether of a traumatic or neoplastic nature, it is important to consider some distinctive features of the morphology and topographical anatomy of the face, since this is a highly conspicuous region in which the faulty or inadequate treatment of tissue changes will have obvious consequences. One tension lines of the skin such feature involves the (Fig. 1.1a ), known also as the relaxed skin tension lines (RSTLs). Scars can be made less conspicuous by taking these tension lines into account when suturing facial skin injuries. The aesthetic units of the face are an important consideration in the treatment ofl arger soft-tissue defects (Fig. 1.1b ). Failure to take these units into account will produce a poor cosmetic result. The Facial Skeleton Skin tension lines and aesthetic units The incisions in facial operations should be placed along skin tension lines ( a) whenever possible. The aesthetic units ( b) should be considered in the closure of soft-tissue defects in order to achieve a satisfactory cosmetic result. Fig.1.2 The cranial bones Knowing the various components of the bony facial skeleton (Fig. 1.2 ) and their relationship to one another is important in trauma management and also in the diagnosis and treatment ofi nflammatory diseases of the facial skeleton and their complications. The upper jaw bone, or maxilla , houses the maxillary sinus and articulates laterally with the zygomatic bone 1.2 ). The (zygoma) via the zygomatic process (Fig. upper part of the maxilla borders the nasal bone , and its frontal process projects upward to the frontal bone . The zygoma also has a frontal process that connects superiorly with the frontal bone lateral to the orbit. The zygoma communicates posteriorly with the zygomatic arch . External Nose The shape of the external nose is defined by the nasal bones, a pair of rectangular bones in the upper nasal dorsum, and by the paired lateral cartilages (upper nasal cartilages) and alar cartilages (major alar cartilages) in the central and lower portions of the nose (Fig. 1.3 ). The lateral portions of the nasal alae also contain several small accessory cartilages, called the The diagram shows the cranial bones that are relevant to rhinologic disorders. minor alar cartilages , which are embedded in the lateral soft tissues of the nose. The shape and stability of the alar cartilages, each of which consists of a medial and lateral crus , chiefly de- Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 12. 1 Anatomy, Physiology, and Immunology of the Nose, Paranasal Sinuses, and Face Fig.1.3 Fig.1.4 Structure of the external nose Anatomy of the nasal base Cartilaginous nasal septum Lateral crus of alar cartilage a The anatomically important cartilaginous structures are projected onto the nasal base. b The nasal septum is subluxed toward the left side, partially obstructing the nasal airway. termine the appearance of the nasal tip and the shape of the nares. As a result, they are also important in maintaining an effective nasal airway. Besides the medial crura, the inferior septal margin and the connective-tissue septum (columella) are also responsible 1.4 a ). Subfor stabilizing the base of the nose (Fig. luxation of the inferior septal margin can also hamper nasal breathing by partially obstructing the nasal airway (Fig. 1.4 b ). has a major bearing on the aerodynamics of nasal airflow (see also 1.3, Basic Physiology and Immunology of the Nose, pp.10–13). The anterior bony opening of the nasal cavity, called the piriform aperture , is bounded laterally and inferiorly by the maxilla and superiorly by the nasal bone (Fig. 1.2 ). The interior of the nose behind the nasal valve is divided by the nasal nasal septum is septum into two main cavities. The composed of an anterior cartilaginous part and two posterior bony parts. Abnormalities in the shape of the nasal septum (see also 3.2, Nasal Deformities, p. 30), which may consist of a deviated septum, tension septum, spurs or ridges, are a frequent cause of nasal airway obstruction. The choanae are the paired posterior openings through which the nasal cavities communicate with the nasopharynx. Nasal Cavities The nasal cavities begin anteriorly at the nasal vestibule, which is bordered posteriorly by the internal nasal valve (limen nasi) located between the posterior border of the alar cartilage and the anterior border of the lateral cartilage. This valve area is the narrowest portion of the upper respiratory tract and, as such, Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 3
  • 13. 4 I Nose, Paranasal Sinuses, and Face Fig.1.5 Structure of the lateral nasal wall Orifice of anterior ethmoid cells Superior meatus Ostium of maxillary sinus Frontal sinus Olfactory epithelium The relationship of the middle meatus to the sinus ostia is of special importance. See also 1.3 (p. 7). Ostium of sphenoid sinus Sphenoid sinus Ostium of frontal sinus Orifice of posterior ethmoid cells Nasolacrimal duct Orifice of eustachian tube Upper lip Inferior meatus Middle meatus The nasal cavity is bounded laterally by the lateral nasal walls, which are formed by the ethmoid bone and maxilla, and posteriorly by the palatine bone and the pterygoid process of the sphenoid bone. Several functionally important structures are located on the lateral nasal wall: the nasal turbinates and their associated passages (meati), sinus ostia, and the orifice of the nasolacrimal duct (Fig. 1.5). The inferior turbinate consists of a separate bone that is attached to the medial wall of the maxillary sinus. The opening of the nasolacrimal duct is located in the corresponding inferior meatus ( 1.1). The middle and superior turbinates are part of the ethmoid bone. In rare cases, a rudimentary “supreme turbinate” is also present above the superior turbinate. The middle turbinate has by far the greatest functional importance, because most of the drainage tracts from the surrounding paranasal sinuses open into the middle meatus (see also 1.3, Anatomy of the Ostiomeatal Unit, p. 7). The nasal cavity is bounded superiorly by the cribriform plate of the ethmoid bone. This thin bony plate has numerous openings for the passage of the fila olfactoria and also forms the boundary of the anterior cranial fossa. The floor of the nasal cavity is formed 1.1 Nasolacrimal duct The nasolacrimal duct is part of the lacrimal apparatus, which also includes the lacrimal gland, the lacrimal ducts, and the lacrimal sac. It runs in a bony canal between the medial canthus of the eye and the inferior nasal meatus. Attachment of inferior turbinate Attachment of middle turbinate Superior turbinate mostly by the hard palate, which is formed in turn by the two palatine processes of the maxilla and the horizontal laminae of the palatine bone. Paranasal Sinuses The paranasal sinuses are air-filled cavities that communicate with the nasal cavities (Fig. 1.6). All but the sphenoid sinus are already present as outpouchings of the mucosa during embryonic life, but except for the ethmoid air cells, they do not develop into bony cavities until after birth. The frontal sinus and sphenoid sinus reach their definitive size in the first decade of life. The maxillary sinus is present at birth but remains very small until the second dentition, because the presence of tooth germs in the maxilla limit the extent of the sinuses. The maxillary sinus, frontal sinus, and anterior ethmoid cells drain into the nasal cavity through the middle meatus—i.e., below the middle turbinate (Fig. 1.5). The posterior ethmoid cells drain into the nasal cavity through the superior meatus. The ostium of the sphenoid sinus is located in the anterior wall directly above the choanae. The anatomical connections between the nasal cavity and paranasal sinuses are functionally important and play a key role in the pathogenesis of many rhinologic diseases that involve the paranasal sinuses (see also 1.3, Anatomy of the Ostiomeatal Unit, p. 7). The maxillary sinus borders the nasal cavity laterally, and the orbital floor separates the upper part of the sinus from the orbit. Behind the maxillary sinus is the pterygopalatine fossa, which is traversed by the maxil- Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 14. 1 Anatomy, Physiology, and Immunology of the Nose, Paranasal Sinuses, and Face 1.2 Ethmoid roof and cribriform plate Ethmoid roof The roof of the ethmoid labyrinth is formed mainly by the portion of the frontal bone that covers and closes the ethmoid cells superiorly. The ethmoid roof is continuous medially with the cribriform plate, the lateral lamina of which represents the continuation of the attachment of the middle turbinate and is very easily injured during surgical manipulations in this region (a ethmoid roof and anterior ethmoid at the level of the crista galli). The levels of the ethmoid roof and cribriform plate can vary considerably, even in the same patient, depending on the vertical extent of the lateral lamina. Computed tomography scans should be taken preoperatively to define the individual anatomy of the anterior skull base region (b–e coronal scans of the anterior skull base in a patient with conspicuous nasoethmoidal opacity caused by nasal polyps). Crista galli Orbita Lamina papyracea Lateral lamina of cribriform plate Septum Middle turbinate Cribriform plate b Crista galli c Ethmoid roof Lateral lamina Cribriform plate Lamina papyracea d e Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. a 5
  • 15. 6 I Nose, Paranasal Sinuses, and Face Fig.1.6 Paranasal sinuses Frontal sinus Sphenoid sinus Ethmoid cells Maxillary sinus Frontal sinus Ethmoid cells this region must have a detailed knowledge of the relations of these structures to the ethmoid labyrinth. The sphenoid sinus is located at the approximate center of the skull above the nasopharynx. Its posterior wall is formed by the clivus. It relates laterally to the cavernous sinus, the internal carotid artery, and cranial nerves II–VI, and it is very closely related to the optic canal. The optic nerve and internal carotid artery may run directly beneath the mucosa of the lateral wall of the sphenoid sinus, without a bony covering. The sphenoid sinus is bordered superiorly by the sella turcica and pituitary and by the anterior and middle cranial fossae. The frontal sinus is located in the frontal bone, its floor forming the medial portion of the orbital roof. The sinus, which is highly variable in its extent, is bounded behind by the anterior cranial fossa. Inflammations of the frontal sinus can give rise to serious complications because of its close proximity to the orbit and cranial cavity (orbital cellulitis, epidural or subdural abscess, meningitis). Maxillary sinus Vascular Supply Sphenoid sinus The external nose derives most of its blood supply from the facial artery, which arises from the external carotid artery, and from the ophthalmic artery, which springs from the internal carotid artery. The internal nose receives blood from the territories of the external and internal carotid arteries: the terminal branches of the sphenopalatine artery, which arises from the maxillary artery, and the anterior and posterior ethmoid arteries, which arise from the ophthalmic artery. A detailed knowledge of the vascular supply is particularly important in the management of intractable epistaxis (nosebleed), which requires vascular ligation or angiographic embolization as a last recourse (see also 3.3, Epistaxis, p. 35). The venous drainage of the facial region is handled by the facial vein, retromandibular vein, and internal jugular vein. The regional lymphatic drainage of the face and external nose is handled mainly by the submandibular lymph nodes, while the nasal cavity is additionally drained by the retropharyngeal and deep cervical lymph nodes. Diagram of the sinuses projected onto the cranial surface. lary artery along with branches of the trigeminal nerve and autonomic nervous system. The floor of the maxillary sinus is closely related to the roots of the second premolar and first molar teeth. This creates a potential route for the spread of dentogenic infections, and a tooth extraction may create a communication between the oral cavity and maxillary sinus (oroantral fistula). Superior and medial to the maxillary sinus are the ethmoid air cells—a labyrinthine system of small, pneumatized sinus cavities that are separated from one another by thin bony walls and extend posteriorly between the middle turbinate (medial border) and orbit to the sphenoid sinus. The orbital plate of the ethmoid bone, called also the lamina papyracea, forms the lateral bony wall that separates the ethmoid air cells from the orbit. Paranasal sinus inflammations can spread through this lamina to involve the orbit (orbital complications). The posterior ethmoid cells are closely related to the optic nerve. The ethmoid roof and cribriform plate ( 1.2) form the bony boundary that separates the ethmoid cells from the anterior cranial fossa. The surgeon who operates in Nerve Supply The facial skin receives its sensory innervation from terminal branches of the trigeminal nerve that enter the facial region through the supraorbital, infraorbital, and mental foramina (Fig. 1.2). Only the skin over the mandibular angle and the lower portions of the auricle are supplied by the great auricular nerve. The facial muscles are classified as mimetic or mastica- Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 16. 1 Anatomy, Physiology, and Immunology of the Nose, Paranasal Sinuses, and Face 1.3 Anatomy of the ostiomeatal unit The term “ostiomeatal unit” describes the area on the lateral nasal wall where the ostia of the paranasal sinuses (except for the sphenoid sinus) open into the nasal cavity in a duct-like fashion. Even minor changes (e.g., anatomical variants, mucosal swelling) can hamper ventilation in this region, leading to pathologic sequelae in the paranasal sinuses (see below). The functionally significant anatomic structures of the ostiomeatal unit are the uncinate process, the semilunar hiatus, the frontal recess, the ethmoid bulla, the ethmoid infundibulum, and the maxillary sinus ostium (a coronal section is shown at right). The frontal sinus is connected to the ostiomeatal unit via the frontal recess, which has an hourglass-like shape. The uncinate process is a thin fibrous or bony process on the lateral nasal wall that arises slightly behind the anterior border of the middle turbinate and may narrow the passage from the nasal cavity to the ostiomeatal complex, depending on its degree of development. Located between the posterior border of the uncinate process and the first ethmoid cell (the ethmoid bulla) is another slitlike passage within the ostiomeatal complex, known as the semilunar hiatus. The space between the uncinate process, ethmoid bulla, and lamina papyracea of the ethmoid bone is called the ethmoid infundibulum. The ostiomeatal unit is bounded medially (toward the nasal cavity) by the middle turbinate and laterally by the lamina papyracea. The main clinical significance of this region relates to the sites of narrowing in the ostiomeatal unit. For example, hyperemia tory, each of these groups receiving different motor innervation. While the mimetic muscles of the face develop from the blastema of the second branchial arch (the hyoid arch) and accordingly are supplied by the facial nerve, the masticatory muscles trace their embryonic development to the first branchial arch (the mandibular arch) and are therefore supplied by mandibular nerve branches arising from the trigeminal nerve. and swelling of the mucosa in the setting of a common cold can obstruct the narrow passages in the ostiomeatal unit, preventing adequate ventilation of the dependent paranasal sinus system and setting the stage for a rhinogenic inflammation of the paranasal sinuses (sinusitis). Frontal recess Lamina papyracea Middle turbinate Ethmoid bulla Seminular hiatus Infundibulum Ostium of maxillary sinus Uncinate process Ostiomeatal unit Functional Anatomy of the Ostiomeatal Unit The nose and paranasal sinuses are regarded as a functional unit. Many rhinologic disorders are transmitted from the nasal cavity into the paranasal sinus system. The ostiomeatal unit is the collective term for various anatomical structures located about the middle meatus. It represents the region on the lateral nasal wall that receives drainage from the anterior ethmoid cells, frontal sinus, and maxillary sinus ( 1.3). It is important to know the anatomical details of this region in order to understand the pathophysiology of acute and especially chronic paranasal sinus inflammations and the surgical procedures that are used in the causal treatment of these conditions. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 7
  • 17. 8 I Nose, Paranasal Sinuses, and Face 1.2 Morphology of the Nasal Mucosa Besides the anatomical structure of the external nose and nasal cavity, the nasal mucosa plays an essential role in numerous functions of the nose owing to its “gateway” location in the respiratory tract (see also 1.3, Basic Physiology and Immunology of the Nose, pp.10–13). This deals with the morphologic structure of the nasal mucosa. Understanding this structure is necessary for an understanding of functional processes. The anterior part of the nasal cavity (the nasal vestibule), like the external nose, is covered by skin composed of a multilayer, keratinizing squamous epithelium. Anterior to the head of the inferior turbinate, this keratinized epithelium gives way to a nonkeratinized squamous epithelium, a nonciliated columnar epithelium, and finally a ciliated respiratory epithelium. Along with the submucous tissue, this ciliated epithelium forms the typical mucosal lining of the nasal cavity and paranasal sinuses (Fig. 1.7). A small area on the upper nasal septum, superior turbinate, and part of the middle turbinate, located adjacent to the cribriform plate, is covered by olfactory mucosa and is called the olfactory region. and MHC-II–bearing dendritic cells, which function as antigen-presenting cells. Respiratory Mucosa Epithelium The epithelium of the respiratory mucosa is composed of ciliary cells, goblet cells, and basal cells and provides an initial, mechanical barrier against infection. The ciliary cells dominate the surface of the respiratory epithelium. Each ciliary cell has approximately 150–200 cilia, which are composed of microtubules and are interlinked by “dynein arms.” This cytoskeleton of the ciliary cells and the activity of dynein, a specialized protein, enable the typical, synchronous beating of the cilia in the respiratory epithelium. This ciliary action propels a blanket of mucous secretions (from the goblet cells) and serous secretions (from the nasal glands) toward the nasopharynx, mechanically cleansing the inspired air in a mechanism called mucociliary transport (see also 1.3, Basic Physiology and Immunology of the Nose, pp.10–13). The basal cells represent the morphologic connection between the columnar epithelium and goblet cells on the one hand and the epithelial basement membrane on the other. They are distinguished from the other epithelial cell types by an increased expression of certain adhesion molecules (e.g., intracellular adhesion molecule-1, ICAM-1) and increased cytokine synthesis (e.g., interleukin 1). Besides the four cell types mentioned, the epithelium also contains immunocompetent cells, mostly CD8-positive T cells, along with smaller numbers of mast cells, macrophages, Lamina Propria The lamina propria of the nasal mucosa is separated from the epithelium by a basement membrane. Some areas of the lamina propria, especially about the inferior turbinate, show a marked preponderance of vascular structures known as venous erectile tissue or sinusoids. They consist of thin-walled and thick-walled venous capacitance vessels, which are important not only in warming the inspired air and producing secretions but also in controlling the tumescence of the nasal mucosa. Besides the venous capacitance vessels there are capillaries and, in deeper areas, arterial vessels. The lamina propria also contains numerous nasal glands, which mainly produce a serous secretion. The immunocompetent cells in the lamina propria consist of CD4-positive T lymphocytes along with CD8-positive cytotoxic cells and suppressor cells such as CD4-/ CD8-negative T lymphocytes, mature B lymphocytes, Ig-plasma cells, mast cells, and macrophages. These cellular elements demonstrate the importance of the nasal mucosa, which acts in concert with local host reactions to mediate inflammatory and allergic responses in the nose (see also 1.3, Basic Physiology and Immunology of the Nose, pp.10–13). Nerve Supply Finally, the nasal mucosa is endowed with a rich nerve supply. It receives its sensory innervation from the trigeminal nerve and its autonomic innervation from the pterygopalatine ganglion. The parasympathetic fibers of this ganglion induce vasodilation and stimulate the secretory activity of the nasal glands, while the sympathetic fibers produce vasoconstriction and inhibit glandular secretions. Olfactory Mucosa Topography: The olfactory mucosa (see 1.4 for details on structure and function) covers the olfactory region, which occupies the anterior superior part of the nasal septum and adjacent areas of the lateral nasal wall, Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 18. 1.2 Morphology of the Nasal Mucosa including the side of the superior turbinate facing the septum and part of the middle turbinate. The junction of the olfactory mucosa with the respiratory mucosa is variable in its location. Stimulus processing system: Although it covers an area of only a few square centimeters, the olfactory mucosa contains between 10 and 20 million bipolar sensory cells. The olfactory sensory cells have dendritic epithelial processes as well as basal axons that pass through the basement membrane between the supporting cells and basal cells and then join into bundles that are ensheathed by Schwann cells. These axon bundles, called the fila olfactoria, pass through foramina in the cribriform plate of the ethmoid bone and enter the cranial cavity. There they unite to form the olfactory nerve and pass to the olfactory bulb in the brain, the primary olfactory center. The latter is connected via the olfactory tract to the secondary olfactory center (olfactory cortex) in the temporobasal cortex, which is responsible for the perception of smells and their association with other sensory impressions. The secondary olfactory center also has projections to the limbic system that connect with the autonomic centers in the thalamus and hypothalamus; this creates a pathway that mediates the emotional and affective phenomena that are associated Fig.1.7 1.4 Olfactory mucosa Microscopic anatomy: Besides receptor cells, the epithelium of the olfactory mucosa is composed of microvilli, supporting cells, and basal cells. The lamina propria additionally contains serous glands (olfactory glands) and vessels. The function of the microvilli and of the olfactory glands located in the lamina propria of the olfactory mucosa is not yet fully understood. The microvilli most likely represent extra chemoreceptors in the olfactory epithelium, which perform their function along with the classic receptor cells. As for the olfactory glands, it is assumed that the secretions from these glands, released at the surface of the epithelium, also play a role in mediating the olfactory sense. Recent studies have shown that the secretion layer on the epithelium contains a specific protein that has a high affinity for most odorous substances, and thus could facilitate or even mediate their binding to the sensory cells. with smells. The olfactory cortex has connections with the tertiary olfactory centers (including the hippocampus, anterior insular region, and reticular formation), which are believed to have polysensory associative functions. Respiratory nasal mucosa a Epithelium b Glands Venous sinusoids a Structure of the lamina propria in histologic section. Cilia Microvilli b Scanning electron micrograph of cilia and microvilli. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 9
  • 19. 10 I Nose, Paranasal Sinuses, and Face 1.3 Basic Physiology and Immunology of the Nose To understand the pathologic processes that are important in inflammatory and allergic diseases of the nose, it is necessary first to understand the physiologic functions. As the threshold of the respiratory tract in humans, the nose is of major importance in conditioning the air before it reaches the lower airways. To understand this complex process, we must know something about the physics of nasal airflow, which also affects the warming and humidification of the inspired air. Due to its exposed position, the nasal mu- cosa is in constant primary contact with the environment and thus with a variety of potential pathogens. As a result, the nose is equipped with a variety of defense mechanisms (mechanical defenses, specific and nonspecific immune responses). As part of the supraglottic vocal tract, the nose also contributes to speech production (see 18.1, pp. 386–389). Finally, the nose contains the olfactory sensory cells, giving it an essential role in olfaction (see p.13). Physical Principles of Nasal Airflow Fig.1.8 During inspiration, the air stream enters the nasal vestibule in an oblique vertical direction. Aerodynamically, this air is in a state of laminar flow, meaning that there is no mixing of the different air layers. When the inspired air reaches the nasal valve located between the vestibule and nasal cavity, it passes through the narrowest site in the upper respiratory tract (limen nasi). Just past the nasal valve, the crosssection of the airway becomes greatly expanded, creating a “diffuser effect” that transforms most of the laminar flow of the inspired air into turbulent flow, in which different air layers are swirled together. Besides the velocity of the air, the degree of change in airflow characteristics at this stage is very strongly influenced by the specialized anatomy of the nasal cavity, which is subject to substantial individual differences. Septal deviation and cartilaginous or bony spurs on the septum can be as significant in this regard as turbinate hyperplasia or septal perforation. To a degree, the transition from laminar to turbulent flow within the nose is functionally desirable because it slows the flow velocity of the inspired air. This prolongs its contact with the nasal mucosa, contributing to olfaction and making it easier for the nose to clean, humidify, and warm the inspired air (see below). Nasal Cycle The “nasal cycle” is a physiologic phenomenon marked by an alternation between luminal narrowing and widening of the nasal cavities. This alternate congestion and decongestion of the nasal mucosa is effected mainly through reactions of the venous capacitance vessels of the inferior and middle turbinates, which are regulated by the autonomic nervous system (Fig. 1.8). The nasal cycle Middle turbinate Inferior turbinate This coronal computed tomography scan shows mucosal swelling in the right nasal cavity, predominantly on the inferior and middle turbinates, and mucosal decongestion in the right nasal cavity. Conditioning of the Inspired Air Inspired air is warmed and humidified in the nose before reaching the lower airways. Turbulent flow and other special physical conditions promote the necessary contact of the inspired air with the nasal mucosa. Moreover, the favorable relationship between the relatively small nasal cavity and the comparatively large mucosal surface area, which is further enlarged by the turbinates, also promotes the functionally important interaction between the inspired air and the mucosa. Humidification is accomplished by secretion and transudation from the nasal glands, the epithelial goblet cells, and the vessels of the lamina propria. Temperature regulation is controlled by the intranasal vascular system and especially the venous erectile tissue, which is particularly abundant in the inferior turbinates. The temperature in the anterior portions of the nasal cavity is lower than in the posterior regions. This temperature gradient produces a gradual warm- Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 20. 1.3 Basic Physiology and Immunology of the Nose ing of the inspired air, while on expiration, moisture and heat are returned to the nose through condensation. The warming capacity of the nasal mucosa is so efficient that even with ambient temperatures below zero, the temperature of the inspired air is raised by 25 C on entering the nasopharynx, with a relative humidity of over 90%. Disturbances in the conditioning function of the nose can result from age-related drying of the mucosa due to involution of the goblet cells and glands. They can also result from chronic inflammatory changes or extensive resections of the mucosa during intranasal surgery. Fig.1.9 Mucociliary transport Gel layer Cilia 8 Protective Functions of the Nasal Mucosa Here the protective functions of the nose are separated into two parts to facilitate learning, although in life the various defense mechanisms are interrelated and should not be thought of as separate entities. Nonspecific Defense Mechanisms Mechanical defenses: The most important mechanical defense mechanism of the nasal mucosa is the mucociliary apparatus, which physically cleanses the inspired air. The mucociliary transport system consists of the cilia of the respiratory epithelium and a mucous blanket composed of two layers: a deeper, less viscid “sol layer” in which ciliary motion occurs, and a superficial, more viscid “gel layer” (Fig. 1.9). The physiology of ciliary movements is described in 1.5. Disturbances of mucociliary transport can have various causes, such as increased viscosity and thickness of the periciliary sol layer, hampering ciliary movements, or changes in the viscoelasticity of the gel layer resulting in ineffectual mucus transport. Finally, various pathogenic mechanisms can produce changes in the cilia themselves, regardless of the viscosity of the mucous blanket. For example, an acute viral infection of the upper respiratory tract can lead to desquamation of the epithelium, with a loss of ciliated cells. Also, certain micro-organisms can directly affect ciliary motility by reducing the beat frequency of the cilia. Finally, ciliary dyskinesia syndromes are congenital disorders based on morphologic changes in the cilia such as absence of the dynein arms. This results in uncoordinated, dyskinetic ciliary movements that prevent effective mucus transport (see also Paranasal Sinus Inflammations). Nonspecific protective factors: The nasal mucosa also has a number of other, nonspecific defense mechanisms in the form of protective factors in the mucous blanket (Table 1.1). Sol layer Microvilli Cilia on the respiratory epithelium beat in a coordinated, metachronous pattern in the periciliary fluid (deeper sol layer), which transports the superficial gel layer toward the nasopharynx (arrow). 1.5 Physiology of ciliary motion Ciliary motion consists of three phases and is initiated by adenosine triphosphate (ATP)-splitting proteins, which cause a movement of the filaments within the cilia (sliding filament theory). The superficial gel layer is propelled toward the nasopharynx by a coordinated but metachronous beating of the cilia. The dynamics of ciliary motion has been likened to a “field of grain swaying in the wind.” The cilia beat at a high frequency (10–20 times per second), but their motion is influenced by external factors such as temperature and humidity. Cellular defenses: The mucosa has nonspecific defense mechanisms at the cellular level as well. The predominant phagocytic cells are neutrophilic granulocytes, monocytes, and macrophages. They are accompanied by “natural killer cells” (NK cells), which comprise a small percentage of the peripheral lymphocytes and protect mainly against viral infections of the nasal mucosa. Specific Immune Responses Besides the nonspecific defense mechanisms of the nasal mucosa noted above, the nose possesses a specific immune system that can be viewed as a separate immunologic unit. It is made up of the nasal mucosa itself and the lymphoepithelial tissue of Waldeyer’s ring (see below). Recent discoveries indicate that the structures of Waldeyer’s ring, especially the pharyngeal and palatine tonsils, function as inductive components that are active in the absorption, processing, and presentation of antigens, whereas the nasal mucosa itself is purely an effector organ in which, for example, foreign material is phagocytized by immunocompetent cells. The local, specific immune system of the nasal mucosa is based on the actions of antibodies, which are responsible for the humoral immune response, and of Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 11
  • 21. 12 I Nose, Paranasal Sinuses, and Face Table 1.1 Nonspecific protective factors in nasal secretions Substance group Example Interferon Proteases Cathepsin, elastase, chymase, tryptase Protease inhibitors α1-Protease inhibitor, C1 inactivator Lysozyme Antioxidants Catalases, glutathione, ascorbic acid cule ICAM-1, expressed by the epithelial cells, helps to prevent viral infections by acting as a receptor for more than 90 % of rhinoviruses. Finally, the endothelial cells of the blood vessels play an important role in the specific immune responses of the nasal mucosa. The vascular endothelial cells are activated by various inflammatory mediators— e.g., interleukin 1, tumor necrosis factor-α (TNF-α), and they regulate the transendothelial diapedesis of immunocompetent cells into the surrounding tissue through the expression of various adhesion molecules (Figs. 1.10, 1.11). Speech Production immunocompetent cells, which are responsible for the cellular immune response. Humoral immune response: Antibodies are formed in the paraglandular plasma cells. Most notably, IgA is an immunoglobulin that is characteristic of the respiratory mucosa and therefore of the nasal mucosa. The plasma cells also synthesize IgM and the less common IgG. When released, the immunoglobulins (especially IgA) are absorbed by the glandular cells of the lamina propria, provided with a secretory component, and re-released as secretory antibodies (sIgA). Cellular immune response: Representatives of the cellular immune response of the nasal mucosa include mast cells, macrophages, various polymorphonuclear leukocytes (neutrophils, basophils, eosinophilic granulocytes), lymphocytes, and the cells of the reticuloendothelial system, which occur chiefly as dendritic (Langerhans) cells in the nasal mucosa. T lymphocytes are of special importance in the control and memory functions of the immune response, while B lymphocytes can differentiate into plasma cells and thus have a key role in the humoral immune response of the mucosa in connection with local antibody production. Eosinophilic granulocytes are found mainly in association with chronic sinusitis and nasal polyps. Their granules contain cytotoxic substances that can damage tissues by the lysis of cell membranes. Basophilic granulocytes are involved in immediate allergic reactions, although the mast cells are by far the most dominant cell type in this phase. The mast cells are also chiefly responsible for histamine release in the early phase of an allergic reaction. Basophilic granulocytes (the only representatives of polymorphonuclear leukocytes) and mast cells also have a specific receptor (FcεR) for binding IgE. On contact with the corresponding allergenic substance, this can incite a devastating allergic reaction that may culminate in anaphylactic shock. The epithelial cells of the nasal mucosa also have an immune function. In particular, the adhesion mole- Various organ systems are involved in the production of voice and speech. The anatomically separate functions of the respiratory tract, glottis, supraglottic vocal tract, and central nervous system must be coordinated in order to produce a normal voice sound. The “supraglottic vocal tract” refers to the air-containing regions located above the level of the vocal cords. The rigid portions of this tract, whose condition is subject to only minor variations under physiologic conditions (e.g., due to mucosal swelling), include the nose, paranasal sinuses, and portions of the nasopharynx. Their role in articulation is most apparent under pathologic conditions. “Hyponasal speech” (rhinophonia clausa) occurs when these segments of the vocal tract contribute less to sound production as a result of partial or complete nasal obstruction or mass lesions in the nasopharynx. Conversely, “hypernasal speech” (rhinophonia aperta) develops when the nasopharynx and nasal cavities overcontribute to sound production. This occurs when velopharyngeal closure is absent or incomplete (cleft palate, velar palsy due to various causes). Olfaction The human olfactory system consists of the intranasal olfactory mucosa with its specialized olfactory epithelium and associated central pathways. The sensory cells consist of bipolar receptor cells whose proximal processes join to form the fila olfactoria, which are relayed through additional neurons and are distributed to the primary, secondary, and tertiary olfactory centers (see olfactory anatomy, p. 9). From a purely functional standpoint, an olfactory impression can be received only during inspiration, and only water-soluble and lipid-soluble substances are perceived. Even subtle changes in the chemical properties of a molecule can produce a clearly perceptible difference in the quality and quantity of the olfactory impression. The precise sequence of events that are involved in olfaction is still uncertain. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 22. 1.3 Basic Physiology and Immunology of the Nose Fig.1.10 Transendothelial migration of immunocompetent cells Fig.1.11 Chronic inflammation of the nasal mucosa a Neutrophilic granulocyte Endothelium P selectin ligand PECAM-1 2 3 E selectin ligand 1 b Eosinophilic granulocyte Vessel lumen P selectin E selectin ICAM-1 LFA-1 L selectin The interaction between immunocompetent cells and endothelial cells in an inflammatory reaction is mediated by various adhesion molecules and proceeds in the following steps: 1. Inflammatory mediators trigger the release of endothelial selectins. The interaction with their ligands initiates the migration of cells along the endothelium. 2. Activated integrins on the cells allow firm binding to the endothelial ligand, usually a member of the immunoglobulin supergene family. 3. The interaction between ICAM-1 and LFA-1 appears to play an important role in the extravasation process. The cells migrate between endothelial junctions, where expressed PECAM-1 is decreased during activation. ICAM = Intercellular adhesion molecule LFA = Lymphocyte function-associated antigen PECAM = Platelet/endothelial cell adhesion molecule Sections from the lamina propria of the nasal mucosa. Increased numbers of lymphocyte function-associated antigen-1 (LFA-1)-labeled leukocytes (brown stain) resulting from transendothelial diapedesis are found in the setting of a chronic inflammatory reaction (a) compared with a control specimen (b) (immunohistochemistry, ABC method with hemalum counterstain). It is important clinically to differentiate between olfactory disturbances and taste disorders, because the senses of smell and taste are closely interrelated. Patients often believe that they have a dysfunction of both senses, even though an olfactory disturbance is the sole cause of the complaints in more than twothirds of cases (see Table 2.2, p. 21). Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 13
  • 23. 2 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 24. I Nose, Paranasal Sinuses, and Face 1 Anatomy, Physiology, and Immunology of the Nose, Paranasal Sinuses, and Face 2 3 Diseases of the Nose, Paranasal Sinuses, and Face Diagnostic Evaluation of the Nose and Paranasal Sinuses 2.1 History and Clinical Examination of the Nose 16 History 16 Clinical Examination 16 2.2 Special Rhinologic Tests 19 Testing Nasal Patency 19 Allergy Testing 19 Olfactometry 21 2.3 Imaging of the Nose and Paranasal Sinuses 22 Conventional Radiographs 22 Computed Tomography (CT) 22 Magnetic Resonance Imaging 23 Ultrasound 25 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 25. 16 I Nose, Paranasal Sinuses, and Face 2.1 History and Clinical Examination of the Nose Aside from special rhinologic tests, which are reviewed in 2.2 (see p.19), the specific rhinologic history and clinical examination of the nose play a key role in further diagnostic and therapeutic decisionmaking. History Clinical Examination Before the examiner asks about specific rhinologic symptoms, patients should be given an opportunity to describe their complaints “in their own words,” as in any history. The history should begin with questions about general, relatively nonspecific symptoms such as obstructed nasal breathing and nasal discharge. It is important to determine, for example, whether the nasal obstruction (“stuffy nose”) has been present for some time or is of recent onset, possibly in connection with trauma to the nose. Additional questions should elicit whether the complaints are unilateral, bilateral, or alternate between the sides and whether they are seasonal or present year-round. In patients with nasal discharge, the consistency of the secretions should be assessed: is the discharge watery, mucopurulent, or blood-tinged (which may suggest a tumor)? To exclude allergic rhinitis, the patient should be questioned about sneezing attacks, itchy eyes (conjunctival irritation), cough, and respiratory complaints (evidence for allergic involvement of the lower respiratory tract). If the history suggests that the disease may have an allergic cause, a specific allergy history should be taken. This includes the family and personal history (bronchial asthma, atopic dermatitis, food allergies) as well as details on the household and occupational environments, giving particular attention to pets, indoor plants, and potential allergen exposure at the workplace (e.g., in a bakery or hair salon). Headaches may signify an accompanying paranasal sinus inflammation. Dryness of the nasal mucosa is a common finding in colds but can also result from changes in air quality, previous nasal surgery, or the chronic use of vasoconstricting nose drops or sprays that contain corticosteroids. Olfactory dysfunction is another possible symptom of rhinologic diseases, and the patient should always be questioned about this. Inspection The clinical examination begins with a visual inspection. Findings such as mouth breathing may direct the examiner to suspect nasal airway obstruction. The shape of the external nose may suggest intranasal abnormalities (e.g., a cartilaginous nasal deviation with a tension septum). It is particularly important to evaluate the nasal base (see Fig. 1.4), for which the patient’s head should be tilted back. In this position, the examiner can also test the stability of the nasal alae. If the alar cartilages are too soft, they will be indrawn even during normal, unforced inspiration. Skin changes such as erythema or swelling can occur with orbital complications of paranasal sinus inflammations (erythema and swelling of the upper and lower lids), in erysipelas (“butterfly”-shaped erythema of the midfacial skin), or with nasal furuncles, which present with circumscribed redness and swelling in the nasal vestibule. Palpation Palpation is most useful for detecting bony discontinuities. In patients with suspected neuralgias, it is also done to check for tenderness over the supraorbital, infraorbital, or mental foramina. In patients with a recent trauma history, palpation of the external nose will disclose any mobility or crepitus suggesting a fracture of the nasal pyramid. The midfacial bones (especially the bony orbital rim) are also palpated to check for step-offs indicating a fracture line. Soft-tissue swelling can limit the accuracy of this examination, however. Anterior Rhinoscopy The rhinologic examination itself begins with anterior rhinoscopy to evaluate the nasal vestibule and the anterior portions of the nasal cavity (Fig. 2.1). Technique: The examiner holds the nasal speculum in the left hand and braces the index finger on the patient’s right nostril. The speculum is inserted into the nose with the blades closed. During the examination, the physician uses the right hand to position the pa- Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 26. 2 Diagnostic Evaluation of the Nose and Paranasal Sinuses Fig. 2.1 Anterior rhinoscopy Fig. 2.2 Nasal endoscopy Technique for inspecting the nasal cavity. Positions of the patient and examiner. tient’s head and gently opens the speculum to spread open the nostril to allow inspection of the nasal cavity. The speculum should not be opened too far, as this would cause discomfort. The head should be tilted slightly forward for evaluating the nasal floor, inferior turbinate, and the anterior portions of the septum. The head is tilted backward to obtain a limited view of the middle meatus and middle turbinate. Often this region cannot be adequately assessed by anterior rhinoscopy alone due to anatomical constraints. As a result, endoscopy is commonly used to examine this region as well as the posterior portions of the nasal cavity and the nasopharynx (see below). When anterior rhinoscopy has been completed, the speculum is carefully withdrawn with the blades slightly open to avoid avulsing hairs from the nasal vestibule. In many cases the nasal mucosa should be decongested with vasoconstrictors prior to the examination, as this makes it easier to examine the interior of the nose. At the same time, it is also important to assess the “original” condition of the nasal mucosa, and so the nose should be examined before and after decongestion of the mucosa. Posterior Rhinoscopy Nasal endoscopy has become the most important and rewarding clinical examination method in rhinologic diagnosis. Prerequisites: Nasal endoscopy requires practice because, unlike anterior rhinoscopy, it provides only close-up views of small intranasal areas. Besides rigid endoscopes, which are available in 4-mm and 2.8mm diameters and assorted viewing angles (e.g., 0 , 30 , 120 ), flexible endoscopes are also available for inspecting the nose and nasopharynx and exploring all of the pharynx and larynx in one sitting. Their main disadvantages compared with rigid scopes are their weaker light intensity and poorer image resolution. Also, it takes two hands to operate a flexible endoscope, while a rigid scope leaves one hand free for manipulating instruments. The patient is seated for the examination (Fig. 2.2). As in anterior rhinoscopy, the preparations include decongestion of the nasal mucosa. A topical anesthetic should also be applied. Diagnostic nasal endoscopy is performed with a 4-mm 30 telescope. The 2.8-mm scope is used only in a very narrow nasal cavity or in children. 8 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 8 8 Decongestants should always be properly diluted when used in children. Nasal Endoscopy 8 Indication: Anterior rhinoscopy is used not only for nasal examination but also for minor therapeutic procedures such as intranasal packing for epistaxis, foreign-body removal, and polypectomy. Children: Smaller instruments (pediatric specula) are available for anterior rhinoscopy in children. Aural specula can also be used to examine the nose in infants or small children. Posterior rhinoscopy was formerly done to evaluate the nasopharynx and posterior nasal cavity (choanae, posterior ends of the turbinates, posterior margin of the vomer). With the establishment of endoscopic examination techniques in rhinology, this procedure, which requires special patient cooperation, is now considered obsolete. 17
  • 27. 18 I Nose, Paranasal Sinuses, and Face Fig. 2.3 Nasal endoscopy Nasal endoscope shown in an anatomic specimen (sagittal section). The tip of the scope is in the nasopharynx. Fig. 2.4 Endoscopy of the nasopharynx Posterior pharyngeal wall Eustachian tube orifice Torus tubarius Transnasal endoscopic appearance of the nasopharynx. Fig. 2.5 Endoscopy of the middle meatus Technique: First the examiner advances the endoscope into the nasopharynx (Fig. 2.3) and inspects the eustachian tube orifice, torus tubarius, posterior pharyngeal wall, and roof of the nasopharynx (Fig. 2.4). While the transnasal nasopharyngeal inspection can provide very detailed views (e.g., for early detection of nasopharyngeal cancer), it should still be supplemented by transoral postrhinoscopic endoscopy (see 5.2, p.104). Nasal endoscopy is particularly useful for evaluating the ostiomeatal unit (see 1.3, p. 7), as this pathophysiologically important region generally cannot be adequately evaluated by anterior rhinoscopy alone. To inspect the middle meatus, the endoscope is first advanced toward the head of the middle turbinate. This should provide a good overview of the middle meatus (Fig. 2.5). To advance farther into the ostiomeatal unit, the scope must negotiate the narrow passage between the uncinate process and the middle turbinate (asterisk in Fig. 2.5). Normally, this can be done only with a narrow-gauge scope (2.8 mm). The 4-mm endoscope can be used at this site only in patients who have had previous intranasal sinus surgery with resection of the uncinate process. Direct endoscopic inspection of the paranasal sinuses is possible only to a limited degree. In some cases, the sphenoid sinus can be examined with a thin telescope passed through the natural ostium in the anterior sinus wall. If endoscopic exploration of the maxillary sinus is required (e.g., for a suspected tumor), it can be done either through the inferior meatus after perforating the lateral nasal wall or by a transfacial approach with incision of the maxillary sinus mucosa and perforation of its anterior wall. Uncinate process Middle turbinate * Normal appearance of the middle meatus, with the middle turbinate and uncinate process. The asterisk marks the narrow passage through which the endoscope can be advanced into the ostiomeatal unit. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 28. 2 Diagnostic Evaluation of the Nose and Paranasal Sinuses 2.2 Special Rhinologic Tests While the examination methods described thus far are practiced routinely, special rhinologic test proce- dures are carried out only if there is specific evidence that suggests a particular disorder. Testing Nasal Patency 2.1 Simple methods can be used for the preliminary assessment of nasal patency. One such method is to hold a reflective metal plate under the nose; the degree of fogging will give a crude impression of the patency of the tested nasal cavity. Nasal patency in infants can be tested subjectively by holding a wisp of cotton in front of each nostril. Today the most standardized procedure for the assessment of nasal patency is active anterior rhinomanometry (Fig. 2.6). This procedure measures and graphically records the difference in pressure (ΔP) from the naris (P2) to the nasopharynx (P1) and the respiratory air volume per unit time (V). One nostril is occluded for this test while the nasal air stream is measured on the opposite side. The accuracy of this test is most limited in patients with severe nasal airway obstruction, and the test cannot be performed when one nasal cavity is completely obstructed. Acoustic rhinometry is described in 2.1. The differential diagnosis of nasal airway obstruction is outlined in Table 2.1. Acoustic rhinometry is a measuring technique that is based on the principle of acoustic reflection and can be used to determine intranasal cross sections. Unlike rhinomanometry, it does not measure dynamic respiratory function but the cross sections of the nasal cavity at various sites, which are averaged together. The main advantages of this method over rhinomanometry are that it is faster and easier to perform and does not depend on patient cooperation. While these features are desirable in the examination of pediatric patients, it should always be considered that acoustic rhinometry measures static parameters and, unlike rhinomanometry, does not assess the patency of nasal airflow. Allergy Testing While the history and nasal endoscopic findings can provide initial, relatively nonspecific evidence of an allergic etiology for rhinitis, allergy testing is used to verify and differentiate this condition. Various in-vivo and in-vitro methods are available for allergy testing. Skin Tests When a small amount of allergen is placed in contact with the skin, it can evoke a local or systemic (!) allergic reaction in a previously sensitized individual. The most widely used method is the prick test, in which the skin is superficially pricked with standard test substances that contain the suspicious antigens. The local skin reaction is compared with the reaction to a simultaneously applied positive control (histamine solution) and negative control (saline solution). A positive skin prick test proves that sensitization has occurred but does not prove an allergic etiology for the rhinitis. Acoustic rhinometry Table 2.1 Differential diagnosis of nasal airway obstruction • Acute and chronic rhinitis (e.g., allergic, atrophic) • Sinusitis • Deviated septum (congenital, acquired) • Nasal pyramid fracture • Septal perforation • Nasal polyps • Cephalocele • Adenoids • Tumors of the nose, paranasal sinuses, and nasopharynx • Foreign bodies (especially in small children) • Drugs – Adverse effects: oral contraceptives, antihypertensive agents (e.g., reserpine, propranolol, hydralazine), antidepressants (e.g., amitriptyline) – Drug abuse: imidazoline derivatives (e.g., oxymetazoline hydrochloride, xylometazoline hydrochloride) Serologic Tests The total immunoglobulin E (IgE) assay—e.g., paper radioimmunosorbent test (PRIST)—can be used for the quantitative determination of nonspecific total IgE, and various tests are available for specific IgE determination—e.g., radioallergosorbent test (RAST), enzyme allergosorbent test (EAST), etc. Specific IgE testing is recommended because of the low sensitivity and specificity of the total IgE assay. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 19
  • 29. I Nose, Paranasal Sinuses, and Face Fig. 2.6 Active anterior rhinomanometry a Nasopharynx P1 Nasal septum Air stream Right nasal cavity b Expiration P1 Occlusion of nasal vestibule V [cm3/s] Left nasal cavity Inspiration P1 P2 Transnasal ΔP [Pa] P2 Face mask V c Expiration V [cm3/s] 20 Inspiration Right side of nose Transnasal ΔP [Pa] Faulty measurement with pressure leak through naris (ΔP too low) Left side of nose Normal nasal breathing Obstructed nasal breathing a In this example, the left nostril has been occluded. A pressure sensor measures the pressure P1 in the left nasal cavity (= pressure in the nasopharynx), and a second sensor measures P2 in a firmly attached face mask. The difference between the pressures, ΔP, is plotted against the respiratory volume flow V. b The curve (green) starts at the zero baseline. It passes through the right upper quadrant during inspiration, crosses back over the baseline at the end of inspiration, passes through the lower left quadrant during expiration, and returns to the origin at the end of the respiratory cycle. A flatter curve (shown in red) indicates a stenosis in the shaded area of the diagram. c When patency is tested in the left nasal cavity, it is customary to draw the curve in the left upper and right lower quadrants. In practice, the measurements from both nasal cavities are charted in one diagram (after Grevers G; see p. 430). Nasal provocation test: This test is of greatest value in allergic rhinitis, as it is the only method in which a specified allergen is placed in direct contact with the nasal mucosa. The technique involves the selective application of an allergen solution to the head of the inferior turbinate. Rhinomanometry (see above), performed before and 20 minutes after application of the allergen, confirms the local allergenic effect of the test substance by showing a significant reduction of nasal patency due to reactive mucosal swelling. Since provocative testing involves placing the allergen directly on the turbinate, it may incite a severe allergic response or even anaphylactic shock, and proper emergency equipment should be easily accessible in the examination room. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 30. 2 Diagnostic Evaluation of the Nose and Paranasal Sinuses Olfactometry Subjective Olfactory Testing Complaints of olfactory dysfunction become more frequent with ageing. They may be caused by a variety of underlying disorders (Table 2.2). In subjective olfactory testing, various substances are held separately in front of each nostril before and after decongestion of the nasal mucosa. Several types of test substance are used: pure odorants that stimulate only the olfactory nerve (coffee, cocoa, vanilla, cinnamon, lavender), odorants with a trigeminal component (menthol, acetic acid, formalin), and substances that also have a taste component (chloroform, pyridine). Patients with a complete loss of smell (anosmia) cannot perceive pure odorants but can at least sense or taste the other substances. Because it is difficult for laypeople to differentiate between smell and taste, many patients initially complain of a taste disturbance when they actually have an olfactory disturbance. Pure taste disorders are very rare. The relationship between taste and smell must be considered during the diagnostic work-up, and therefore both sensory modalities should be tested (see also 4.2, Taste Testing, p. 76). After a detailed history has been taken, the patient is examined by anterior rhinoscopy or endoscopy to rule out anatomical and functional obstructions of nasal airflow to the olfactory groove. Malingering should be suspected in patients who deny the perception of trigeminal stimulants. Testing can also be performed with ready-to-use test kits (e.g., Sniffin’ Sticks). It is likely that these standardized tests will increasingly supplant the classic subjective smell tests, owing to their better reproducibility. Table 2.2 Causes of olfactory disturbances Classification Example Transport of odorants Nasal obstruction Deviated septum, mucosal swelling, polyps, tumor Scar tissue occluding the olfactory groove After intranasal surgery Perception: damage to the olfactory epithelium caused by: Toxic substances Objective Olfactory Testing Objective olfactory testing is far more costly and is generally performed only at large centers. Pure odorants and trigeminal nerve stimulants are presented separately to the patient, and the responses are measured by the computer-controlled recording and analysis of olfactory evoked potentials. Objective olfactometry is used mainly in disability examinations. SO2, NO, ozone, heavy metals, varnishes Drugs Viral infections Influenza Radiotherapy (rare) Stimulus conduction and processing Avulsion of fila olfactoria Skull base fracture Aplasia of the olfactory bulb (rare) Kallmann syndrome Injury to olfactory centers Contusion or hemorrhage due to head injury Neurodegenerative diseases Alzheimer disease, Parkinson disease, diabetes mellitus (rare) Olfactory hallucinations After epileptic seizures, in schizophrenia Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 21
  • 31. 22 I Nose, Paranasal Sinuses, and Face 2.3 Imaging of the Nose and Paranasal Sinuses Imaging procedures are an important tool in the diagnostic work-up of rhinologic diseases. Besides conventional sinus radiographs, the most important imaging modalities at present are computed tomography and magnetic resonance imaging. Conventional Radiographs Computed Tomography (CT) Indications Indications Standard paranasal sinus radiographs in the occipitomental projection (Fig. 2.7 a, b; Water projection) and occipitofrontal projection (Fig. 2.7 c, d; Caldwell projection) are still routinely obtained, particularly in cases of acute inflammation. They are also obtained to evaluate midfacial fractures. Besides an occasional malformation, the main indications for CT scanning of the nose and paranasal sinuses are chronic sinusitis, trauma (especially frontobasal fractures), and tumors. CT sinus scans are compromised by metal-bearing dentures, which cause beam-hardening artifacts that can significantly degrade the image quality. Diagnostic Value The value of sinus radiographs is inherently compromised by the presence of superimposed structures. If previous surgery has been done on the paranasal sinuses, roentgen interpretation is further hampered by scar tissue, which can mimic sinus opacity. It is sometimes difficult to evaluate the sphenoid sinus in the occipitomental projection. If there is a high index of suspicion for sphenoid sinus involvement, a lateral sinus projection should be added to the study. The craniocaudal extent of the frontal and maxillary sinuses can also be evaluated with this technique. Fig. 2.7 Scan Planes Computed tomography can provide nonsuperimposed primary images of the paranasal sinuses in coronal (Fig. 2.8) and axial planes of section (Fig. 2.9). Sagittal images can be reconstructed secondarily from the axial or coronal scans, but they are of poorer quality. Coronal planes are used mainly for CT examination of the paranasal sinuses, and axial scans can be added for special investigations. Standard radiographic projections of the paranasal sinuses b a c Maxillary sinuses Central ray Frontal sinus d Ethmoid cells Central ray Sphenoid sinus a, b The occipitomental projection demonstrates the maxillary sinus and gives a limited view of the sphenoid sinus. c, d The occipitofrontal projection is better for evaluating the ethmoid cells and frontal sinus. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 32. 2 Diagnostic Evaluation of the Nose and Paranasal Sinuses Fig. 2.8 Computed tomography of the paranasal sinuses Orbit Maxillary sinus Cribriform plate Crista galli Frontal sinuses Lamina papyracea (of the orbit) a Ethmoid infundibulum b Orbit Frontal sinus Maxillary sinus Cribriform plate Crista galli Optic canal Ethmoid cells Middle turbinate Inferior turbinate c Sphenoid sinus d Four representative coronal CT scans are shown. Scan Acquisition Interpretation Scans can be acquired using the sequential, singleslice technique (conventional CT) or a continuous spiral technique (spiral or helical CT). The advantages of spiral CT are complete coverage with no interslice gaps (“volume scan”) and a shorter examination time (about 20 seconds), making the images less susceptible to respiratory and motion artifacts. Normally aerated paranasal sinuses exhibit air density on CT scans—i.e., they appear black. The normal mucosal lining of the sinuses is not visualized. The bony sinus walls appear hyperdense (white). Magnetic Resonance Imaging Indications Documentation CT images documented on radiographic film should occupy the whole frame, displaying only the structures that are relevant for making an interpretation. Magnetic resonance imaging (MRI) has fewer indications than CT in patients with paranasal sinus disease. This is primarily because MRI is markedly inferior to CT in defining the bony boundaries of the sinuses. The strength of MRI lies in its superior soft-tissue discrimination (Fig. 2.10). MRI is indicated in diseases Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 23
  • 33. 24 I Nose, Paranasal Sinuses, and Face Fig. 2.9 Computed tomography of the paranasal sinuses a Pterygopalatine fossa b Ethmoid cells Sphenoid sinus Sphenoid sinus Maxillary sinus Maxillary sinus c d Sphenoid sinus Ethmoid cells Orbit Frontal sinus Four axial CT scans are shown. that involve the paranasal sinuses in addition to the cranial cavity or orbit (e.g., tumors and congenital malformations such as encephaloceles). It can also supply information that is useful in differentiating soft-tissue lesions within the paranasal sinuses (mucocele, cyst, polyp), and it can distinguish between solid tumor tissue and inflammatory perifocal reaction. At present, MRI is contraindicated in most patients with electrically controlled devices such as a cardiac pacemaker, insulin pump, cytostatic pump, or cochlear implant. By contrast, modern internal fixation materials such as titanium are usually nonmagnetic and therefore MRI-compatible. Contraindications The standard imaging protocol employs a T1-weighted spin-echo sequence before and after intravenous contrast administration in addition to a proton- and T2weighted turbo spin-echo sequence. Before ordering an examination, the physician should consider the basic physical principle of MRI—i.e., the utilization of magnetic fields and radiofrequency energy. Method Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 34. 2 Diagnostic Evaluation of the Nose and Paranasal Sinuses Fig. 2.10 MRI of the paranasal sinuses Orbit Frontal sinus Maxillary sinus Sphenoid sinus Ethmoid cells Sphenoid sinus Ethmoid cells Frontal sinus Middle turbinate Inferior turbinate Maxillary sinus a Coronal, b axial, and c sagittal magnetic resonance images. Slice Thickness Indications The slice thickness should not exceed 3–4 mm, and the slice increment should be no greater than 0.6 mm. Imaging of the frontal skull base, orbit, parapharyngeal space, and pterygopalatine fossa requires the highest possible spatial resolution with a thin slice thickness (3 mm). The frontal and maxillary sinuses are most easily accessible to ultrasound imaging. The anterior ethmoid cells can be scanned via the medial canthus of the eye, but it should be added that these cells can be examined from this site only by using a small A-mode transducer or a more costly, specialized B-mode transducer; a large linear array (7.5 MHz) cannot be used. Scanning the middle and posterior ethmoid cells by the transocular route is extremely challenging and requires a highly experienced examiner. The sphenoid sinus is inaccessible to ultrasound imaging because of its location. Imaging Planes Primary scan acquisition in MRI can be done in three planes: axial, coronal, and sagittal (Fig. 2.10). Plain, unenhanced T1-weighted images are excellent for defining normal craniofacial anatomy. Ultrasound The paranasal sinuses can also be visualized with ultrasound (A and B mode). Advantages: Ultrasound is particularly useful in the follow-up of acute inflammatory processes, as it can eliminate the need for extra radiographic views. It is also used in children and pregnant women for the same reason. Disadvantages: Ultrasound yields much less detailed images than CT and MRI, and it cannot provide threedimensional rendering. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 25
  • 35. 3 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 36. I Nose, Paranasal Sinuses, and Face 1 Diagnostic Evaluation of the Nose and Paranasal Sinuses Diagnostic Evaluation of the Nose and Paranasal Sinuses 2 3 Diseases of the Nose, Paranasal Sinuses, and Face 3.1 Malformations of the Nose, Paranasal Sinuses, and Face 28 Choanal Atresia 28 Frontobasal Dysraphias 28 3.2 Nasal Deformities 30 Septal Deviation 30 Deformities of the External Nose 31 3.3 Inflammations of the External Nose, Nasal Cavity, and Facial Soft Tissues 48 Purulent Inflammations of the Hair Follicles 48 Erysipelas 49 Inflammations of the Nasal Cavity 49 3.8 Sinus Inflammations 54 Acute Sinusitis 54 Chronic Sinusitis 56 Nasal Polyposis 57 Mucoceles and Pyoceles 58 Rhinosinogenic Complications Nosebleed (Epistaxis) 32 3.4 3.7 Soft-Tissue Injuries and Plastic Surgery 36 Diagnosis 36 Treatment 36 58 3.9 3.6 Tumors of the External Nose and Face 62 Benign Tumors 62 Precancerous Lesions 62 Malignant Tumors 62 3.10 3.5 Tumors of the Nasal Cavity and Paranasal Sinuses 64 Benign Tumors 64 Malignant Tumors 64 Fractures of the Nasal Pyramid and Lateral Midface 40 Nasal Pyramid Fracture 40 Lateral Midfacial Fractures 41 Fractures of the Central Midface and Anterior Skull Base 44 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 37. 28 I Nose, Paranasal Sinuses, and Face 3.1 Malformations of the Nose, Paranasal Sinuses, and Face Malformations involving the nose may be caused by developmental abnormalities of the nasal floor, palate, nasal roof, and internasal region. A variety of dis- Choanal Atresia Epidemiology: Choanal atresia has an incidence of one in 5000 to one in 10,000 births and is more often unilateral than bilateral. The atresia is bony in 90% of cases and membranous in only 10%. 3.1 Embryology of choanal atresia The choanae are the posterior openings that connect the nasal cavities with the nasopharynx. They develop between the third and seventh embryonic weeks, following rupture of the vertical epithelial fold between the olfactory groove and the roof of the primary oral cavity (pronasal membrane). If this process is disturbed, rupture of the oronasal membrane will be absent or incomplete, resulting in the partial (stenosis) or complete closure (atresia) of one or both choanae. Symptoms: Bilateral choanal atresia is an acutely lifethreatening emergency because the neonate, except when crying, is an obligate nasal breather until about the sixth week of life. As a result, the infant experiences episodes of asphyxia at rest when its mouth is closed, especially during periods of sleep, and also during feeding. The resulting hypoxia is manifested by cyanosis, bradycardia, and an erratic respiratory rate with the mouth open or closed. Cyanosis that is present at rest and improves with exertion is called paradoxical cyanosis because of its opposite pattern relative to cyanosis with a cardiac cause. Unilateral choanal atresia may be manifested by a purulent nasal discharge on the affected side. Choanal atresia may be associated with various other anomalies, with fully developed cases presenting as the CHARGE syndrome (coloboma; heart disease; atresia of the choanae; retarded growth, development and/or central nervous system anomalies; genital hypoplasia; ear anomalies or deafness). orders can result, depending on the affected anatomic structures. The clinical suspicion of choanal atresia can be confirmed by examination with a rigid or flexible endoscope (Fig. 3.1). Treatment: The acute care of choanal atresia in asphyxia consists of intubation followed by perforation of the atresia plate. Recurrent stenosis is prevented by inserting a stent and securing it with a suture (to prevent aspiration). The definitive surgical repair of bilateral choanal atresia is performed during the first weeks or months of life. Surgery for unilateral atresia can be postponed until school age, when the anatomy of the region is more similar to that encountered in adults. Frontobasal Dysraphias The incidence of dysraphias involving the anterior skull base is approximately one in 20,000 to one in 40,000 births. The familial pattern of occurrence suggests a genetic component to the disease. For further details on the embryology, see 3.2. Manifestations: Congenital dysraphias of the anterior skull base can have various manifestations that include dorsal nasal fistulas ( 3.3), dermoids ( 3.4), frontonasal extracerebral gliomas, and cephaloceles ( 3.5). Fig. 3.1 Choanal atresia Torus tubarius Diagnosis: Both choanae in newborns should be routinely catheterized in the immediate postnatal period (e.g., with the suction catheter) to exclude choanal atresia. Postrhinoendoscopic view shows partial closure (stenosis) of the left choana accompanied by complete closure (atresia) of the right choana (contrast with normal-appearing choanae in Fig. 2.4, p.18). Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 38. 3 Diseases of the Nose, Paranasal Sinuses, and Face 3.2 Embryology of frontobasal dysraphias 3.4 The skull base may be affected by congenital closure defects, analogous to a dermal sinus or spina bifida involving the lumbar portion of the spine. Dysraphic anomalies of the anterior skull base are caused by exposure to teratogenic agents during the second or third week of embryonic development, when the neural tube is forming from the neural plate, or during the fourth week, when the cerebral ventricles and central canal are forming and the central nervous system is separating from the epidermis and migrating to a deeper level. 3.3 Nasal dermoids, like dorsal nasal fistulas, are lined by keratinized squamous epithelium. Sites of predilection are the dorsal nasal midline and nasal flank, where the lesions present as cystic protrusions. A nasal dermoid may coexist with a dorsal nasal fistula in rare cases. Abscesses may develop as an inflammatory complication. Diagnosis and treatment are the same as described in 3.3. Dorsal nasal fistula Morphology: A dorsal nasal fistula consists of a fistulous tract that is lined by keratinized squamous epithelium and forms a tiny opening on the dorsum or tip of the nose. The fistula may terminate blindly or even extend into the cranial cavity, creating an open communication with the subarachnoid space. Symptoms: Fistulas that terminate blindly are usually manifested clinically at an older age due to inflammation around the fistulous opening. If the fistula communicates with the subarachnoid space, it can lead to severe complications such as cerebrospinal fluid leakage, meningitis, or brain abscess. 3.5 Nasal dermoid Diagnosis: The diagnosis is established by computed tomography or magnetic resonance imaging. Diagnostic catheterization or contrast injection is contraindicated due to the risk of intracranial complications. Treatment: Treatment consists of complete removal of the fistulous tract, which may include excising the dural defect and repairing it by duraplasty. Incomplete removal of the fistula will predispose to recurrent infections. Cephalocele Cephaloceles are herniations of intracranial contents through a bony defect in the skull. Several types are distinguished according to the structures involved: meningocele (congenital protrusion of the leptomeninx), meningoencephalocele (leptomeninx and brain tissue), and meningoencephalocystocele (meningocele plus portions of the ventricular system). Etiology: Most cephaloceles are congenital, but rare cases are post-traumatic (e.g., after a frontobasal fracture). Classification: Cephaloceles of the anterior skull base are classified into two groups. Sincipital cephaloceles are located near the glabella, forehead or orbit, while basal cephaloceles are found mainly in the nasal cavity or nasopharynx. Presentation: Most cephaloceles are manifested clinically during childhood. The sincipital forms appear as a pulsating mass near the glabella, often associated with a broad nasal dorsum and hypertelorism. Fig. a illustrates these features in a girl with an extensive meningocele. The basal forms present a as an intranasal mass, typically with associated nasal airway obstruction. They closely resemble intranasal polyps and should be considered in the differential diagnosis of children with suspected nasal polyps, which are rare in this age group. Diagnosis: Computed tomography (CT) and magnetic resonance imaging (MRI) can supply information on the location and extent of the mass and the associated bony defect. In the case shown in Fig. a, coronal CT with a bone window setting (Fig. b) defines the extensive bone defect in the ethmoid roof (arrows), while CT with a soft-tissue window (Fig. c) more clearly distinguishes the cephalocele from adjacent structures. Treatment: Treatment is always surgical and consists of removing the cephalocele and repairing the dural defect. Any associated anomalies of the orbit and facial skeleton should also be corrected. < Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. Cephalocele b c 29
  • 39. 30 I Nose, Paranasal Sinuses, and Face 3.2 Nasal Deformities A basic distinction is drawn between deformities of the external nose and intranasal deformities. They are frequently combined, however, as deformities of the external nose are generally associated with a variable degree of nasal septal curvature and may even be caused by them (e.g., cartilaginous nasal deviation Septal Deviation Definition: A congenital or traumatically acquired bending or bowing of the nasal septum. Symptoms: Almost everyone has some degree of bowing, spurring, or ridging of the cartilaginous or bony nasal septum. Mild forms do not cause symptoms and have no pathologic significance (Fig. 3.2 a). More pronounced degrees of septal curvature can obstruct nasal breathing and may also cause olfactory impairment due to inadequate ventilation of the olfactory groove. Deficient nasal airflow can also lead to paranasal sinus sequelae such as headaches and recurrent sinusitis. A large septal spur that comes into contact with the nasal turbinates can cause epistaxis (Fig. 3.2 b). Diagnosis: Septal subluxation is a special form in which the anterior septal margin is displaced from the median plane (Fig. 1.4 b, p. 3). This condition is readily identified by external inspection of the nasal base. Further clinical examination consists of anterior rhinoscopy or endoscopy (Fig. 3.2 a, b), which can verify the morphologic changes in the nasal septum. The degree of nasal obstruction can be objectively evaluated by rhinomanometry (see p.19). For medicolegal reasons, olfactory testing should always be done prior to surgical treatment (see p. 21). Treatment: The treatment of choice is surgical straightening of the deviated septum (septoplasty). This procedure involves removing the deviated cartilaginous and bony portions of the septum along with any spurs and ridges and reimplanting them as needed until the septum occupies a tension-free position in the median plane. The indication for septoplasty is basically any septal deviation that is causing subjective complaints with functional impairment of nasal breathing. with a deviated septum, humped nose with a tension septum). For learning purposes, however, septal deviation is classified as an intranasal deformity and is described separately from the various external deformities. Fig. 3.2 Septal pathology a Middle Turbinate Septum Inferior turbinate b Bony spur Inferior turbinate a Endoscopic appearance of a nasal septum deviated toward the left side, partially obstructing the nasal airway. b Endoscopic appearance of a bony septal spur that touches the inferior turbinate, causing epistaxis (left nasal cavity). The indication for septoplasty should be weighed very carefully in children and adolescents under 15–17 years of age, and a very conservative approach should be taken in patient selection. Indiscriminate use of this procedure in younger patients can damage the growth zones of the septum, causing long-term problems. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 40. 3 Diseases of the Nose, Paranasal Sinuses, and Face Deformities of the External Nose Causes and forms: Deformities may be congenital or traumatically acquired. Virtually any bony and cartilaginous structures of the external nose may be affected. An accompanying septal deviation is present in many cases. The most common deformities are a crooked nose, humped nose, saddle nose, and broad nose, which may occur separately or in combinations (Fig. 3.3). Diagnosis: Besides inspection of the external nose, in which the affected cartilaginous and bony structures are identified, the diagnostic workup should include anterior rhinoscopy or endoscopy to evaluate the shape and position of the nasal septum. Fig. 3.3 Deformities of the external nose Crooked nose Humped nose Photographic documentation should always be obtained preoperatively for medicolegal reasons. Treatment: Since deformities of the external nose are frequently associated with intranasal changes, most cases have both a functional and an aesthetic indication for corrective surgery. The treatment of choice is “functional septorhinoplasty,” with correction of the nasal septum and external nose. In most cases the bony nasal skeleton has to be osteotomized at multiple sites in order to achieve the desired nasal shape and position. The humped nose additionally requires dorsal hump removal. Saddle nose is corrected by filling the dorsal concavity with a cartilage graft taken from the septum, auricle, or rib. Saddle nose Broad nose The preoperative appearance of various nasal deformities is shown on the left side, the postoperative appearance on the right side. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 31
  • 41. 32 I Nose, Paranasal Sinuses, and Face 3.3 Nosebleed (Epistaxis) Nosebleed is a relatively common, usually harmless symptom that may reflect a number of diseases of variable severity. By knowing the potential causes, Causes Nosebleed may have a local or systemic cause. Possible local causes (Table 3.1) include mucosal hyperemia due to an acute inflammation (rhinitis), allergies, and ambient conditions that dry the mucosa, increasing the fragility of the intranasal vessels (e.g., air conditioning). Local manipulations (nose picking) can also cause a nosebleed, usually in Kiesselbach’s area (a richly vascularized area of septal mucosa at the junction of the nasal cavity and vestibule, Fig. 3.4). Other possible local causes of epistaxis are congenital or acquired abnormalities of the nasal septum, such as pronounced septal spurs or ridges (see Fig. 3.2 b, p. 30). Finally, nosebleed can result from a septal perforation (Fig. 3.5). A perforated septum can have several causes, including a septal fracture with a superinfected septal hematoma (septal abscess), autoimmune disease (e.g., Wegener granulomatosis, see 3.10, p. 50), or a previous septoplasty (see p. 30) leading to mucosal perforation and cartilage necrosis. Epistaxis may also be symptomatic of an underlying systemic disease (Table 3.2). Besides vascular and circulatory diseases, typical examples are the various forms of hemorrhagic diathesis (e.g., Osler disease, see 3.7, p. 35), infectious diseases, and endocrinopathies. Diagnosis Nosebleed requires a simultaneous, coordinated protocol of diagnostic and therapeutic actions. One possible algorithm is shown in Fig. 3.6. The diagnostic work-up begins with blood pressure measurement. Except in very minor cases, the Hb should also be determined, and a coagulation disorder should be excluded by determining the platelet count, bleeding time, thromboplastin time (formerly: Quick), partial thromboplastin time (PTT), and thrombin time. Bleeding site: The nasal cavity is inspected by anterior rhinoscopy or endoscopy following decongestion and local anesthesia of the mucosa. In most cases the bleeding site is in Kiesselbach’s area (Fig. 3.4). It can be difficult to locate the bleeding source, however, when there is profuse bleeding from the posterior the physician can react appropriately in threatening cases. Table 3.1 Local causes of epistaxis Classification Examples Change in the nasal septum Perforation (Fig. 3.5): traumatic, iatrogenic, inflammatory; spurs or ridges (Fig. 3.2 b, p. 30) Mucosal or vascular injury Foreign bodies, rhinoliths, trauma (including nose picking), allergy, acute rhinitis, traumatic aneurysm of the internal carotid artery (very rare) Neoplasia Benign and malignant neoplasms of the nose, paranasal sinuses, and nasopharynx “Idiopathic” Fig. 3.4 Bleeding from Kiesselbach’s area Nasal septum Right inferior turbinate Kiesselbach’s area on the anterior septal mucosa is the site at which epistaxis typically occurs due to a local cause. The right inferior turbinate is visible in the background. parts of the nasal cavity, which are less accessible to inspection. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 42. 3 Diseases of the Nose, Paranasal Sinuses, and Face 3.6 Alternatives to anterior nasal packing and complications A double-lumen balloon catheter is introduced and inflated with water to produce local compression in the nasal cavity and nasopharynx. If the bleeding persists, a posterior nasal pack (Bellocq pack) can be inserted, but it should be used with caution due to the risk of aspirating the pads in the nasopharynx. Systemic complications of anterior and posterior nasal packing: • Arterial hypoxia: fall of oxygen partial pressure with pulmonary dysfunction due to an impaired nasopulmonary reflux mechanism. • Toxic shock: focal staphylococcal infection develops within 24 h after nasal packing, with generalized shock symptoms caused by bacterial toxins. Treatment General measures: The intensity of the bleeding and risk of aspiration can be reduced before the cause and location have been established. The nostrils are compressed against the nasal septum, and the patient is told not to swallow blood running down the pharynx. The patient is kept in an upright posture to reduce blood flow to the head and inhibit the swallowing of blood. An ice bag can be placed on the back of the neck to induce reflex vasoconstriction (see Fig. 3.7). An intravenous line should be placed if bleeding is severe. Silver nitrate cautery: Mild epistaxis from Kiesselbach’s area can often be controlled by selective local cauterization of the bleeding site with silver nitrate. Opposing sites on the nasal septum should not be cauterized due to the risk of septal perforation. Nasal packing: For severe epistaxis, the anterior nasal cavity can be packed with ointment-impregnated gauze strips (see Fig. 3.7) or with ready-made foam packs that expand on contact with fluid. Fig. 3.5 Septal perforation Left middle turbinate Right inferior turbinate The bleeding in this case is from the edges of a septal perforation. The endoscope was introduced into the right nasal cavity. The left middle turbinate and right inferior turbinate are visible in the background. Table 3.2 Systemic causes of epistaxis Classification Examples Vascular and circulatory diseases Atherosclerosis, arterial hypertension Infectious diseases Influenza, measles, typhus Endocrine changes or diseases Pheochromocytoma, pregnancy, diabetes mellitus Hemorrhagic diathesis • Coagulopathies • Platelet disorders – Thrombocytopenias – Thrombocytopathies Both nasal cavities should always be packed in order to produce adequate counterpressure. Alternatives to anterior nasal packing are shown in 3.6. Intranasal packing should not remain in place for more than 2–3 days. Balloon catheters should be progressively deflated starting on the second day; otherwise they may cause irreversible tissue necrosis. Long-term mucosal hygiene should be maintained after the packing is removed. Congenital: e.g., hemophilia A and B, Willebrand disease Acquired: e.g., anticoagulant therapy, hepatocellular insufficiency • Vasopathies Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. Idiopathic thrombocytopenic purpura, platelet proliferation disorders, platelet distribution disorders Congenital Acquired: uremia, dysproteinemia, adverse effects of dextran and acetylsalicylic acid (ASA) therapy Schönlein–Henoch purpura, Osler disease ( 3.7) 33
  • 43. 34 I Nose, Paranasal Sinuses, and Face Fig. 3.6 Flowchart for the diagnosis and treatment of epistaxis Epistaxis General measures: – Upright posture – Ice bag on back of neck – Compress the nostrils – Tell the patient not to swallow blood – Place an i.v. line Lab tests: – Hb – Platelet count – Clotting time – Coagulation: TPT, PTT, TT Blood pressure? Elevated Normal or decreased Antihypertensive agent Volume replacement If necessary, give platelet concentrate or fresh frozen plasma Decongest and anesthetize nasal mucosa Inspect nasal cavity by anterior rhinoscopy or endoscopy Kiesselbach’s area Light bleeding Silver nitrat cautery of bleeding site Other site in the anterior nose Posterior sites Changes in nasal septum (perforation, spur, etc.) Bellocq pack ( 3.6) Local surgical treatment (e. g., septoplasty) Heavier bleeding Bilateral anterior nasal pack or balloon tamponade Bleeding persists Surgical ligation of bleeding vessel (Fig. 3.8) or angiographic embolization Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 44. 3 Diseases of the Nose, Paranasal Sinuses, and Face Vascular ligation or embolization: The most common source of bleeding from the posterolateral part of the nasal cavity is the sphenopalatine artery (branch of the maxillary artery), which can be coagulated or clipped under endoscopic control. The ligation or angiographic embolization of a larger arterial trunk may be considered as a last recourse. When this is done, the source of the bleeding must be accurately identified since the nasal lining is supplied by various arteries (Fig. 3.8). Prevention of recurrent bleeding: Besides the conservative treatments noted above, some causes of epistaxis require surgical treatment since nasal packing alone is of only temporary, symptomatic benefit ( 3.7). Fig. 3.7 3.7 Surgical prevention of recurrent epistaxis The main indications for surgery are changes in the nasal septum such as septal spurs (Fig. 3.2 b, p. 30), ridges, and perforations (Fig. 3.5). Treatment consists of straightening the nasal septum (septoplasty, see p. 30) or closing the septal perforation (e.g., by implanting an auricular cartilage graft and using local mucosal flap advancement). In diseases that are associated with vascular changes, such as Osler disease, telangiectatic areas on the septal mucosa can be treated with a surgical laser. The figure shows numerous punctate telangiectasias in the left nasal cavity in Osler disease. If laser treatment is inadequate, other surgical options are available. In a Saunders dermoplasty, for example, the telangiectatic septal mucosa is resected and replaced with a free skin graft (e.g., from the supraclavicular area). Middle turbinate Anterior nasal packing Inferior turbinate Ice bag Treatment of a patient with epistaxis. Ointment-impregnated gauze strips are layered into both nasal cavities. An ice bag is placed on the back of the patient’s neck. Fig. 3.8 Vascular ligation for severe epistaxis Anterior ethmoid artery Posterior ethmoid artery Ophthalmic artery Sphenopalatine artery Maxillary artery Internal carotid artery External carotid artery Pterygopalatine fossa Common carotid artery Depending on the bleeding source, various vessels can be ligated through a cervical approach, by the transnasal endoscopic route, or by a transmaxillary route in the pterygopalatine fossa. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 35
  • 45. 36 I Nose, Paranasal Sinuses, and Face 3.4 Soft-Tissue Injuries and Plastic Surgery Facial soft-tissue injuries are still a common occurrence in recreational and traffic accidents. When improperly managed, they can result in disfiguring scars and deformity. Poor cosmetic results are particularly Diagnosis Before a traumatic facial wound is treated, possible coexisting fractures should be excluded by clinical examination and, if necessary, by imaging studies such as biplane skull films, standard sinus projections (see Fig. 2.7, p. 22), and computed tomography (CT) scans. Especially with bite wounds, a smear should be taken for microbiologic examination. Every patient with facial injuries should be asked about tetanus immunization. objectionable in this very conspicuous region. This deals with necessary diagnostic measures and also reviews the most important techniques of facial plastic surgery. Fig. 3.9 Closure of facial soft-tissue wounds a Single Z-plasty b Multiple Z-plasty Treatment Prior to surgical treatment, measures are taken to reduce micro-organism counts and prevent infection (tetanus, rabies), especially in patients with bite wounds. In the interest of maximum tissue preservation, only tissues that are definitely necrotic should be debrided from facial wounds. c W-plasty Wound margins should never be reapproximated under tension, as this would result in aesthetic and functional deficits such as incomplete eyelid closure. In most soft-tissue injuries to the nose, adequate treatment consists of primary reapproximation and suturing of the wound margins. d Broken-line closure Scar Camouflage Two fundamental local principles in facial soft-tissue surgery are the relaxed skin-tension lines (RSTLs, see Fig. 1.1 a, p. 2) and the aesthetic units (see Fig. 1.1 b). The RSTLs are a particularly important consideration when there are no soft-tissue or skin defects and only a direct closure is required, since scars are easier to camouflage when they are oriented along the RSTLs. The techniques described below are also useful for revising a functionally and/or aesthetically objectionable result, such as lengthening a heavily contracted scar. Z-plasty (Fig. 3.9 a, b): When a wound margin runs perpendicular to the RSTLs, it can be reoriented with a single or multiple Z-plasty and lengthened in the direction of the scar axis. Auxiliary incisions and skin areas to be removed Direction of tension along RSTLs Direction of advancement The techniques of scar revision can also be used in primary wound care. The wound area should be broadly undermined to eliminate tension on the reapproximated wound margins. The colored dots mark the original and transposed location of the skin areas. The solid lines represent the wound margins. Broken lines indicate auxiliary incisions. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 46. 3 Diseases of the Nose, Paranasal Sinuses, and Face Fig. 3.10 Local flap techniques a Horizontal advancement flap b Bilobed flap c Rhomboid flap Outlined skin area Defect Direction of advancement Direction of tension along RSTLs a Small “Burow triangles” are excised at the ends of the incisions, allowing the two rectangular flaps to be advanced for defect closure. b The bilobed flap is a butterfly-shaped advancement flap used to close a defect. c The rhomboid flap can be used on the nasal flank, as illustrated, or on the cheek. d The skin between the defect and superficial flap is undermined, and the island flap is pulled into the defect on its subcutaneous pedicle. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 37
  • 47. 38 I Nose, Paranasal Sinuses, and Face Fig. 3.11 Forehead flap Larger defects of the nose can be reconstructed with a forehead flap based on the supraciliary and supratrochlear arteries. a The skin surrounding the defect is circumscribed, mobilized, and turned downward to provide intranasal lining. b Next the forehead flap is raised and partially backed with cartilage (composite graft) for coverage of the external defect. c The forehead defect can usually be closed directly. W-plasty (Fig. 3.9 c): The principal effect of this technique is to lengthen the scar. Broken-line closure (Fig. 3.9 d): The effect of this technique is to “optically disperse” the scar, making it more irregular and less noticeable. Fig. 3.12 Pedicled myocutaneous flap Repair of Tissue Defects Soft-tissue defects (traumatic or post-tumor resection, see p. 62) often cannot be adequately managed by primary wound closure with reapproximation of the skin margins. Smaller tissue defects can be repaired with local flaps such as a sliding flap, bilobed flap, rhomboid flap, or island flap (Fig. 3.10, p. 37). A larger defect of the nose can be covered by turning down a forehead flap (Fig. 3.11), if necessary after first reconstructing the nasal skeleton with cartilage and bone grafts. Local flaps are often inadequate for more extensive defects of the external nose (e.g., tumor, dog bite), which may require more complex reconstructive procedures using an autologous transfer. This may consist of a pedicled flap (e.g., the myocutaneous pectoralis major flap, Fig. 3.12) or a microvascular free flap. In a microvascular free transfer, the autologous tissue is removed with its supply vessels, which are anastomosed to corresponding arteries and veins at the recipient site. Very extensive defects in the nasal region, like those created by a tumor resection, are repaired in multiple sittings using more complex flap transfers from the scalp (Fig. 3.13). If the graft must also provide a degree of stability (e.g., alar cartilage of the external nose), this can be accomplished with a composite graft harvested from the auricle (Fig. 3.14) or from the costal or septal cartilage. The myocutaneous pectoralis major flap is frequently used in the head and neck and is useful for repairing large defects in the facial region. Based on the thoracoacromial artery, the flap is composed of skin, subcutaneous soft tissue, and portions of the pectoralis major muscle. It is mobilized, swung into the tissue defect, and sutured into place. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 48. 3 Diseases of the Nose, Paranasal Sinuses, and Face Fig. 3.13 Scalp flap a b The Converse scalp flap is usually based on the superficial temporal artery. Owing to its size and width, one of its applications is for total nasal reconstruction. Backing material (e.g., costal or auricular cartilage) should be added to the flap when it is mobilized and inset in order to obtain proper nasal height. c Fig. 3.14 Composite graft a b e c d a The nasal alar defect is repaired with a composite graft of cartilage and skin from the auricle to restore adequate stability to the nasal vestibule. b, c A woman with a nasal alar defect caused by a dog bite, shown before (b) and after (c) debridement of the wound margins. d Appearance after inset of the auricular composite graft. e Appearance 6 months later. The healed graft shows an excellent color and texture match with its surroundings. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 39
  • 49. 40 I Nose, Paranasal Sinuses, and Face 3.5 Fractures of the Nasal Pyramid and Lateral Midface Bony injuries to the nasal pyramid and midface are still common in sports and traffic accidents. Most of the injuries are closed fractures. The initial findings may be deceptive, due to hematoma-induced soft-tissue swelling. Nasal Pyramid Fracture formation (Fig. 3.16 a). The hematoma may become infected, giving rise to a septal abscess (Fig. 3.16 b), which in turn can lead to cartilage necrosis with loss of the nasal septum and dorsal saddling. Alternatively, the infection may spread to the cranial cavity by the vascular route, causing meningitis. The nasal pyramid is predisposed to fractures because of its exposed location. The fractures are classified as open or closed on the basis of concomitant soft-tissue injuries. Diagnostic procedure: Inspection may show obvious deviation of the external nose (Fig. 3.15 a) or a simple depression of the lateral nasal wall. Swelling of the surrounding soft tissues is also present, usually caused by a hematoma. Intranasal inspection by anterior rhinoscopy or endoscopy is done to check for concomitant mucosal injuries and especially to evaluate the nasal septum, which also may be fractured. Crepitus noted on palpation confirms the suspicion of a fracture. Further diagnostic measures include radiographs of the nose in the lateral projection (Fig. 3.15 b) and standard sinus projections to exclude bony involvement of the lateral midface (see below). Treatment: Surgical treatment is generally indicated due to the potential for permanent nasal deformity. An open fracture requires immediate surgical care accompanied by tetanus prophylaxis or a tetanus booster. If the fracture is displaced and closed, it can be safely reduced during the initial week after the injury. The displaced or depressed bone fragments can be reduced manually or with the aid of a special instrument (elevator) (Fig. 3.17). After the reduction, the nasal cavities should be packed to provide “internal splinting,” and a plaster cast is applied externally. Complications: When a septal fracture is covered by an intact soft-tissue envelope, there is a danger of subperichondrial hemorrhage with hematoma Fig. 3.15 Nasal pyramid fracture a The clinical appearance, showing deviation of the external nose with an intact soft-tissue envelope. b The lateral radiograph of the nose demonstrates a fracture line (arrow). a Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. b
  • 50. 3 Diseases of the Nose, Paranasal Sinuses, and Face Fig. 3.16 Complications of septal fracture Septal hematoma a Symmetrical sites of boggy swelling over the nasal septum following a septal fracture, with subperichondrial bleeding under the intact mucosa. b Septal abscess with symmetrical bulging and erythema of the mucosa, with a purulent nasal discharge. Septal abscess Subperichondrial hematoma Fig. 3.17 Reduction of a nasal pyramid fracture Traumatizing force Reduction a b Lateral Midfacial Fractures Lateral midfacial fractures are usually caused by blunt trauma to the side of the face. Affected structures of the bony facial skeleton are the maxillary sinus, orbit, and the zygoma or zygomatic arch (see Fig. 1.2, p. 2 and Fig. 1.6, p. 6). An isolated fracture of the orbital floor with a partial herniation of the orbital contents into the maxillary sinus is a special type of lateral midfacial fracture called a blow-out fracture (see Fig. 3.20 b). Symptoms: A depressed fracture of the zygoma presents clinically with facial asymmetry. Depression of the zygomatic arch frequently causes limited mouth opening. Fractures of the orbital floor can cause diplopia on upward gaze due to entrapment of the inferior rectus muscle. Sensory disturbances involving the cheek, ipsilateral upper lip, and lateral nasal wall suggest a direct or indirect fracture-induced lesion of the infraorbital nerve, which enters the buccal soft tissues below the infraorbital margin and is commonly involved by fractures of the orbital floor. Diagnosis: a Laterally displaced fragments are reduced by external digital pressure. b If the nasal pyramid is depressed, the fragments have to be elevated with an instrument from within the nasal cavity. Inspection: Swelling is usually present due to subcutaneous hemorrhage (periorbital or “monocle” hematoma, Fig. 3.18). Asymmetry of the affected facial half is most likely to occur with depression of the zygoma or zygomatic arch, depending on the location and extent of the fracture (Fig. 3.19). Enophthalmos signifies involvement of the orbital floor (herniation of orbital contents). It is prudent to seek ophthalmologic consultation in these cases. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 41
  • 51. 42 I Nose, Paranasal Sinuses, and Face Fig. 3.18 Unilateral periorbital hematoma Fig. 3.19 Facial asymmetry caused by a depressed fracture of the zygoma The periorbital hematoma in this patient is the superficial sign of a lateral midfacial fracture. The right cheek is flattened relative to the opposite side due to a depressed fracture of the zygoma. Fig. 3.20 Radiographic imaging of lateral midfacial fractures a b a Sinus radiograph demonstrates the displaced bone fragments (arrows). b Sinus radiograph of a blow-out fracture shows a typical softtissue density (arrow) caused by herniated orbital contents (“hanging drop” sign). Palpation: Concomitant soft-tissue swelling can make it difficult or impossible to palpate sites of bony discontinuity or displacement. The following areas should be examined: • Frontozygomatic suture (upper part of the lateral orbital rim) • Infraorbital margin (anterior bony margin of the orbital floor) • Zygomatic arch (often difficult to evaluate due to soft-tissue swelling) Sensory testing: Wisps of cotton can be used to test sensory function on the healthy and affected sides. Radiographs: Whenever a lateral midfacial fracture is suspected, standard sinus radiographs should be obtained (occipitomental and occipitofrontal projections, see Fig. 2.7, p. 22) to define the extent of the bony discontinuity or displacement (Fig. 3.20 a, b, c c Coronal computed tomogram of a blow-out fracture. Fig. 3.21 a). The zygomatic arches may be poorly visualized in standard projections, and so a “bucket handle” view should be added when a concomitant zygomatic arch fracture is suspected (Fig. 3.24 a). CT scans may also be helpful to obtain a more discriminating view of the fracture and also to exclude an involvement of the anterior skull base (see 3.6, Fig. 3.20 c, Fig. 3.23 b, and Fig. 3.24 b). Treatment: Surgical treatment is unnecessary for undisplaced, asymptomatic fractures, but it is indicated for displaced fractures or fractures that are causing symptoms such as sensory deficits in the distribution of the infraorbital nerve, diplopia on upward gaze, enophthalmos, restricted jaw opening, or facial asymmetry. Treatment consists of reduction and fixation of the bone fragments using miniplates, interosseous wiring, or both (Fig. 3.21 b and Fig. 3.22). In all cases the patient should be cautioned to avoid nose blowing. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 52. 3 Diseases of the Nose, Paranasal Sinuses, and Face Fig. 3.21 Displaced lateral midfacial fracture on the left side Fig. 3.22 Internal fixation of an orbital rim fracture a A fracture of the left infraorbital margin has been stabilized by wire and miniplate fixation. The orbital contents are retracted upward with a spatula. b Fig. 3.23 Depressed fracture of the zygoma a The sinus radiographs show a displaced lateral midfacial fracture on the left side with separation of the frontozygomatic suture and a displaced orbital floor fracture before (a) and after (b) reduction and stabilization with miniplates. Fig. 3.24 Depressed fracture of the zygomatic arch b a b Depressed fracture of the zygomatic arch (arrows), demonstrated by the bucket-handle view (a) and axial CT scan (b). a Sinus radiograph of a depressed zygomatic fracture on the right side (the patient had been kicked by a horse). b Axial computed tomogram in the same patient shows the displaced body of the zygoma (arrow), which has penetrated the orbital cone from the lateral side. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 43
  • 53. 44 I Nose, Paranasal Sinuses, and Face 3.6 Fractures of the Central Midface and Anterior Skull Base Although fractures of the central midface and anterior skull base (frontal skull base, rhinobase) are sepa- rate entities, they are on a clinical continuum and are therefore discussed in the same . Classification: Central midfacial fractures: The Le Fort classification (Fig. 3.25) describes various midfacial fracture patterns ranging from isolated detachment of the alveolar process (Le Fort I, Fig. 3.26) to separation of the midfacial bones from the anterior skull base (Le Fort III). The dura along the fracture line tends to become torn at sites where it is firmly adherent to the bone of the skull base (e.g., cribriform plate, sphenofrontal suture, sellar tubercle, spheno-occipital synchondrosis). Frontobasal fractures: These are bony injuries to the anterior skull base and adjacent paranasal sinuses (frontal and sphenoid sinuses, ethmoid labyrinth). The Escher classification distinguishes four types of frontobasal fractures based on the location and extent of the fracture lines (Fig. 3.27). Etiopathogenesis: Fractures of the central midface and frontal skull base generally occur in multiply injured patients (usually vehicular accidents), but they can also result from “trivial” trauma or even a surgical procedure (e.g., endoscopic sinus surgery), since some bony portions of the anterior skull base are quite thin (e.g., the cribriform plate of the ethmoid bone). Frontobasal fractures occupy a special place among skull fractures because they are usually an “indirectly open” injury that creates a communication between the cranial cavity and the environment. Ascending infection can occur via the adjacent paranasal sinuses in frontobasal fractures and can lead to life-threatening intracranial complications (e.g., meningitis, brain abscess). Symptoms: Most patients present with a unilateral (see Fig. 3.18) or bilateral periorbital hematoma, depending on the nature and direction of the traumatizing force. A dish face is seen in combined fractures (Le Fort II–III, Escher III) where the midface has been separated from the skull base and displaced inward. Cerebrospinal fluid (CSF) rhinorrhea is one of the few reliable signs of an anterior skull base fracture with associated dural injury. It can also occur with petrous bone fractures, in which case CSF leakage occurs via the eustachian tube. Particularly in fresh head injuries, CSF leak from a dural tear may be obscured by heavy bleeding or may be contained by bone fragments, prolapsed brain tissue, swollen mucosa, or foreign bodies. Severe craniocerebral trauma can also result in vision loss caused by ocular destruction or injury to the optic nerve (nerve contusion, rupture of the nerve in an intact sheath due to sagittal brain motion within the skull). Diplopia due to oculomotor palsy from damage to the third, fourth, or sixth cranial nerve is somewhat rare and occurs only if the fracture line runs through the cavernous sinus. Extensive injuries with sites of bone dehiscence can lead to cerebral prolapse, with Fig. 3.25 Le Fort classification a Le Fort I b Le Fort II c Le Fort III Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. Central midfacial fractures are classified into three groups: a Le Fort I: isolated detachment of the alveolar process (see also Fig. 3.26). b Le Fort II: pyramidal fracture with detachment of the maxilla. c Le Fort III: craniofacial dysjunction.
  • 54. 3 Diseases of the Nose, Paranasal Sinuses, and Face Fig. 3.26 Le Fort I a b Before an ENT examination is performed, the patient’s vital functions should be stabilized by the anesthesiologist or neurosurgeon. Facial soft-tissue injuries are often extensive but may provide little information on possible associated bony injuries at the level of the skull base. A basic impression is gained by palpation of the facial bones (Fig. 3.28) and inspection of the nasal cavity by rhinoscopy or endoscopy. Profuse bleeding from softtissue injuries, including intranasal lesions, often makes it difficult to adequately evaluate the injury in the acute stage, and it may not be possible at this time to confirm or exclude a CSF leak in multiply injured patients, many of whom are intubated. The next step after nasal inspection is to inspect the oral cavity and oropharynx. Otoscopy or otomicroscopy should also be performed to exclude a concomitant petrous bone fracture. A clear, watery nasal discharge should raise suspicion of a CSF leak (Fig. 3.29), which requires differentiation from ordinary nasal mucus. Various CSF tests (e.g., glucose test, β2-transferrin assay) are available for this purpose ( 3.8). Intracranial complications (especially bleeding) should also be excluded. Intraoperative photos of a multiply injured patient with a Le Fort I fracture on the right side. brain tissue herniating externally or into the nasal cavity. Anosmia can result from a fracture of the cribriform plate with avulsion of the fila olfactoria, or it may signify damage to more central structures in the setting of a cerebral concussion or contusion. Diagnosis: Patients with craniocerebral trauma require interdisciplinary care. Computed tomography supplies additional important information on the location and extent of injuries. Neurosurgeons order CT scans with a soft-tissue window as an initial study for excluding intracranial bleeding, hematoma, and pneumocephalus. This type of study is not useful for the assessment of bony lesions. While indirect signs such as the presence of intracranial air (Fig. 3.30 c) suggest a strong likelihood of dural injury with a frontobasal fracture, only a bone-window CT scan can reliably evaluate or exclude a fracture. So whenever a frontobasal fracture is suspected, high-resolution CT scans (2-mm slice thickness, bone window) of the paranasal sinuses should be obtained in the axial and coronal projections. The Fig. 3.27 Escher classification Frontobasal fractures are classified into four groups: a Escher I: high fracture. b Escher II: central fracture. c Escher III: low fracture. d Escher IV: latero-orbital fracture. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 45
  • 55. 46 I Nose, Paranasal Sinuses, and Face Fig. 3.28 Palpation of the bony facial skull a Bony orbital margin b Zygoma c Maxilla Fig. 3.29 Cerebrospinal fluid (CSF) rhinorrhea d Nasal pyramid 3.8 CSF rhinorrhea appears clinically as a watery nasal discharge. axial scans are for evaluating the anterior and posterior walls of the frontal sinuses (Fig. 3.30 a) and sphenoid sinus (Fig. 3.30 b), while the coronal scans more clearly define the ethmoid roof and cribriform plate (Fig. 3.30 c, d). The preliminary testing of hearing and balance is possible only if the patient is conscious and responsive to verbal commands. Olfactory testing to exclude anosmia often cannot be performed in the acute stage but should be done at a later time. For medicolegal reasons, it should always precede surgical treatment (see Olfactometry, p. 21). e Mandible Detection of cerebrospinal fluid (CSF) In the glucose test, a dipstick is used to test the glucose content of the collected discharge. The presence of blood in the sample can give a false-positive reading, since blood has twice the sugar content of CSF. This test is therefore very nonspecific. The immunoelectrophoretic determination of β2-transferrin is a more accurate method. This protein is normally present only in CSF. Since it is also detectable in the serum in very rare cases, the patient’s serum should additionally be tested for comparison. The advantages of this method are that it is noninvasive, supplies a result within 24 hours, and can be repeated as often as needed (for follow-up). The test procedure is relatively costly and complex, however. restoration of normal occlusion. The urgency of surgical intervention for a frontobasal fracture is shown in Table 3.3. Three main surgical approaches to the anterior skull base are available (Fig. 3.31). The choice depends on the individual situation and is made in consultation with the other involved specialties (e.g., neurosurgeon, maxillofacial surgeon, ophthalmologist). Treatment: Every confirmed fracture of the anterior skull base should be treated surgically in operable patients, regardless of whether or not a CSF leak has been detected. The patient should also be instructed not to blow the nose. With an isolated central midfacial fracture that does not involve the anterior skull base, surgical treatment of the maxilla should be provided by a maxillofacial surgeon to ensure the Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 56. 3 Diseases of the Nose, Paranasal Sinuses, and Face Fig. 3.30 CT examination of frontobasal fractures a Axial computed tomography scans demonstrate a fracture of the anterior and posterior walls of the frontal sinuses (arrows) (a) and a clivus fracture (arrow) that extends anteriorly into the sphenoid sinus (b). The coronal scans show air in the cranial cavity (c) and a fracture of the ethmoid roof (d) (arrow). b c d Fig. 3.31 Surgical approaches to the anterior skull base Transfrontal intradural or extradural approach Transfacial frontoorbital extracranial approach Endoscopic approach Dura Table 3.3 Indications for the surgical treatment of frontobasal fractures Vital indications (operate immediately) • Life-threatening rise of intracranial pressure due to intracranial hemorrhage • Bleeding from the nose or sinuses that is refractory to conservative treatment • Bleeding from an open skull injury that is refractory to conservative treatment Absolute indications (operate as soon as possible) • Open brain injury • Dural tear from an indirectly open head injury • Penetrating foreign bodies and impalement injuries • Early complications (e.g., meningitis, encephalitis, brain abscess) • Late complications (e.g., meningitis, brain abscess, osteomyelitis) • Orbital complications Relative indications (operate in 1–2 weeks) • Displaced bone fragments • Fractures involving the drainage tracts of the paranasal sinuses (“ostiomeatal unit”) • Acute or chronic sinusitis at the time of the injury • Post-traumatic sinus inflammation, mucopyocele formation • Supraorbital nerve injury due to an adjacent fracture Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 47
  • 57. 48 I Nose, Paranasal Sinuses, and Face 3.7 Inflammations of the External Nose, Nasal Cavity, and Facial Soft Tissues Inflammatory diseases of the nasal skin usually have a bacterial cause and may be manifested on the exposed skin and the dermal appendages. Although these diseases fall primarily within the scope of dermatology, the otolaryngologist is frequently faced with inflammations of this type that can lead to lifethreatening complications unless adequately treated. Inflammation of the nasal cavity (rhinitis) predominantly involves the nasal mucosa. While it can have a variety of causes, it always exhibits a more or less Purulent Inflammations of the Hair Follicles Pyodermas of the hair follicles are common purulent inflammations that can occur at almost any age. The main causative organisms are staphylococci. If the disease is confined to the hair follicles, it is termed folliculitis. If the infection spreads to deeper tissues and forms a central core of purulent liquefaction, it is called a furuncle. Symptoms: Nasal furuncles present as painful, tender, erythematous swellings about the nasal tip and nares (Fig. 3.32). There may be concomitant edematous swelling of the upper lip. The changes are confined to the outer skin and do not involve the mucosa. Fever is sometimes present. pronounced combination of characteristic symptoms. Although rhinitis and sinusitis are on a continuum owing to the special anatomical and physiological relationships of the nose and paranasal sinuses (see 1.1–1.3, pp. 2–13), the diseases are covered separately in this unit for learning purposes. The various forms of rhinitis are discussed according to their etiology, noting that the great majority of cases seen in clinical practice are mixed forms that have more than one cause. Treatment: The treatment of choice is high-dose parenteral administration of an antibiotic that is active against staphylococci, such as flucloxacillin sodium or dicloxacillin sodium, combined with the local application of an antibiotic-containing ointment (chlortetracycline HCl). Also, the upper lip should be moved as little as possible, and so the patient should be placed on a liquid or semisolid diet and speak as little as possible. An essential goal of these measures is to prevent the potentially lethal complication of intracranial spread. Complications: Inadequate treatment or manipulations of the nasal furuncle itself can result in hematogenous spread to intracranial structures, since the veins of the nose and upper lip drain via the angular and ophthalmic veins into the cavernous sinus. If tenderness in the medial canthus of the eye raises a sus- Fig. 3.32 Nasal furuncle Clinical appearance before (a) and after (b) antibiotic treatment. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 58. 3 Diseases of the Nose, Paranasal Sinuses, and Face Fig. 3.33 Facial erysipelas Patients typically present with generalized facial swelling and erythema. The possible portals of entry are visible over the nasal dorsum. If facial erysipelas spreads lateral to the nose and about the eyelids, there is a risk of intracranial involvement by hematogenous spread of the causative organisms, as with a nasal furuncle. Treatment: The treatment of choice is the parenteral administration of penicillin. Moist compresses soaked in an antiseptic solution can also be applied locally. Inflammations of the Nasal Cavity Acute Rhinitis picion of thrombophlebitis of the angular vein, the vessel should be surgically ligated and divided. Erysipelas Etiopathogenesis: The principal causative organisms are beta-hemolytic group A streptococci. Less common pathogens are streptococci of other groups, Staphylococcus aureus, and gram-negative rods (e.g., Klebsiella pneumoniae), which gain entry to the skin through minor injuries (usually on the face and limbs). The inflammation spreads diffusely in the skin and subcutaneous tissue. Symptoms: Facial erysipelas (Fig. 3.33) usually begins with a high fever and a feeling of tension in the soft tissues, followed rapidly by broad areas of erythema and swelling, which are sharply demarcated from unaffected skin. The tissue is warm to the touch, and small blisters occasionally form. 3.9 Differential diagnosis of facial soft-tissue swelling Lupus erythematosus (LE), the most common form of cutaneous LE, is an inflammatory dermatosis that frequently affects the face, spreading in a butterfly-shaped pattern over the cheeks, forehead, and nose. The differential diagnosis also includes allergic contact dermatitis, which may be induced by cosmetics, toilet articles, sun creams, or exposure to airborne plant pollens. In strongly sensitized patients who wear a face mask, even a single contact can incite a severe, acute allergic reaction with erythema and edematous swelling of the facial soft tissues. Finally, the differential diagnosis should include angioedema, which is also associated with facial swelling that chiefly affects the eyelids and lips (see also 4.4, p. 87). Epidemiology: Acute rhinitis (common cold) is the most prevalent infectious disease. Given its frequency and the fact that the disease does not confer postinfection immunity, acute rhinitis has assumed major epidemiologic and economic significance. Etiopathogenesis: Rhinoviruses and coronaviruses comprise almost half of the causative organisms of acute viral rhinitis. Other pathogens are influenza viruses and adenoviruses. The infection is transmitted by the airborne route (droplet infection). Cold exposure and other environmental factors can increase the susceptibility of the host to infection. The incubation period is 3–7 days. Symptoms: The disease begins with an initial dry stage characterized by malaise (lethargy, headache, fever) and local discomfort in the nose and nasopharynx (burning, soreness). This is followed by a catarrhal stage marked by a watery, initially serous nasal discharge and nasal obstruction due to mucosal swelling, which mainly involves the turbinates. The viruses damage the mucociliary transport system, which hampers the normal clearing of secretions. With a profuse nasal discharge, inflammatory changes often develop about the nasal vestibule. Viral damage to the epithelium promotes bacterial colonization, which alters the consistency of the clear nasal discharge, causing it to become mucopurulent (Fig. 3.34). The local and systemic symptoms usually subside in about a week. Treatment: Treatment consists of supportive measures to relieve nasal obstruction and prevent sinusitis and other sequelae by the use of decongestant nose drops. Nose drops should be used no longer than absolutely necessary (generally no more than one week) due to the risk of tachyphylaxis (see also rhinitis medicamentosa, p.11) with severe rebound swelling of the nasal mucosa. Various other options are available for relieving the discomfort of acute rhinitis, including chamomile steam inhalation, “light baths,” and infrared therapy. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 49
  • 59. 50 I Nose, Paranasal Sinuses, and Face Fig. 3.34 Acute rhinitis 3.10 Middle turbinate Endoscopic inspection of the left nasal cavity shows inflammatory changes in the mucosa with mucopurulent nasal secretions. Antibiotics may also be prescribed in patients with bacterial superinfection or paranasal sinus involvement. Nonspecific Chronic Rhinitis Etiopathogenesis: Chronic inflammation of the nasal mucosa can have various underlying causes. Besides recurrent acute inflammations with progressive damage to the mucosa, nonspecific chronic rhinitis can develop due to anatomic changes (e.g., marked septal deviation, septal spur) or other lesions of the nasal cavity (polyps, tumors) and nasopharynx (adenoids, see 5.3, p.108). Environmental factors such as sustained extreme temperatures or air pollutants can also bring on this condition. Symptoms: Patients present clinically with obstructed nasal breathing and a mucous nasal discharge. They also complain of frequent throat clearing and occasional hoarseness. Treatment: The most important step is to eliminate the cause by removing chronic irritants from the environment or by surgically correcting any intranasal pathology (e.g., septoplasty, p. 30). Supportive measures such as decongestant nose drops or nasal irrigation with saline solution are of only temporary benefit. Specific Chronic Rhinitis This category includes inflammations of varying causes that may be manifested in the nose ( 3.11). Wegener granulomatosis (Wegener disease) Wegener granulomatosis is a granulomatous disease that starts with the formation of primary granulomas in the connective tissue and later progresses to vascular involvement in the form of a necrotizing vasculitis. In the head and neck region, the nose is predominantly affected. Lesions may also develop in the trachea and middle ear. Symptoms consist of nasal airway obstruction, a bloody nasal discharge, and severe crusting in the nasal cavity and nasopharynx. As the disease progresses, soft-tissue and cartilage destruction may occur as a result of superinfection or necrotizing granulomas, manifested clinically by mucosal ulcerations, septal perforation, and cartilaginous saddle nose. Allergic Rhinitis Diseases of the nose and paranasal sinuses have undergone a disproportionate rise during the past few decades. Meanwhile, the spectrum of rhinologic diseases has changed from a qualitative standpoint as well. As allergic diseases have become more prevalent, there has also been a notable rise in the incidence of allergic rhinitis. Etiopathogenesis and classification: Allergic inflammation of the mucosa is triggered by an immediate, IgE-mediated reaction of the immune system to any of a number of foreign substances, particularly pollens and animal allergens. Allergic rhinitis is classified as seasonal (hay fever) or perennial according to the presence of the allergen in the environment. Seasonal allergic rhinitis in Central Europe is caused mainly by pollens from alder, hazel, birch, grasses, rye, mugwort, and plantain. Clinical symptoms appear between February and September, depending on the individual allergen spectrum of the patient, and disappear at the end of the pollen season. By contrast, perennial allergic rhinitis is caused by year-round allergen exposure that incites a permanent inflammation of the nasal mucosa. The predominant causative allergens are house dust, pet dander, and molds. The disease may also be caused by certain foods (e.g., strawberries, nuts, eggs, fish) as well as occupational exposure to allergens (e.g., bakers and hairdressers). A new occupational allergen, especially prevalent in health workers, is latex, which is used to manufacture disposable gloves. Symptoms: The clinical manifestations include obstructed nasal breathing and sneezing attacks, a watery nasal discharge, and itching of the nose and eyes (conjunctivitis). Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 60. 3 Diseases of the Nose, Paranasal Sinuses, and Face 3.11 Causes of specific chronic rhinitis Tuberculosis Tuberculosis can involve the nasal mucosa as a primary infection following the inhalation of infectious droplets, forming a primary complex approximately 6 weeks after infection. Another manifestation is lupus vulgaris, the most common postprimary form of cutaneous tuberculosis. Ulcerative cases are marked by increasing necrosis within the tubercular granulomas, which can cause a mutilating destruction of nasal skin and cartilaginous structures. Lupus vulgaris may also arise from the nasal mucosa itself, causing the contiguous destruction of nasal structures from the inside. Sarcoidosis Sarcoidosis is a common, granulomatous systemic disease of unknown etiology that predominantly affects women under 40 years of age. Although the lymph nodes, lung, joints, and skin are chiefly affected and involvement of the upper respiratory tract is relatively rare, nasal symptoms may be the initial manifestation of the disease. Involvement of the external nose is called lupus pernio because the characteristic skin changes resemble chilblains (pernio). Involvement of the nasal mucosa mainly affects the septum and inferior turbinate, which develop yellowish, submucous nodules that have the gross appearance of intramucosal granulomas. Rhinoscleroma This chronic inflammatory disease is extremely rare and is manifested in the nose, oral mucosa, and upper respiratory tract. It is transmitted by Klebsiella pneumoniae (subspecies rhinoscleromatis). Rhinoscleroma presents the features of atrophic rhinitis (see below): fetid nasal discharge, dry mucosa, and crusting. The nasal mucosa shows inflammatory infiltrates that may progress to granulations and also involve the nasal vestibule. Actinomycosis The gram-positive anaerobe Actinomyces israelii can cause this disease, usually in immunocompromised patients. Symptomatic involvement of the nose and paranasal sinuses is somewhat uncommon. Changes in these regions may include firm infiltrates in the nasal mucosa that resemble a nasal furuncle. There have also been sporadic reports of granulations 3.12 Nasal hyperreactivity Because the nasal mucosa is reactive to physical, chemical, and pharmacologic stimuli, which may take the form of allergens, pollutants (cigarette smoke, dust, fumes), or even position changes or exertion, the term “nasal hyperreactivity” (analogous to “bronchial hyperreactivity”) has lately been coined as a collective term for a heightened reactivity of the nasal mucosa to these agents. Some of the diseases that lead to nasal hyperreactivity are marked by signs of inflammation and others chiefly by disturbances of autonomic nervous regulation, with an altered response of the associated receptors on vessels, nerves, and glands of the mucosa. forming on the nasal mucosa and in the paranasal sinuses. Untreated, the inflammation can spread and cause severe tissue destruction with a fatal outcome. Syphilis Nasal involvement by syphilis occurs mainly in the tertiary stage of the disease. It is manifested by the appearance of isolated gummata or by diffuse gummatous infiltration of the nasal cavity. Untreated, the disease causes progressive destruction of the surrounding tissue, and eventual bone destruction can occur. Infants with congenital syphilis contracted in utero may also manifest nasal changes that include a purulent and sometimes bloody nasal discharge, which may be mistaken for “normal” infant rhinitis. Malleus Malleus is a rare infectious disease (causative organism: Pseudomonas mallei) that is transmitted to humans from horses and occasionally from house pets. When the nasal mucosa is the portal of entry, it exhibits inflammatory swelling, pustule formation, and ulceration with a viscous nasal discharge containing blood and pus. Fungal infections Aspergillosis is the most common fungal infection causing chronic specific rhinitis, with fungal colonization occurring mainly in the paranasal sinuses (see Sinusitis in 3.8, pp. 54– 57). In rare cases and especially in immunocompromised patients, the infection may take an aggressive, fulminating course with the destruction of surrounding structures, resulting in a very high mortality. Mucormycosis resembles aspergillosis in its symptoms and course. The invasive form of mucormycosis still has a relatively high mortality rate despite the availability of systemic antimycotics, but it mainly affects patients with a weakened immune status. Rhinosporidiosis is another very rare disease caused by the spore-forming fungus Rhinosporidium seeberi. Highly vascular, friable granular lesions develop in the anterior portions of the nose and may spread to involve the paranasal sinuses and nasopharynx. Diagnosis: The diagnostic workup should include a detailed allergy history (do the symptoms present year-round or only during contact with certain animals or plants; do they disappear during vacation?). With seasonal allergic rhinitis, inspection of the nasal cavity typically reveals a bluish-purple discoloration of the mucosa (Fig. 3.35). With perennial rhinitis, the mucosa is bright red and shows inflammatory changes. Careful allergy testing (see 2.2, p.19) is necessary to identify the antigens involved. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 51
  • 61. 52 I Nose, Paranasal Sinuses, and Face Table 3.4 Drugs used in the treatment of allergic rhinitis Category Agent Dosage form Applications per day Comments Cromoglycate ED, NS 4 Agent of first choice Nedocromil ED, NS 2 Successor to cromoglycate 2. α-Sympathomimetic Xylometazoline NS 3 Only initially as an adjunct 3. Local H1 antagonists New, alternative to 1 Azelastine NS 2 ED, NS 2 1. Mast cell stabilizers Levocabastine 4. Local steroids Strong anti-inflammatory action (superior to groups 1 and 3) Mometasone NS 1–2 Triamcinolone acetonide NS 1–2 Fluticasone NS 1–2 Budesonide NS 2 Flunisolide NS 3 5. Systemic H1 antagonists Fexofenadine hydrochloride T 1–2 Also relieve conjunctival symptoms Nonsedating Levocetirizine T 1 Nonsedating Desloratadine T 1 Nonsedating Clemastine T, A 3 Sedating Ebastine T 1–2 Nonsedating Ipratropium bromide NS 2 Effective only for drainage 6. Anticholinergic A: ampules; ED: eye drops; NS: nasal spray; T: tablets (source: Grevers; see p. 430). Treatment: Fig. 3.35 Allergic rhinitis Middle turbinate Septum Inferior turbinate The best treatment strategy is to avoid contact with the allergen or eliminate allergenic irritants from the environment. Since the avoidance strategy is not always possible for practical reasons, most patients with allergic rhinitis receive pharmacologic treatment. The various drugs and their properties (mast-cell stabilizers, local and systemic H1 antihistamines, local steroids) are reviewed in Table 3.4. Further information on immunotherapy (hyposensitization) and surgical options can be found in 3.13. Typical endoscopic appearance of the nasal mucosa in allergic rhinitis. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 62. 3 Diseases of the Nose, Paranasal Sinuses, and Face 3.13 Long-term treatment options for allergic rhinitis In immunotherapy or hyposensitization therapy, a specially prepared antigen is administered subcutaneously to induce a systemic tolerance to the foreign protein. The disadvantages of this therapy include adverse effects, ranging from mild local reactions to severe systemic symptoms, a protracted course of treatment, and a significant percentage of nonresponders. Lately, however, there have been efforts to design a “brief immunotherapy” that will shorten the duration of treatment. If the response to conservative treatment is unsatisfactory and the principal complaint is nasal obstruction (i.e., hyperplasia of the nasal mucosa), surgical treatment is indicated. The main goal in these cases is to reduce the size of the turbinates by coagulation (turbinate cautery), laser treatment, or mucotomy (resecting a tissue strip from the lower edge of the inferior turbinate). If septal pathology is also present (septal deviation, septal spur or ridge), a concomitant septoplasty should be performed. With associated sinus complaints, endoscopic sinus surgery may also be required ( 3.16, p. 57). Vasomotor Rhinitis Vasomotor rhinitis resembles allergic rhinitis in its clinical features, but there is no evidence that the patient has been previously sensitized. The pathogenesis of vasomotor rhinitis is believed to involve neurovascular autonomic disturbances in regulating the tonus of the nasal mucosal vessels. The symptoms consist of obstructed nasal breathing, watery nasal discharge, and sneezing. The history shows that the symptoms are related to a temperature change, the consumption of hot liquid or alcohol, or less specifically to “emotional stress.” On inspection, the appearance of the nasal mucosa is similar to that in allergic rhinitis. Medical therapy includes the use of antihistamines or corticosteroid-containing nasal sprays. In the Kneipp system of therapy, ice-cold water is sniffed up the nose as a way of “training” the neuroautonomic regulation of the blood supply to the nasal mucosa. The last recourse for intractable vasomotor rhinitis is surgical reduction of the turbinates by electrocoagulation, laser ablation, or mucotomy, especially in cases with pronounced inferior turbinate hyperplasia. If significant septal deviation is present, a septoplasty should be performed. Atrophic Rhinitis Symptoms: Atrophic rhinitis is characterized by pronounced dryness of the nasal mucosa. Severe cases, especially with secondary bacterial colonization, are marked by a fetid nasal odor that is not perceived by the patient due to degeneration of the olfactory epithelium. The etiology of primary atrophic rhinitis is unknown. Secondary forms can have various causes including an extensive prior tumor resection, the excessive use of nose drops, drug abuse (cocaine), or previous radiotherapy for nasal and sinus tumors. Iatrogenic causes include a botched septoplasty or an excessive turbinate reduction (conchotomy). Endoscopic examination reveals a broad nasal cavity lined with dry, crusted mucosa. Treatment should begin with conservative, symptomatic measures (saline “nasal douche,” soothing mucosal ointments). Under no circumstances should decongestant nose drops be used, as the vasoconstriction would exacerbate the patient’s symptoms. If conservative treatments prove inadequate, an attempt can be made to reduce the nasal cavity surgically by the submucous implantation of cartilage grafts. This creates a relative increase in surface area in relation to the volume of the nasal cavity. Hormonal Rhinitis Synonym: pregnancy-associated rhinitis Hormonal rhinitis occurs mainly during pregnancy and is believed to be caused by estrogen-induced swelling of the mucosa with nasal airway obstruction. The symptoms diminish as term approaches and disappear after the delivery. Rhinitis Medicamentosa This disease occurs mainly as a side effect from the long-term use of decongestant nose drops. It can also result from the use of certain antihypertensive drugs—e.g., rauwolfia alkaloids, beta-blockers, angiotensin-converting enzyme (ACE) inhibitors—and from oral contraceptive use, in which case the rhinitis is attributed to a vasoactive estrogen effect. Clinical symptoms consist of obstructed nasal breathing, dry mucosa, and occasional olfactory disturbances. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 53
  • 63. 54 I Nose, Paranasal Sinuses, and Face 3.8 Sinus Inflammations Sinus inflammations (sinusitis) generally develop in association with rhinitis, and so the term “rhinosinusitis” is often applied to these disorders. Despite the continuum that exists between rhinitis and sinusitis, they are discussed as separate entities in this textbook for teaching purposes. Inflammations that are Acute Sinusitis Etiopathogenesis: While acute sinusitis in children predominantly affects the ethmoid cells due to incomplete pneumatization of the other sinuses (see 1.1, p. 4), acute sinusitis in adults affects the following sinuses in descending order of frequency: maxillary sinus, ethmoid cells, frontal sinus, and sphenoid sinus. The inflammation may involve one, several, or all of the paranasal sinuses (pansinusitis). Acute sinusitis generally results from the spread of an intranasal inflammation (rhinitis), since the mucosa of the paranasal sinuses communicates with that of the nasal cavity (rhinogenic sinusitis). Accordingly, the causative viruses of acute rhinitis (see p. 49) are etiologically important in addition to the common bacterial organisms Haemophilus influenzae and Streptococcus pneumoniae. Although rhinitis has a very marked tendency to involve the contiguous sinus mucosae, acute rhinitis does not invariably lead to symptomatic sinusitis. The extent of the inflammation in the sinus system and the associated symptoms depend on various factors: • Individual functional anatomy (see Chapter 1, p. 2) • Individual immune status • Specific virulence of the causative organism Besides rhinogenic sinusitis, there are also rare instances of dentogenic sinusitis arising from a dental root infection, an apical granuloma, or a maxillary sinus fistula following a tooth extraction ( 3.14). Symptoms: The clinical picture is marked by the features of acute rhinitis combined with a variable degree of headache, which is exacerbated by bending over. Generally the pain is most intense over the affected sinuses (see also Fig. 1.6, p. 6). Thus, the pain of maxillary sinusitis is greatest over the maxillary sinus and the adjacent midface and temple. Ethmoid sinusitis is most painful over the bridge of the nose and the medial canthus of the eye, and frontal sinusitis over the anterior wall and floor of the frontal sinus, with pain radiating toward the medial canthus. The pain of sphenoid sinusitis is fairly nonspecific, confined chiefly to the nasal cavity are covered in the previous . This unit deals with acute and chronic sinusitis in addition to nasal polyposis, mucoceles, pyoceles, and rhinosinogenic complications—diseases in which clinical symptoms arising from the paranasal sinuses are the dominant features. 3.14 Special forms of sinusitis Other forms are nosocomial sinusitis resulting from prolonged nasal intubation, barosinusitis caused by pressure changes during flying or diving, and swimmer’s sinusitis caused by the entry of infectious micro-organisms into the sinus during swimming. marked by a dull, aching pressure located at the center of the skull and radiating to the occiput. Diagnosis: Rhinoscopy or nasal endoscopy often reveals pus tracking along the middle meatus of the nasal cavity (Fig. 3.36), but a purulent track may not be seen if the mucosa is greatly swollen. With isolated sphenoid sinusitis, pus may be found about the ostium in the anterior wall of the sphenoid sinus or on the posterior wall of the pharynx. Sinus radiographs (see also Fig. 2.7, p. 22) may show partial opacification of the affected sinus due to mucosal swelling (Fig. 3.37 a) or may demonstrate a fluid level if the sinus contains free pus (Fig. 3.38). An alternative to radiography, especially for follow-up and in children and pregnant women, is ultrasonography (Amode or B-mode), which avoids radiation exposure. Treatment: Conservative treatment options should be exhausted before surgery is considered. The latter may be necessary in cases where the complaints of acute sinusitis do not respond to conservative treatment modalities and in cases with persistent sinus empyema. Conservative therapy: Ventilation and drainage of the paranasal sinuses can be improved by the use of decongestant nose drops, nasal spray, or by inserting a cotton pack soaked with nose drops into the middle meatus. In more severe forms associated with fever and significant malaise, antibiotics (e.g., amoxicillin) should be administered. Heat therapy (electric light bath) and the inhalation of chamomile or sage are recommended as adjuncts. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 64. 3 Diseases of the Nose, Paranasal Sinuses, and Face Fig. 3.36 Acute sinusitis Fig. 3.39 Complication after sharp puncture of the maxillary sinus Middle turbinate Septum Inferior turbinate Ethmoid cells A purulent track (arrows) is visible in the middle meatus of the left nasal cavity. Fig. 3.37 Acute maxillary sinusitis a b Occipitomental radiographs of the paranasal sinuses. a Prior to antibiotic therapy, the radiograph shows partial opacification of the left maxillary sinus (arrows). b Follow-up after the conclusion of treatment. Fig. 3.38 Acute ethmoid sinusitis Coronal computed tomography shows diffuse opacification of the left maxillary sinus and left anterior ethmoid bone. The orbit contains two small air bubbles (arrows) signifying perforation of the maxillary sinus roof. Surgical therapy: Maxillary sinusitis can be treated by maxillary sinus puncture following decongestion and topical anesthesia of the nasal mucosa. Two approaches are available: first, “sharp puncture” through the inferior meatus, passing the needle below the inferior turbinate; and second, “blunt puncture” via the natural maxillary sinus ostium in the middle meatus. In the sharp puncture technique, there is a significant risk of complications due to air embolism if air is inadvertently injected into the sinus after a medication has been instilled. Another potential danger is perforation of the lateral sinus wall, resulting in a buccal abscess or perforation of the sinus roof causing infection of the orbital contents (Fig. 3.39). A frontal sinus empyema can be surgically drained through a “Beck puncture” ( 3.15). There should be little hesitation in using this procedure, since the frontal sinus directly borders the cranial cavity, posing a risk of meningoencephalitis or frontal brain abscess. Occipitofrontal sinus radiograph demonstrates a fluid level (arrow) in the left ethmoid labyrinth. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 55
  • 65. 56 I Nose, Paranasal Sinuses, and Face 3.15 Diagnosis: Rhinoscopy, endoscopy: The nasal cavity is inspected by rhinoscopy or endoscopy, giving particular attention to changes in the nasal septum, the condition of the turbinates (turbinate hyperplasia, pneumatized middle turbinate, concha bullosa), and the appearance of the ostiomeatal unit (mucosal swelling, polyps, tumors, etc., see also 1.3, p. 7). Other causes of impaired ventilation and drainage in the nasal cavity itself (e.g., tumors) should also be excluded. Frontal sinus irrigation For the Beck puncture, the skin and subcutaneous soft tissues are divided at the medial border of the eyebrow, and the anterior wall of the frontal sinus is opened with a drill. Secretions and pus are aspirated from the frontal sinus, and the sinus is irrigated with decongestant nose drops and an antibiotic solution. Chronic Sinusitis Etiopathogenesis: Besides intranasal anatomic changes such as septal deviation and septal spurs, a variety of other diseases of a chronic inflammatory, allergic, traumatic or neoplastic nature can lead to chronic sinusitis. The common pathogenic mechanism is impaired ventilation of the ostiomeatal unit (see 1.3, p. 7) due to stenosis or obstruction of this region. This hampers drainage of the dependent sinus systems, particularly the adjacent maxillary sinus and anterior ethmoid cells. As the mucosa becomes swollen, especially in the narrow anatomical passages of the ostiomeatal unit, a vicious cycle becomes established that initially leads to recurrent bouts of acute inflammation and eventually culminates in a persistent, chronic sinusitis. Chronic sinusitis frequently affects the maxillary sinus and ethmoid cells, while the frontal and sphenoid sinuses are less commonly involved. Imaging studies: Today, computed tomography is considered the only acceptable modality for imaging the paranasal sinuses if chronic sinusitis ist suspected. Conventional sinus radiographs are of very limited value in diagnosing chronic sinusitis due to artifacts from superimposed structures. Also, only CT scans can accurately define the key anatomic structures that are important for accurate preoperative planning (Fig. 3.40). Treatment: Conservative treatment options include decongestant nose drops (for no more than one week), heat therapy (electric light cabinet, microwaves, infrared), and broad-band antibiotics (e.g., amoxicillin) for acute exacerbations of sinusitis with fever and malaise. Mucolytics can also be administered for supportive therapy. With an allergic etiology, appropriate antiallergic therapy should also be provided (see p. 52). All of these conservative therapies are of symptomatic benefit and cannot eliminate the cause of chronic sinusitis. The only definitive treatment is sinus surgery ( 3.16). Symptoms: The character of the pain is variable and can range from a feeling of pressure to persistent or recurrent headaches. Many patients also complain of nasopharyngeal drainage (postnasal drip), and some complain of obstructed nasal breathing. Fig. 3.40 Chronic sinusitis a b Middle turbinate Septum Septal spur Inferior turbinate a Septal deviation with a prominent septal spur have caused narrowing of the left nasal cavity. b Corresponding coronal computed tomography also demonstrates the marked septal deviation and ridges. The opacifica- Septal deviation and ridges Left ethmoid labyrinth tion of the left ethmoid labyrinth reflects the chronic inflammation resulting from impaired ventilation and drainage of the middle meatus and ostiomeatal unit. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 66. 3 Diseases of the Nose, Paranasal Sinuses, and Face 3.16 Endoscopic sinus surgery The modern surgical treatment of chronic sinusitis is performed intranasally under endoscopic or microscopic control. The principle of endoscopic sinus surgery is to enlarge the tight passages in the middle meatus and ostiomeatal unit including the natural ostia of the maxillary sinus and, if necessary, the frontal sinus. A preliminary septoplasty may be necessary in patients with functionally significant septal deviation (Fig. 3.40 a). The hazards of intranasal sinus surgery are based mainly on the close proximity of the sinuses to the anterior cranial fossa, optic nerve, and (in the case of the sphenoid sinus) to the internal carotid artery. The prerequisites for any type of intranasal sinus surgery, then, are a detailed knowledge of sinonasal anatomy and technical proficiency in handling the endoscope or microscope, which should be gained in diagnostic procedures and by practice on anatomic specimens. The surgeon should also be well versed in the radiographic anatomy of this region. Nasal Polyposis Pathogenesis and morphology: Nasal polyposis is a very complex condition that develops in response to a variety of noxious stimuli, appearing morphologically as edematous, polypoid hyperplasia of the sinus mucosa (usually in the anterior ethmoid cells and maxillary sinus) and projecting into the nasal cavity in the form of polyps (Fig. 3.41). Etiology: Besides genetic causes, nasal polyps are attributed mainly to chronic irritation of the mucosa, like that occurring in chronic rhinitis or sinusitis. They can also form in response to allergic rhinitis and acetylsalicylic acid (ASA) intolerance (ASA pseudoallergy). The functional anatomy of the ostiomeatal unit, with its slitlike passages, appears to have causal significance in nasal polyposis, as in chronic sinusitis, because it controls the ventilation and drainage of the frontal and maxillary sinuses. The opposing mucosal surfaces in these areas are often separated by a distance of less than 1 mm. If they come into contact, this will impair the mucociliary clearance mechanism and hamper the normal transport of harmful substances toward the nasopharynx. Most polyps form at these narrow passages. Whether, when, and to what extent these pathologic changes lead to symptomatic polyposis varies in different individuals and may depend partly on the timing of diagnosis and treatment. Nasal polyps are rarely observed in children. Most occur in a setting of cystic fibrosis. Fig. 3.41 Nasal polyposis Middle turbinate Septum Polyp Inferior turbinate A nasal polyp has prolapsed from the middle meatus into the main part of the left nasal cavity. Symptoms: The clinical manifestations of nasal polyps depend on their extent and may consist of obstructed nasal breathing, hyposmia or anosmia (due to obstruction of the olfactory groove), headache (due to impaired ventilation and drainage in the paranasal sinuses), snoring, rhinophonia clausa, and frequent throat clearing due to associated postnasal drainage. Spread to the lower airways can lead to laryngitis with hoarseness and bronchitic symptoms. Diagnosis: As in chronic sinusitis, the diagnosis is established by careful rhinoscopic or endoscopic evaluation of the nasal cavity, giving particular attention to the lateral nasal wall. The imaging modality of choice is computed tomography. Further diagnostic measures consist of allergy tests and olfactory testing. Treatment: Treatment may begin with symptomatic conservative measures such as the use of corticoidcontaining nasal sprays and systemic antihistamines. Systemic steroids may also be tried. A partial or even complete remission of nasal polyps can sometimes be achieved with these measures alone. Many cases will require surgical treatment, however. Besides intranasal polypectomy, which is performed mainly in older or higher-risk patients, an important current option is intranasal sinus surgery using endoscopic or microsurgical technique (see also Treatment of Chronic Sinusitis, p. 57). Prognosis: Given the complex and poorly understood etiopathogenesis of nasal polyposis, which is not considered a single entity, the prognosis is guarded even with modern surgical techniques, and even the Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 57
  • 67. 58 I Nose, Paranasal Sinuses, and Face 3.17 Primary ciliary dyskinesia Fig. 3.42 Frontal sinus mucocele A frontal sinus mucocele appears as a rounded bulge in the anterior wall of the sinus (arrows). Primary ciliary dyskinesia is an autosomal-recessive disease characterized by morphologic changes in the cilia (absence of dynein arms, transposition of microtubules), leading to a marked reduction in beat frequency and dyskinetic ciliary movements that are ineffectual for mucus transport. The impaired function of the mucociliary apparatus is manifested by symptoms of primary ciliary dyskinesia, which consist mainly of recurrent sinusitis and nasal polyposis, eustachian tube catarrh, otitis, bronchitis, and bronchiectasis. Life expectancy in affected patients depends mainly on the severity of pulmonary involvement. most meticulous ablative sinus surgery cannot prevent a recurrence. As a result, there is often no alternative to long-term medical prophylaxis with topical steroid sprays. Mucoceles and Pyoceles A mucocele is a cystlike, mucus-containing sac that can form within a paranasal sinus. A pyocele is a mucocele that contains purulent material as a result of superinfection. Pathogenesis: A mucocele may be caused by adhesions (postinflammatory, post-traumatic, or postoperative) that obstruct drainage from the paranasal sinus system. Mass lesions (polyps, tumors) can also obstruct and obliterate the drainage tracts, leading to mucocele formation. The outflow obstruction causes the mucocele to exert increasing pressure on the surrounding sinus walls, resulting in progressive thinning of the bone. In this way the mass can erode into adjacent structures such as the orbit or even the cranial cavity. The most common site of occurrence is the frontal sinus, followed by the ethmoid cells, maxillary sinus, and sphenoid sinus. Symptoms: A frontal sinus mucocele usually presents as an isolated, tense swelling over the anterior wall of the frontal sinus (Fig. 3.42). It may also cause inferolateral displacement of the orbital contents, especially if it has eroded through the sinus floor. On the other hand, swelling in the cheek area with upward displacement of the orbital contents is more characteristic of a maxillary sinus mucocele (Fig. 3.43 a). Proptosis, limited ocular movements, and diplopia may also occur, depending on the location of the mass. Unlike mucoceles in the frontal sinus, ethmoid cells (Fig. 3.44) and maxillary sinus, sphenoid sinus mucoceles (Fig. 3.45) often have nonspecific clinical manifestations, with complaints similar to those of sphenoid sinusitis (headache radiating to the vertex and occiput). Diagnosis: A prior surgical history is often helpful in making a diagnosis. The clinical appearance may also be suggestive (Fig. 3.42, Fig. 3.43 a), whereas inspection of the nasal cavity by rhinoscopy or endoscopy usually does not advance the diagnosis. On the other hand, modern sectional imaging modalities (computed tomography and magnetic resonance imaging, Fig. 3.43 b, Fig. 3.44, Fig. 3.45) can make it possible to delineate the mucocele from surrounding tissues and differentiate it from a malignant tumor. Treatment: The treatment of choice is surgical removal of the mucocele. Rhinosinogenic Complications There are various mechanisms by which serious and even life-threatening complications can arise from inflammatory diseases of the paranasal sinuses. Complications with inflammatory involvement of the orbit (orbital complications) are distinguished clinically from bone and soft-tissue complications (osteomyelitis) and from intracranial complications. Orbital Complications Inflammatory complications with orbital involvement most commonly arise from the ethmoid cells or frontal sinus and less commonly from the sphenoid or maxillary sinus. They occur with highest frequency in children under 6 years of age. Four different clinical grades of severity are distinguished, requiring a graded therapeutic approach. Ophthalmologic consultation should be obtained. Orbital edema: The initial stage is marked by a doughy swelling and erythema of the eyelids (Fig. 3.46). Ocular mobility is normal, and the globe itself is not dis- Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 68. 3 Diseases of the Nose, Paranasal Sinuses, and Face Fig. 3.43 Maxillary sinus mucocele a Fig. 3.44 Ethmoid mucocele a Mucocele b b Mucocele Orbital contents Mucocele a A mucocele of the right maxillary sinus has caused upward displacement of the orbital contents. b Corresponding coronal computed tomography demonstrates the sac protruding through the orbital floor. placed. The differential diagnosis should include dacryocystitis, the most common disease of the lacrimal sac, which is characterized by tenderness, erythema, and accompanying edema at the medial canthus of the eye. The treatment of choice is conservative and relies on nose drops (which may be applied in an intranasal cotton pack; see Treatment of Acute Sinusitis, p. 55) and antibiotics. Corticosteroids may also be administered if required. Periosteitis: While lid edema persists, pain develops at the medial canthus of the eye. Conservative medical treatment is still adequate at this stage in most cases. Subperiosteal abscess: The inflammatory process has penetrated the bony barrier between the paranasal sinus and orbit, separating the orbital periosteum from the lamina papyracea and raising the pressure within the orbit. This stage is marked by an initial limitation of ocular movement with associated proptosis. Chemosis may already be present in exceptional cases. The treatment of choice is surgical drainage of the abscess, which today is done endoscopically. Nose drops and antibiotics are also administered. Ophthalmo- An ethmoid mucocele on the left side has displaced the orbital contents laterally. Coronal (a) and axial (b) computed tomography scans. logic consultation is advised for medicolegal reasons. Orbital cellulitis: The final stage of orbital complications is associated with proptosis and limited eye movements, pain, chemosis, and visual deterioration or even blindness. Orbital cellulitis is a life-threatening emergency that requires immediate surgical decompression. This should be done with antibiotic coverage, as for a subperiosteal abscess. An “orbital apex syndrome” can develop when the cellulitis spreads to involve the anatomic structures at the orbital apex (cranial nerves II–VI, ophthalmic Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 59
  • 69. 60 I Nose, Paranasal Sinuses, and Face Fig. 3.45 Sphenoid sinus mucocele Mucocele Bone and Soft-Tissue Inflammations (Osteitis and Osteomyelitis) Osteomyelitis occurs mainly as a complication of frontal sinusitis when the bacterial inflammation spreads to the bony anterior wall of the frontal sinus, the frontal bone, and the surrounding soft tissues. The main danger of frontal osteomyelitis is that the infection may spread to other bony structures of the calvaria. Symptoms: The patient presents clinically with a tender, doughy, erythematous swelling over the forehead (Fig. 3.47). The surrounding facial soft tissues are also involved in most cases. Diagnosis: Cranial CT scans should always be obtained to define the extent of the inflammation. A sagittal magnetic resonance image demonstrates a sphenoid sinus mucocele. Fig. 3.46 Orbital edema Treatment: The treatment of choice is surgical eradication of the affected bone under antibiotic coverage. Bone affected by inflammatory changes should be generously resected to prevent the further spread of inflammation. Intracranial Complications Intracranial complications also arise from the frontal sinuses in most cases. The ethmoid cells and sphenoid sinus are a more frequent nidus for these complications in children due to their lack of aeration. A rhinosinogenic inflammation has spread to the orbit. The initial stage is marked by orbital edema on the left side with an erythematous, doughy swelling of the upper and lower lids. artery and vein). Progressive thrombophlebitis can also lead to cavernous sinus thrombosis and other intracranial complications (see below). Epidural, subdural and intracerebral abscesses: The clinical manifestations of these lesions are frequently nonspecific. As the disease progresses, it may produce signs of increased intracranial pressure with nausea, headache, vomiting, and occasional papilledema, somnolence, or seizures. The diagnosis relies critically on computed tomography (Fig. 3.48) or magnetic resonance imaging (Fig. 3.49) due to the nonspecific clinical features. The treatment of choice for the various types of abscess is surgical drainage with high-dose antibiotic coverage. Meningitis: The main clinical manifestations are stiff neck, headache, fever, nausea, and photophobia. Some cases show increasing somnolence and clouding of consciousness, and seizures are occasionally observed. Cranial CT scans should be obtained whenever meningitis is suspected, particularly to exclude an intracranial abscess. The neurologist confirms the diagnosis by CSF sampling. In rhinogenic meningitis and with other forms, treatment relies mainly on surgical drainage of the affected sinuses under antibiotic coverage. Neurologic therapies may also be indicated (e.g., in patients prone to seizures). Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 70. 3 Diseases of the Nose, Paranasal Sinuses, and Face Fig. 3.47 Osteomyelitis of the frontal bone Fig. 3.48 Epidural abscess Typical features are a doughy swelling over the forehead with concomitant soft-tissue swelling, especially about the eyelids on both sides. Sinus Thrombosis and Thrombophlebitis These complications, while rare, can lead to permanent neurologic deficits if diagnosed too late. They can be fatal in extreme cases. Cavernous sinus thrombosis may present clinically with orbital edema, signs of venous congestion in the optic fundus (ophthalmologist!), chemosis, and occasional diplopia and proptosis with limited ocular movements. Magnetic resonance imaging should be performed and will often show definite evidence of sinus thrombosis. If magnetic resonance imaging (MRI) is unrewarding in patients with suggestive clinical signs, digital subtraction angiography (DSA) should be performed. As with all other intracranial complications, treatment consists of surgical drainage under antibiotic coverage. Axial CT scan of an epidural abscess (arrows), which has developed as an intracranial complication of frontal sinusitis. Fig. 3.49 Rhinosinogenic brain abscess a b Coronal (a) and sagittal (b) magnetic resonance images of a pediatric rhinosinogenic brain abscess originating from the right frontal sinus. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 61
  • 71. 62 I Nose, Paranasal Sinuses, and Face 3.9 Tumors of the External Nose and Face The majority of facial tumors are malignancies, consisting mainly of basal cell carcinomas and spindle cell carcinomas. Other malignant neoplasms, precancer- ous lesions, and benign tumors are much less common in this region. Benign Tumors Fig. 3.50 Rhinophyma The most important benign facial tumor is rhinophyma (Fig. 3.50 a), a connective-tissue and sebaceous hyperplasia with angiectatic changes occurring over the cartilaginous nose. Most patients have preexisting rosacea, and so concomitant erythema is usually present. Although rosacea is more common in women than men, usually begins after age 20 and has a peak incidence at 40–50 years of age, rhinophyma is seen almost exclusively in older men. The differential diagnosis should include the cutaneous manifestations of lymphatic leukemia, cutaneous T-cell lymphoma, and sarcoidosis. The treatment of choice is surgical ablation of the hyperplastic tissue in layers, allowing the wound area to heal by spontaneous epithelialization (Fig. 3.50 b). a b Typical clinical appearance of rhinophyma before and after ablation of the hyperplastic tissue areas. Basal Cell Carcinoma Precancerous Lesions Synonym: basaloma Besides actinic keratosis and Bowen’s disease, a chronic skin inflammation caused by carcinoma in situ, precancerous lesions include cutaneous horn and malignant lentigo. The latter is attributed to chronic sun exposure, grows slowly, and may progress to malignant melanoma. Epidemiology: Basal cell carcinoma has a peak incidence between 60 and 70 years of age but may be seen in patients as young as 40. Precancerous lesions of the facial skin should be watched closely, as they may progress to a malignant tumor. Details on these precancerous lesions, which are generally rare, can be found in textbooks of dermatology. Malignant Tumors The most common facial malignancies are of epithelial origin, predominantly basal cell carcinomas and squamous cell carcinomas (spindle cell carcinomas). By contrast, melanomas, sarcomas, lymphomas, and cutaneous infiltration by leukemia are relatively rare in the facial region. Etiology: Uncertain. In addition to a genetic predisposition, prolonged sun exposure in people with very sun-sensitive skin appears to have causal significance. Clinical manifestations: The tumor is classified as a malignant neoplasm because of its local invasiveness, but it has no tendency to metastasize. Basal cell carcinomas can vary greatly in their morphologic features. Solid basalomas are particularly rare in the facial region; they show central crusting and a stringof-beads margin (Fig. 3.51). Diagnosis and treatment: After the diagnosis is confirmed by biopsy, treatment consists of surgical excision with frozen-section control of all margins. A special form, sclerodermiform basaloma, irregularly infiltrates the surrounding skin and often has illdefined gross margins. This can lead to problems of surgical excision, as the size of the defect is often underestimated preoperatively. Following tumor removal with a margin of healthy tissue, the surgical defect is reconstructed in the same sitting (see 3.4, p. 36). Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 72. 3 Diseases of the Nose, Paranasal Sinuses, and Face Fig. 3.51 Basal cell carcinoma Fig. 3.52 Spindle cell carcinoma of the nose a Before surgery b 1 month after surgery c 4 months after first operation d 1 year after first operation Typical clinical appearance of the lesion. Spindle Cell Carcinoma Synonym: spinalioma Epidemiology: Spindle cell carcinoma (Fig. 3.52 a) is the second most common malignant tumor of the external nose and also tends to occur in older individuals. Etiology: The etiology is uncertain, but it is very likely that exposure to ultraviolet radiation has causal significance. a Preoperative clinical appearance. b Following tumor resection and reconstruction with a midline forehead flap. c Following division of the midline forehead flap and replacement of the flap pedicle. d Final result. The principle of this operation is shown in Fig. 3.11 on p. 38. Clinical manifestations: Unlike basal cell carcinoma, spindle cell carcinoma is a “classic” malignant tumor in that it can metastasize to regional lymph nodes. Treatment: Treatment consists of surgical tumor removal. Various plastic reconstructive techniques can be used, depending on the location and size of the defect (Fig. 3.52 a–d and Figs. 3.9–3.14, p. 36). Patients with regional lymph-node metastases should undergo a neck dissection in the same sitting, followed by postoperative radiotherapy. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 63
  • 73. 64 I Nose, Paranasal Sinuses, and Face 3.10 Tumors of the Nasal Cavity and Paranasal Sinuses Benign tumors of the nasal cavity and paranasal sinuses are relatively rare. Malignancies of this region occur mainly in older patients and, since they develop in preexisting cavities, may remain asymptomatic for years. Benign Tumors tomography (Fig. 3.53 b) is the imaging modality of choice for the accurate localization of osteomas. Besides epithelial and connective-tissue neoplasms, benign intranasal and sinus tumors may arise from smooth muscle, peripheral nerves, or blood vessels. Inverted Papilloma Sinonasal papillomas, especially inverted papillomas, constitute a special category of epithelial masses. The inverted papilloma has certain characteristics that still prompt discussion on its etiology and appropriate management. It is a locally aggressive tumor, and transformation to squamous cell carcinoma is periodically described. Its growth characteristics resemble those of various virus-induced cutaneous and mucosal lesions (e.g., warts, condylomas, laryngeal papillomas). But while a viral etiology has been discussed, it remains unproved. Symptoms and diagnosis: The clinical manifestations of inverted papilloma are as nonspecific as those of other sinonasal tumors and include nasal airway obstruction, headache, and occasional epistaxis. The lesion often has a polyp-like appearance when inspected by nasal endoscopy. In many cases only histologic examination can establish the diagnosis. Imaging (computed tomography) is helpful in defining the tumor extent. Treatment: The treatment of choice is surgical removal. The special growth characteristics of this tumor require adequate exposure to allow for complete removal. Osteomas Osteomas are benign bone tumors that may occur as isolated masses, especially in the ethmoid cells and frontal sinus, or may form extensive masses that grow along the skull base (Fig. 3.53). Symptoms and diagnosis: Many of these tumors are detected incidentally on x-ray films of the skull (Fig. 3.53 a). Often they do not become symptomatic until they obstruct drainage tracts to or from the paranasal sinuses, leading secondarily to headaches and recurrent bouts of sinusitis. Computed For medicolegal and other reasons, it is essential to define the relationship of the osteoma to the skull base and other landmarks prior to surgical treatment. Treatment: As soon as an osteoma becomes symptomatic, it should be surgically removed. Otherwise there is no need for therapeutic intervention. Malignant Tumors Malignant tumors of the nasal cavity and paranasal sinuses are far more common than benign masses. Histologically, the great majority (> 80%) are tumors of the epithelial series (e.g., squamous cell carcinoma, adenocarcinoma, adenoid cystic carcinoma). Neoplasms of mesenchymal origin, such as osteosarcomas and chondrosarcomas, as well as malignant lymphomas are much less common. Metastases from other malignancies are occasionally found, with the primary tumor residing in the kidney, lung, breast, testis, or thyroid gland. The main sites of predilection are the nasal cavity and maxillary sinus, followed by the ethmoid cells, frontal sinus, and sphenoid sinus. Symptoms: Because many tumors originate in the paranasal sinuses themselves, they often do not produce clinical manifestations until they have reached an advanced stage. Symptoms that are suspicious for malignancy include sudden onset of obstructed nasal breathing combined with bloody rhinorrhea and a fetid nasal odor, especially in patients over 50 years of age. A malignant tumor should also be considered in the differential diagnosis of unilateral sinusitis that is refractory to treatment. Advanced tumor stages may be marked by swelling of the buccal soft tissues, swelling at the medial canthus of the eye, headache, facial pain, and hypoesthesia or numbness of the cheek due to infraorbital nerve involvement. Orbital infiltration can lead to displacement of the orbital contents, diplopia, or proptosis. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 74. 3 Diseases of the Nose, Paranasal Sinuses, and Face Fig. 3.53 Osteoma a b a Anteroposterior skull radiograph demonstrates a mass of osseous density in the ethmoid labyrinth (arrows). b Computed tomography defines the relationship of the lesion (arrows) to neighboring structures with much greater clarity. Diagnosis: The clinical examination includes endoscopic inspection of the nasal cavity (Fig. 3.54) and a search for regional lymph-node metastases by bimanual palpation of the cervical soft tissues. Since sinus tumors are apt to invade the nasal cavity secondarily, endoscopy alone may provide little information on the extent of the mass. For this reason, computed tomography and/or magnetic resonance imaging should always be performed (Fig. 3.55) and should cover the cervical soft tissues to check for nodal metastases. The disease can be staged based on the results of the examination. The principles of sinonasal tumor staging are outlined in Table 3.5. Fig. 3.54 Squamous cell carcinoma of the anterior ethmoid Treatment: Treatment is individualized according to the histology and extent of the malignant tumor, and the treatment plan should be coordinated with the radiotherapist and medical oncologist. Since the great majority of lesions are squamous cell carcinomas, however, the treatment of choice will usually consist of surgery and postoperative radiation (Fig. 3.56). The goal of radical tumor removal may require a very extensive procedure with partial or complete removal of the maxilla or partial resection of the anterior skull base. As a result of close interdisciplinary cooperation with neurosurgeons, maxillofacial surgeons and ophthalmologists, as well as modern intensive-care options, even very extensive sinonasal malignancies can now be managed by surgical treatment. Since only about 20% of sinonasal malignancies metastasize to regional lymph nodes, a neck dis- Nasal septum Tumor A blood-tinged mass is visible in the right middle meatus between the middle turbinate and lateral nasal wall. The true extent of the tumor cannot be determined from the endoscopic findings alone. section is necessary only in patients who have clinically positive cervical nodes. Many of these cases will require postoperative radiotherapy ( 3.18). Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 65
  • 75. 66 I Nose, Paranasal Sinuses, and Face Fig. 3.55 Imaging of malignant sinonasal tumors a b Orbital contents Tumor c d Tumor a Coronal computed tomography with a bone window demonstrates an extensive sinonasal carcinoma with sites of bone destruction in the anterior skull base and orbit (arrows). b Coronal magnetic resonance (MR) imaging in the same plane more clearly demonstrates the soft-tissue relationship of the tumor to the brain tissue and orbital contents. c Sagittal MR image. d Axial MR image. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. Tumor
  • 76. 3 Diseases of the Nose, Paranasal Sinuses, and Face Fig. 3.56 Melanoma of the nasal cavity and maxillary sinus a b Nasal cavity Maxillary sinus 3.18 Esthesioneuroblastoma Esthesioneuroblastoma is a rare neurogenic malignancy that arises from the sensory cells of the olfactory region and generally occurs in adults. Its etiology is still uncertain, but it is believed that some cases are embryogenically induced. Clinically, esthesioneuroblastoma remains asymptomatic for some time due to its location in the olfactory groove between the upper portions of the nasal septum and the attachment of the middle turbinate. When advanced, the tumor causes obstructed nasal breathing, recurrent epistaxis, and particularly hyposmia or anosmia. Some of these tumors become symptomatic only after invading the cranial cavity or orbit, causing headache or visual deterioration. In a few cases, cervical lymph-node metastases are the primary manifestation of the disease. Diagnosis is based on endoscopy (see image below) and especially computed tomography or magnetic resonance imaging; only these modalities can accurately define the tumor extent. Treatment is based on a combination of tumor resection and postoperative radiotherapy. Tumor Middle turbinate c Septum Table 3.5 Principles for the staging of sinonasal tumors Regions Nasal cavity Upper level Maxilloethmoid angle, ethmoid cells, sphenoid sinus, frontal sinus Inferior, superior and medial portions of maxillary sinus Tumor stage Tumor extent Example: maxillary sinus carcinoma T1 1 subregion Floor of maxillary sinus T2 > 1 subregion or 1 region Floor and medial portion of maxillary sinus T3 Invasion of adjacent region Invasion of nasal cavity T4 a The tumor extends into the nasal vestibule, where it is visible to external inspection. b Corresponding axial computed tomography shows tumor tissue occupying the right maxillary sinus and nasal cavity. c At surgery, the tumor is exposed and resected through a lateral rhinotomy. Nasal floor and roof Midlevel Tumor Subregions Tumor crosses organ boundaries Skull base, cranial nerves, orbit, sphenoid sinus, frontal sinus, skin* * Tumor involves at least one of the regions listed. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 67
  • 77. 4 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 78. II Oral Cavity and Pharynx 4 5 6 Pharynx and Esophagus The Salivary Glands Lips and Oral Cavity 4.1 Basic Anatomy and Physiology of the Lips and Oral Cavity 70 Anatomy 70 Physiology 74 4.2 Methods of Examining the Lips and Oral Cavity 76 Visual Inspection 76 Palpation 76 Taste Testing 76 Imaging Procedures 76 4.3 4.4 Inflammations of the Lips and Oral Cavity 80 Viral Infections 80 Bacterial and Fungal Infections 84 Superficial Tongue Lesions 86 Angioedema 87 Immunologic Diseases 87 4.5 Tumors of the Lips and Oral Cavity 90 Benign Tumors 90 Precancerous Lesions 90 Malignant Tumors 90 Malformations of the Lips and Oral Cavity 78 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 79. 70 II Oral Cavity and Pharynx 4.1 Basic Anatomy and Physiology of the Lips and Oral Cavity The lips and the soft tissues of the cheek function as the outer boundary of the oral vestibule and oral cavity, which form the initial part of the digestive tract. The tongue is situated such that the body of the tongue is within the oral cavity, while the base (root) of the tongue is in the oropharynx, forming its anterior boundary. For learning purposes, however, the tongue as a whole is included in the chapter on the oral cavity. Functionally, the lips and oral cavity comprise the initial part of the upper digestive tract and thus play a key role in food ingestion. Speech production additionally developed during the course of phylogenesis. Finally, a large percentage of the taste receptors are located in the oral cavity. Anatomy Knowledge about the lymphatic drainage of the lips is important for understanding the lymphogenous metastasis of malignant tumors of the lips. The submandibular and submental lymph nodes receive the lymphatic drainage from the lips. The upper lip receives its sensory innervation from the infraorbital nerve, the lower lip from the mental nerve. Oral Vestibule The oral vestibule is bounded externally by the lips and cheeks and internally by the alveolar processes and teeth (Fig. 4.1). When the teeth are in occlusion, the oral vestibule communicates with the oral cavity via a space behind the last molar. The oral cavity opens into the pharynx at the faucial isthmus (see 5.1, p. 98). Lips and Cheeks The lips and cheeks, the morphologic framework of which is formed largely by the mimetic muscles, are lined on their mucosal side by nonkeratinized squamous epithelium. Lips: The longer upper lip and shorter lower lip are connected to each other by the labial commissures at the corners of the mouth. The lips are separated from the cheek by the nasolabial fold, an oblique sulcus that runs laterally and inferiorly from the nasal alae. The lamina propria of the lips contains numerous seromucous salivary glands (see Fig. 6.2, p. 133), the secretions from which drain into the oral vestibule. The orbicularis oris muscle forms the muscular foundation of the lips (Fig. 4.2). The lips receive their blood supply from the superior and inferior labial arteries, which arise from the facial artery. The lips are drained primarily by the facial vein, which also communicates with the orbital veins via the angular vein above the upper lip. With inflammatory lesions of the lip (e.g., furuncles), infectious organisms can spread into the cranial cavity via connections between the orbital veins and cavernous plexus, resulting in complications (see 3.8, p. 59). Cheeks: The cheeks, which form the lateral boundaries of the oral vestibule, also contain small salivary glands in their mucosa. The buccinator forms the muscular framework of the cheek. Like the orbicularis oculi, the buccinator is a mimetic muscle (Fig. 4.2) and receives its motor innervation from branches of the facial nerve. The Bichat fat pad (buccal fat pad) is located between the buccinator muscle and the overlying masseter muscle, the fibers of which run almost perpendicular to the buccinator. This fat pad smoothes the cheek contour by filling in the depression at the anterior border of the masseter muscle. The excretory duct of the parotid gland runs through the buccinator muscle and opens into the mucosa of the cheek opposite the upper second molar. Masticatory Muscles The masseter muscle, located in the posterior part of the cheek, covers the vertical ramus of the mandible and the mandibular angle from the outside. It is one of the masticatory muscles, along with the temporalis muscle and the medial and lateral pterygoid muscles (Fig. 4.2). These muscles form both a functional and phylogenetic unit and accordingly are all supplied by the mandibular nerve (third division of the trigeminal nerve). Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 80. 4 Lips and Oral Cavity Fig. Anatomy of the lips, oral vestibule and oral cavity Hard palate Palatine glands Veli pelatini muscles Uvula and soft palate Palatopharyngeal arch Palatine tonsil Greater and lesser palatine arteries and nerves Buccinator muscle Palatoglossal arch Faucial isthmus Dorsum of tongue Palatoglossus muscle Palatopharyngeus muscle Uvular muscle Gingiva Oral vestibule Fig. Anatomy of portions of the mimetic and masticatory muscles The diagram shows the superficial and deep masticatory muscles, the buccinator muscle, and the orbicularis oculi muscle. Lateral pterygoid muscle Medial pterygoid muscle Temporalis muscle Infraorbital foramen Parotid duct Pterygopalatine fossa Buccinator muscle Orbicularis oculi muscle, marginal part Orbicularis oculi muscle, labial part Teeth The human dentition consists of two sets of teeth that vary in their individual shapes. The deciduous teeth are replaced by the permanent teeth, eight of which occupy each half of the maxilla and mandible: • Two incisors • One canine • Two premolars • Three molars Each tooth consists of a crown and a root, which terminates at the apex. The area between the crown and root is the neck (cervix), which protrudes from sockets (dental alveoli) in the alveolar processes of the maxilla and mandible. The crown projects freely into the oral Masseter muscle Mental foramen cavity and is covered externally by enamel. Internally, each tooth has a pulp chamber that contains connective tissue, nerve fibers, and blood vessels and is connected to the alveolus via the root canal. The teeth are anchored in the alveoli by the cementum, the bony alveolar wall itself, and the gingiva. These anchoring and supporting structures are known collectively as the periodontium. The alveolar processes in the maxilla also form the floor of the maxillary sinuses—a fact that has major practical relevance. Normally, the roots of the second premolar and first molar are very closely related to the maxillary sinus (see also Fig. 1.5, p. 4 and Fig. 1.6, p. 6). Occasionally, the bony shell between the periodontium and maxil- Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 71
  • 81. 72 II Oral Cavity and Pharynx Fig. Anatomy of the lingual muscles Longitudinalis superior linguae muscle Transversus linguae muscle Lingual septum Palatoglossus muscle Palatopharyngeus muscle Longitudinalis inferior linguae muscle The diagram shows the intrinsic muscles of the tongue and also the extrinsic muscles, consisting of the genioglossus and geniohyoid. The mylohyoid muscle provides the muscular foundation of the oral floor. Foramen cecum Root of tongue Genioglossus muscle Styloglossus muscle Mylohyoid muscle Geniohyoid muscle lary sinus mucosa may even be absent in this region. The arteries that supply the maxilla and mandible (inferior alveolar artery, anterior and posterior superior alveolar arteries) arise from the maxillary artery. The upper teeth receive their innervation from branches of the maxillary nerve, the lower teeth from branches of the mandibular nerve. Oral Cavity The oral cavity is bounded anteriorly and laterally by the alveolar ridge and teeth, superiorly by the hard and soft palate (Fig. 4.1, p. 71), and posteriorly by the faucial isthmus. This narrow opening between the oral cavity and pharynx is bordered by the soft palate with the uvula and by the dorsum of the tongue at its junction with the tongue base. Palate: The hard palate is formed by the palatine processes of the maxilla anteriorly, the incisive bone, and the horizontal plates of the palatine bones posteriorly. The oral cavity is sealed posteriorly by the soft palate with its pendulant process, the uvula. The palatal muscles that form the framework of the soft palate are the tensor veli palatini and especially the levator veli palatini, which elevates the soft palate during swallowing to keep food from entering the nose. The muscles of the soft palate are completed by the palatoglossus, which runs in the anterior faucial pillar (palatoglossal arch), and by the palatopharyngeus muscle of the posterior faucial pillar (palatopharyngeal arch, Fig. 4.1). The uvula also has its own muscle, called the muscle of the uvula. The palatal mucosa, like the mucosa of the lips and cheeks, contains numerous salivary glands (palatine glands, see also Fig. 6.2, p.133). The motor innervation of the soft palate is described in 4.1. The palatal mucosa receives its sensory innervation from the greater and lesser palatine nerves (which arise from the second trigeminal nerve division; Fig. 4.1). The blood supply to the palate is derived from the ascending palatine branch of the facial artery. Tongue and oral floor: The tongue is composed of various muscular systems (Fig. 4.3), occupies much of the oral cavity, and is continuous anteriorly and laterally with the floor of the mouth. The muscular foundation of the oral floor is formed by the mylohyoid muscle, which stretches between the anterior portions of the mandible. When the tip of the tongue is raised to expose the undersurface, the sublingual folds and sublingual papillae can be identified on both sides of the frenulum in the anterior part of the oral floor (Fig. 6.3, p.133). 4.1 Motor innervation of the soft palate Developmentally, the individual muscular components of the soft palate are derived from different structures and are therefore supplied by different cranial nerves (mainly by cranial nerves IX and X, see Fig.16.3 and Fig.16.4, p. 315 f., and to a small degree by cranial nerve V). Cranial nerve deficits, especially those involving the lower cranial nerves IX and X, tend to restrict the mobility of the soft palate, causing difficulties in swallowing. During phonation (“ah”), the uvula and faucial pillars deviate toward the unaffected side. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 82. 4 Lips and Oral Cavity Fig. Anatomy of the tongue The body and base of the tongue, viewed from the superior aspect. Palatine tonsil Root of tongue Lingual tonsil Foramen cecum Terminal sulcus Vallate papillae Foliate papillae Body of tongue Filiform papillae Fungiform papillae Tip of tongue The main anatomical subdivisions of the tongue are the apex, the body, and the base or root. The body of the tongue is separated from the base by a V-shaped groove called the terminal sulcus. The tip of this groove is directed toward the tongue base and is formed by the foramen cecum (Fig. 4.4). The mucosa of the tongue differs from the rest of the intraoral mucosa chiefly by the presence of numerous papillae, which project from the surface of the tongue and give it its characteristic roughness. Four types of papillae are distinguished: filiform, fungiform, vallate, and foliate (Fig. 4.5). The latter three types are most important for taste perception. The microscopic taste buds are responsible for specific taste reception. They are most numerous on the vallate and foliate papillae and less so on the fungiform papillae. Small numbers of taste buds also occur in other regions of the oral cavity and pharynx (e.g., the soft palate, the anterior pillar, and the posterior wall of the oropharynx). Each taste bud consists of 30–80 elongated cells that extend superficially to the gustatory pore. This channel is located between the squamous epithelial cells and communicates with the oral cavity. The lingual tonsil is part of the collection of lymphoepithelial tissue known as Waldeyer’s ring (see 5.1, p.101). The tongue and oral floor derive their blood supply from the lingual and sublingual arteries, which branch from the external carotid artery. Homonymous accompanying veins provide for drainage via the facial vein to the internal jugular vein. Lymphatic drainage is handled by the ipsilateral and contralateral submandibular and submental lymph nodes, which drain to the lymph nodes at the junction of the facial and internal jugular veins (upper jugular lymph nodes, see Fig. 16.2, p. 314). The potential for contralateral lymphogenous spread should always be considered in patients with malignant tumors. Developmentally, the tongue is derived from structures of the first through fourth branchial arches (see 16.5, p. 317). This accounts for the complex innervation of the tongue, which is supplied in varying degrees by cranial nerves V, VII, IX, X, and XII (see also Figs. 16.3–16.6, p. 315–317). The tongue derives its motor innervation from the hypoglossal nerve. The terminal sulcus receives its sensory supply from the lingual nerve, which branches from the third division of the trigeminal nerve (see Fig. 6.3, p.133). Sensation to the tongue base region is supplied by the glossopharyngeal and superior laryngeal nerves (from cranial nerve X). The taste buds (sensory innervation) are supplied by the chorda tympani (from cranial nerve VII) in the anterior two-thirds of the tongue and by the glossopharyngeal nerve in the posterior third. The central gustatory pathways are described in 4.2. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 73
  • 83. 74 II Oral Cavity and Pharynx Fig. 4.5 Histology of the tongue a Cutaway view Lingual tonsil Filiform papillae Fungiform papillae Vallate papilla Taste buds b Filiform papillae c Vallate papilla a The overall arrangement of the various papillae. b The epithelium of the filiform papillae bears keratinized, thread-like (filiform) structures that are directed toward the pharynx (original magnification × 40). c The vallate papillae are located at the junction of the body and base of the tongue. The epithelium in the pit surrounding the papilla contains numerous microscopic taste buds (arrows; original magnification × 100). Sources (b, c): Welsch; see p. 430. Physiology both motor and sensory properties. The complex motor functions of the tongue, like its other functions, can be traced to a specialized developmental history, which accounts for the sophisticated nerve supply derived from various cranial nerves (see p. 73 and Figs. 16.3–16.6, pp. 315–317) and for the specialized muscular structure of the tongue (Fig. 4.3, p. 72). The musculature of the tongue consists of extrinsic and intrinsic muscles. The extrinsic muscles are attached to the mandible and to the hyoid bone or styloid process, project into the body of the tongue, and greatly affect the position and movements of the tongue. The intrinsic muscles are composed of longitudinal, transverse, and vertical fiber systems and serve mainly to alter Importance for Food Intake The lips are the gateway to the digestive tract, sealing the oral cavity during chewing and swallowing to prevent the spillage of food. The orbicularis oculi muscle is chiefly responsible for this task. If the function of this muscle is impaired (e.g., due to facial nerve palsy), the resulting deficiency of lip closure can cause eating difficulties as well as drooling from the corners of the mouth at rest. Within the oral cavity itself, the tongue has major functional importance as a “multifunction organ” with Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 84. 4 Lips and Oral Cavity 4.2 Central gustatory pathways All gustatory fibers converge centrally in the area of the ipsilateral solitary tract, which ends at the solitary tract nucleus in the medulla oblongata; there the signal is relayed to the second neuron. The further course of the gustatory fibers is not yet fully understood. According to recent discoveries, the axons initially continue on to the medial parabrachial nucleus, where they synapse with the third neuron. Reportedly the fibers then travel via the dorsal trigeminothalamic tract, some crossed but most uncrossed, to the thalamus. The cortical taste areas themselves are located in the lateral part of the postcentral gyrus and in the adjacent insular cortex. To foot of postcentral gyrus and to insula Posteromedial ventral nucleus of thalamus Dorsal tegmental nucleus Dorsal trigeminothalamic tract Dorsal longitudinal fasciculus Medial parabrachial nucleus Oval nucleus Solitary nucleus, gustatory part VII Solitary nucleus, cardiorespiratory part Spinal nucleus of trigeminal nerve IX Dorsal nucleus of vagus nerve X Area postrema Chorda tympani Sweet, salty, sour Bitter Epiglottis and aryepiglottic folds VII the shape of the tongue. The tongue muscles as a whole are distinguished both by their extreme mobility and their considerable strength. These properties play an essential role in swallowing (see 5.1, p.101); they also influence the normal development of the maxilla and the dentition. The molars have the greatest importance in chewing, because they are located closest to the insertion of the masticatory muscles themselves. This allows very high pressure to be developed between their occlusive surfaces. Taste There are only four basic taste sensations: sweet, sour, salty, and bitter. The sensory experience of “taste” is a much more complex phenomenon, however, and results from a combination of olfactory, thermal, mechanical, and sensory impressions. The precise mechanism that triggers a taste sensation or transmits a gustatory signal at the molecular level remains unknown. Various theories have been advanced ranging from taste mediation by receptor proteins to taste activation through electrostatic interactions. Importance in Phonation and Articulation The musculature of the lips has an essential role in phonation, while “lingual articulation” controls the production of vowels, certain consonants, and palatal sounds through changes in the shape and position of the tongue. Finally, the oral cavity joins with the pharynx, nose, and paranasal sinuses (see 1.3, p.12 and 18.1, p. 386) in forming the “supraglottic vocal tract,” which plays a role in the coordination of vocal sounds. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 75
  • 85. 76 II Oral Cavity and Pharynx 4.2 Methods of Examining the Lips and Oral Cavity Inspection of the lips and oral cavity is an essential part of every otolaryngologic examination. Some problems that cannot be adequately investigated by clinical examination alone (e.g., taste disturbances, tumors) may require additional diagnostic procedures (e.g., taste tests, imaging studies). Disturbances of taste are rare but can be very distressful for the patient. They are reversible in many cases, depending on the cause (see Table 4.1). Visual Inspection Fig. After the lips have been inspected, the oral cavity is examined with the aid of a tongue blade. The examiner holds the instrument in the right hand while using the left hand to position and steady the patient’s head. Physical examination of the oral cavity a b c Dentures should be removed before the examination is started. The sequence of the examination is shown in Fig. 4.6. Tongue mobility is assessed by having the patient stick out the tongue. With hypoglossal nerve palsy, the tongue will deviate toward the affected side (Fig. 4.7). Glossopharyngeal nerve palsy, in which the uvula and palatal arches deviate toward the healthy side (“backdrop sign,” Fig. 4.7 b), is excluded by assessing the mobility of the soft palate. This is done by watching the soft palate while the patient says “ah” several times. Palpation If inspection reveals questionable changes, the affected region or structure should next be palpated to better assess the consistency and depth of the suspicious finding. The cervical lymph nodes should also be palpated. Taste Testing Abnormalities of taste are classified as hypogeusia (diminished sense of taste), hypergeusia (increased sensitivity of taste), or ageusia (absence of the sense of taste). Subjective Taste Testing In the subjective test known as chemogustometry, aqueous solutions of glucose, NaCl, citric acid, and quinine are applied to the tongue in various concentrations to test the threshold of taste perception for the four basic qualities of sweet, salty, sour, and bitter. This test, while easy to perform, does not provide a high degree of reliability or reproducibility. Electrogustometry is another subjective test procedure in which sensations are evoked by applying a constant anodal current to the taste receptors of the tongue. d a Positions of the patient and examiner. b The lips and cheeks are retracted from the teeth and alveolar ridge with a tongue blade to inspect the mucosa and assess the condition of the parotid duct orifice opposite the second upper molar. c The patient elevates the tongue so that the examiner can evaluate the floor of the mouth and the submandibular duct orifices. d The tongue is retracted with the blade so that the lateral oral floor can be examined. This test has methodologic advantages over chemogustometry, providing better quantitative assessment of side-to-side differences and more accurate localization of responses. Objective Taste Testing Objective taste tests based on gustatory evoked potentials, for example (analogous to objective hearing and olfactory tests), are possible in principle but are very costly. They are practiced only at large centers and are used mainly in examinations for disability assessment. Imaging Procedures Since the anatomical structures of the oral cavity are easily accessible, the diagnosis can often be established by clinical examination alone (inspection, palpation, biopsy or local excision of a suspected tumor). As a result, imaging procedures tend to have a limited role in diseases of the lips and oral cavity. Nevertheless, there are various clinical situations (e.g., a tumor Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 86. 4 Lips and Oral Cavity Fig. 4.7 Motor dysfunction of the tongue a Hypoglossal nerve palsy on the left side b Glossopharyngeal nerve palsy on the left side or extensive inflammatory process) in which a sectional imaging procedure can advance the diagnosis. a The tongue deviates toward the affected side when protruded. b The soft palate deviates toward the healthy side during phonation. Table 4.1 Causes of taste disorders Classification Ultrasound Basically, only B-mode instruments are useful for ultrasound examinations of the oral floor and tongue (Fig. 4.8), and real-time scanning is preferred. Transducers with an operating frequency in the 5–10 MHz range are used, depending on the desired penetration depth and resolution. Newer systems have multifrequency transducers that operate at variable frequencies. Computed Tomography and Magnetic Resonance Imaging Normal findings are illustrated in Fig. 5.9 and Fig. 5.10 (pp. 106 f.). Computed tomography and magnetic resonance imaging are not only more cost-intensive than ultrasound but are also more invasive in cases where contrast media are used. Indications: • Pronounced inflammatory changes (e.g., Fig. 4.17, p. 84) • Tumors. Information on tumor extent, depth of invasion, and spread across the midline are important parameters in selecting the optimum treatment modality, especially for lesions involving the tongue and floor of the mouth (see 5.4, p.122). Magnetic resonance imaging offers advantages over computed tomography in its superior soft-tissue discrimination. If an imaging procedure is performed for confirmation (especially of a suspected tumor), the examination should include the soft tissues of the neck to check for regional lymph-node metastases. Examples Congenital Aplasia of the taste buds Endocrine disorders Diabetes mellitus, hypothyroidism, adrenal insufficiency Drug side effects E.g., D-penicillamine, various lipidlowering drugs, ACE* inhibitors, antifungals Peripheral nerve lesions Involvement of the chorda tympani by facial nerve palsy, otitis media or previous middle ear surgery; involvement of cranial nerve IX by tumors or fractures of the skull base; very rarely after tonsillectomy Radiotherapy Radiation damage to the papillae Exogenous chemical agents Alcohol, nicotine, mouthwashes Central taste disorders E.g., head trauma, carbon monoxide poisoning * ACE: angiotensin-converting enzyme. Fig. 4.8 Ultrasound (B-mode) image of the tongue and oral floor Normal ultraDigastric muscle sound anatomy of the oral floor. The transducer is placed submentally, resulting in an upside-down Mylohyoid monitor image. muscle Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 77
  • 87. 78 II Oral Cavity and Pharynx 4.3 Malformations of the Lips and Oral Cavity Malformations of the lips, cheeks, and oral cavity (especially those involving the palate and oral floor) are of epithelial origin. Although they are highly variable in their extent and clinical appearance, they are all based on a common teratogenic mechanism. Cleft Lip and Palate 4.3 Epidemiology: Clefts of the lip, palate, and alveolar ridge can occur in various combinations. They are among the most common malformations, with an incidence of 1 in 500. While the pathogenesis of cleft lip and palate is not yet fully understood, basically it involves a developmental anomaly of the embryonic head. In addition to genetic inheritance clefting can result from a number of external influences, such as viral infections, placental oxygen deficiency, intrauterine bleeding, and exposure to ionizing radiation. Classification: The following main groups are distinguished: • Cleft lip and alveolar ridge • Cleft lip, alveolar ridge, and palate and isolated cleft palate. The bifid uvula is a very mild variant of the cleft palate (Fig. 4.9). Symptoms: Different clefts have a spectrum of clinical manifestations, depending on their morphology and extent: • Hypernasal speech (rhinophonia aperta) due to incomplete closure of the nasopharynx • Recurrent middle ear effusions and inflammations resulting from eustachian tube dysfunction • Variable abnormalities of the nasal septum (septal deviation) or in the shape of the external nose Fig. 4.9 Pathogenesis of cleft lip and palate Bifid uvula The photograph shows the characteristic appearance of a median cleft in the uvula. Fig. 4.10 Basic treatment plan for cleft lip and palate Months Years 0–3 4–6 7–12 13–18 19–24 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 E1E5Pediatrician 1year E4 E7 E8 E9 E3 E6 Orthognathic surgeon Treatment in pri- Treatment in permary dentition manent dentition Feeding plate Phoniatrist Auditory testing, treatment of hearing disorders Speech promo- Speech therapy tion Speech therapist Dentist Caries prevention Operations Lip repair Velum repair (if needed) Prosthesis Palate repair Various corrective operations Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. Rhinoplasty
  • 88. 4 Lips and Oral Cavity 4.4 Rare malformations involving the oral cavity Malformations of the intermandibular fusion zone Anomalies of the intermandibular fusion zone are much rarer than cleft lip and palate. They include dermoids of the tongue, oral floor, and mandible; superficial median neck clefts; and clefts of the lower lip, mandible, and tongue. Illustrative case: dermoid cyst of the oral floor (Fig.) a The patient presents with a submental swelling and b a tense bulging of the entire anterior and lateral oral floor. c A transverse ultrasound scan reveals displacement of the oral-floor musculature by a cystic mass. d An axial T2-weighted magnetic resonance image (MRI) defines the lateral extent of the mass (arrows). e Coronal MRI (T1-weighted, postcontrast) demonstrates the relationship of the mass to the musculature of the oral floor and tongue, and f a sagittal T2-weighted image defines the anteroposterior extent of the mass in the direction of the tongue base. The streaky markings within the cystic mass are a motion artifact due to swallowing. a g The lesion was surgically removed via the anterior oral cavity, yielding a well-circumscribed, thin-walled mass loosely attached to the surrounding tissue and identified histologically as a dermoid cyst. An important differential diagnosis is a dysgenetic salivary-gland cyst (ranula), which also tends to occur in the anterior oral floor (see 6.2, p.143). Transverse facial cleft Another, very rare anomaly is the transverse facial cleft (cleft cheek, macrostomia, lateral facial cleft), caused either by failure of fusion of the maxillary and mandibular processes or failure of the buccal membrane to regress due to fusion of the myoblasts. A transverse facial cleft is marked by bilateral extension of the oral fissure due to lateral displacement of the commissures and is frequently associated with facial dysplasia and auricular dystopia. Oral-floor musculature b Cystic mass c d Tongue musculature g Oral-floor musculature e Cyst Cyst f Diagnosis: Particularly with submucous clefts, the examination should include palpation of the hard palate in order to detect the bony discontinuity in that region. Treatment: The adequate treatment of cleft lip and palate requires close interdisciplinary teamwork among the pediatrician, otolaryngologist, maxillofacial surgeon, orthognathic surgeon, and phoniatrist (see Fig. 4.10). Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 79
  • 89. 80 II Oral Cavity and Pharynx 4.4 Inflammations of the Lips and Oral Cavity Inflammatory diseases of the oral cavity and lips are often on a continuum and can have a variety of causes. An underlying systemic disorder is frequently present. Viral agents, bacteria, fungi, contact allergens, and various autoimmune diseases can incite inflammatory changes in this region, which predominantly affect the mucous membranes. Viral Infections Fig. 4.11 Herpes simplex labialis Herpes Simplex Virus Epidemiology and pathogenesis: Herpes simplex virus (HSV) infections of the oral mucosa are most often caused by HSV type 1 (cutaneous and oral-mucosa strain), while infections with HSV type 2 more commonly affect the genital region. The virus may be transmitted by contact or droplet infection or occasionally through superficial skin injuries. From 85 % to 90% of the adult population are seropositive for HSV, particularly in urban areas. Symptoms: Primary infection with HSV is usually acquired in early childhood and predominantly affects the oral mucosa as herpetic gingivostomatitis (aphthous stomatitis). The appearance of local lesions (bullae) on the oral mucosa is preceded by fever and lethargy consistent with a flulike infection. This is often accompanied by regional lymphadenitis. In rare cases, the nasal mucosa is also involved (herpetic rhinitis). Special clinical forms are reviewed in 4.5. Reactivation of the HSV can occur in response to physical exertion, ultraviolet radiation, a febrile infection, emotional stress, or pregnancy (see also 4.6). Reactivation is most commonly manifested as herpes labialis. The site of predilection is the perioral region, especially the mucocutaneous junction of the lips (Fig. 4.11), but lesions sometimes occur in the mouth and nasal vestibule or on the cheeks, earlobes, or eyelids. Typical clinical appearance with vesicles about the upper and lower lip. 4.5 A particularly severe form of HSV infection, known as Pospischill–Feyrter aphthoid, can occur in immunocompromised children or as a sequel to measles, rubella, or chickenpox. A comparable form of this disease occurs much less frequently in immunocompromised adults and especially in HIV-infected patients. A dreaded complication of primary HSV infection in children is herpetic meningoencephalitis. 4.6 Diagnosis: The diagnosis is generally based on the history and clinical examination. Ordinarily there is no need for viral culturing or costly methods of viral identification (electron microscopy, immunofluorescence microscopy, polymerase chain reaction). A simple method is to demonstrate classic giant cells by the cytologic examination of a Tzanck smear. Complications: A feared complication is secondary bacterial superinfection by Staphylococcus aureus or streptococci. Also known as herpes impetiginatus, this infection frequently heals by scarring, in contrast to non-superinfected cases (Fig. 4.12 a). An occasional complication is postherpetic exudative erythema multiforme, characterized by skin lesions as well as typical Severe forms of herpes simplex virus (HSV) infection Theories on the reactivation of herpes simplex virus (HSV) infection The precise etiology of HSV reactivation is uncertain. Besides reinfection due to an exogenous cause, theories have focused mainly on an endogenous reactivation of the virus. The “precipitating factor” may be the integrated viral DNA in the host cells, which often is not detectable during latent periods but is able to induce the production of an “active” virus. Another theory holds that the herpesviruses persist asymptomatically in the spinal cord, where they may be activated by any of a number of provocative mechanisms and then travel along sensory nerve fibers to corresponding sites on the skin or mucosa. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 90. 4 Lips and Oral Cavity Fig. 4.12 Complications of herpes simplex labialis a days, but some cases (especially immunosuppressed patients) may require a more prolonged course of treatment. Varicella-Zoster Virus Pathogenesis: Chickenpox (varicella) and zoster are different clinical manifestations of infection with the varicella-zoster virus (VZV). Chickenpox occurs predominantly in children and results from primary infection with the varicella-zoster virus. After the cutaneous lesions have healed, the virus persists in the ganglion cells of sensory nerves. Zoster occurs as a reinfection or results from reactivation of the virus in response to various provocative mechanisms—ultraviolet radiation exposure, infectious diseases, or weakened immune defenses due, for example, to immunosuppressant therapy or human immuno-deficiency virus (HIV) infection; hence it requires previous contact with the virus. b a Typical clinical appearance of bacterial superinfection in herpes labialis. b Postherpetic exudative erythema multiforme. Symptoms: Chickenpox presents with a characteristic skin rash consisting of erythematous papules and thin-walled vesicles with watery contents, covering the body but especially pronounced on the head and trunk. Aphtha-like vesicles also consistently appear on the oral mucosa and especially on the hard palate, buccal mucosa, and gingiva. Zoster presents clinically as a segmental disease, with cutaneous and mucosal lesions distributed along a sensory nerve segment and often accompanied by systemic signs such as lethargy, fatigue, and occasional neuralgiform pain in the distribution of the affected nerve. With involvement of the second and third divisions of the trigeminal nerve, aphthae or scalloped ulcerations can be found on the buccal mucosa, palate, and body of the tongue. Treatment: Zoster, like HSV infection, should be treated with a 5–7-day course of acyclovir or famciclovir. Analgesics and anti-inflammatory drugs (especially carbamazepine) can also be beneficial, and antibiotics may be indicated in elderly or immuno-compromised patients to prevent superinfection. The efficacy of adjuvant cortisone therapy for zoster is a controversial issue. Herpangina ulcerative eruptions on the mucous membranes of the mouth, lips and genitals (Fig. 4.12 b). Synonyms: vesicular pharyngitis, ulcerative pharyngitis Treatment: The treatment of herpes simplex labialis should include the use of topical antiseptics to prevent superinfection. Acyclovir, administered as a topical ointment or systemically, is available for severe forms of the disease. Therapy is generally continued for 5–7 Epidemiology and pathogenesis: Herpangina is caused mainly by the group A coxsackievirus (CV), less commonly by the group B CV, and occasionally by retroviruses or echoviruses. The disease predominantly af- Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 81
  • 91. 82 II Oral Cavity and Pharynx Fig. 4.13 Herpangina Fig. 4.14 Candidiasis in human immunodeficiency virus (HIV) infection a Typical clinical appearance, with aphthous lesions on the anterior faucial pillar. b fects young children but also occurs in adults and is often manifested in the spring and fall. Symptoms: Besides systemic symptoms such as fever, malaise, headache, and muscle pain, bullous eruptions surrounded by a red halo appear on the oral mucosa, particularly affecting the anterior faucial pillars (Fig. 4.13), uvula, and palatine tonsils. As a rule, the vesicles rupture in a few days, leaving behind shallow ulcerations. c Differential diagnosis: The gingivostomatitis caused by HSV (see above) is considerably more painful and runs a longer course. Treatment: Treatment is purely symptomatic—anti-inflammatory agents or mouth rinses with chamomile. The disease generally resolves in 14 days without complications. Inflammatory Mucosal Lesions in HIV Infection Inflammatory lesions of the lips and oral cavity, while commonly observed in symptomatic HIV-infected patients, are not caused by the HIV itself but occur secondarily as a result of weakened host defenses. Candidiasis. This disease, caused by Candida albicans, is the most common infection seen in HIV-positive patients (Fig. 4.14). 4.7 Hand-foot-mouth disease Hand–foot–mouth disease is also caused by coxsackieviruses and predominantly affects small children from 6 months to 5 years of age. Clinically, small bullae typically appear simultaneously on the palate, tongue, and gingiva as well as on the palms of the hands, fingers, toes, and soles of the feet. As in herpangina, treatment is symptomatic. The disease generally resolves in 1–2 weeks without complications. Typical whitish plaques on the oral mucosa. Viral infections: Occurrence: Viral pathogens also play a significant role in the setting of HIV infections. The most common infecting viruses are HSV, VZV, and cytomegalovirus (CMV), all of which can be cultured from mucosal lesions in HIV-infected patients. The occurrence of a CMV infection, like an HSV infection, has been identified as a potential cofactor for the progression of HIV disease and tends to affect patients with an advanced immune deficiency. Symptoms: These diseases warrant special discussion, because their clinical features differ from those of the ordinary forms of these viral infections. This pertains to characteristic morphologic signs (e.g., a herpes sim- Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 92. 4 Lips and Oral Cavity 4.8 Recurrent aphthous stomatitis Synonyms: benign aphthous disorders, canker sores, recurrent aphthous ulceration Aphthae are considered the most common inflammatory lesion of the oral mucosa and occur predominantly during the second and third decades of life. Approximately 40% of cases show a familial pattern of occurrence. The etiology is still unclear, although viruses of the herpes group (varicella-zoster virus, cytomegalovirus) have been identified in some cases. Various precipitating factors have been identified: minor trauma, hormonal changes (e.g., premenstrual), concomitant gastrointestinal disease, and “emotional stress.” The disease has also been linked to iron, folic-acid or vitamin B12 deficiency. Signs and symptoms: Aphthae are inflammatory, shallow mucosal ulcerations with slightly raised erythematous borders and a tendency to recur. Three clinical variants of recurrent aphthous stomatitis are distinguished: Minor aphthae (approximately 80–90% of cases): •Superficial, usually small (2–5 mm) ulcerations located in the anterior third of the oral cavity •Heal without scarring, usually in about 1 week Major aphthae (approximately 10%): •Significantly larger (> 10 mm) and deeper ulcerations •Heal with scarring in about 2–4 weeks •Greater severity of complaints •Often accompanied by tender, enlarged regional lymph nodes Herpetiform aphthae (approximately 5%): •Very small aphthae showing a herpes-like arrangement •Mild systemic effects Differential diagnosis: Early differentiation from Behcet’s dis¸ ease (see 4.15, p. 88) is necessary for prognostic reasons and is critical for proper diagnostic and therapeutic management. It is important to watch for accompanying symptoms such as fever, lethargy, joint pain, and ocular signs, since severe oropharyngeal symptoms in themselves can also occur with major aphthae. plex infection may have zoster-like manifestations) and to the course of the disease, which is markedly protracted in this subset of patients and is associated with more severe complaints (Fig. 4.15). Treatment: Acyclovir is beneficial in HSV and VZV infections, but CMV is much less sensitive to this agent. CMV infections are treated with ganciclovir. Special form: Another disease that has been linked to HIV infection since its initial description and is believed to have a viral cause is oral hairy leukoplakia (OHL). The presence of OHL is basically considered pathognomonic for an HIV infection. Today it is believed to be caused by the Epstein–Barr virus (EBV). The clinical presentation is marked by patchy, whitish, slightly raised lesions occurring predominantly on the border of the tongue (Fig. 4.16). Less commonly, the mucosal lesions are found in other regions of the oral cavity (buccal or lip mucosa, oral floor, soft palate). OHL typically runs a painless course, and dysphagia occurs only in cases with Candida superinfection. De- The differential diagnosis should also include the various viral diseases of the oral mucosa such as herpes simplex (see p. 80), herpangina (see p. 81), and hand–foot–mouth disease (see 4.7, p. 72). The treatment of recurrent aphthous stomatitis is symptomatic and may include the frequent topical application of astringents (tincture of myrrh) or mouth rinses with special pain-relieving electrolyte solutions (e.g., Hanks’ solution). Deficits can be corrected by means of iron, folic-acid and/or vitamin B12 replacement. Chronic recurrent lesions may also benefit from the topical application of corticosteroid gel alternating with antiseptic mouth rinses. Fig. 4.15 Cytomegalovirus infection Typical clinical appearance of mucosal ulcerations with grayishwhite plaques. spite their resemblance to leukoplakia (Fig. 4.21), the lesions have not been known to undergo malignant transformation. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 83
  • 93. 84 II Oral Cavity and Pharynx Fig. 4.16 Oral hairy leukoplakia Bacterial and Fungal Infections Oral Floor Abscess Synonym: Ludwig’s angina Epidemiology: Oral floor abscess is a rare disease that can become potentially life-threatening if the inflammatory process spreads to the deep cervical soft tissues and mediastinum. Typical whitish patches on the border of the tongue. Treatment consists of local measures such as the topical application of vitamin A acid and/or podophyllin. Virostatics should not be used due to the high incidence of side effects and the likelihood that OHL will recur within a few days after the drugs are discontinued. HIV-infected patients are also predisposed to bacterial infections of the oral and pharyngeal mucosa. They have an increased incidence of acute and subacute tonsillitis as well as specific bacterial inflammations such as tuberculosis (see p.115), atypical mycobacterial infections, and syphilis (50 % of HIV-infected patients test seropositive for syphilis; see 4.10). Pathogenesis: In many cases, the inflammation originates from the lower molars. Less commonly, the disease develops from mucosal injuries in the oral floor, leading to abscess formation in the tongue muscles or connective-tissue spaces of the oral floor. The disease can also develop as a sign of impaired host resistance, as in the case of diabetic or immunosuppressed patients (especially children). Symptoms and diagnosis: An oral floor abscess is manifested clinically by edematous expansion with a firm, erythematous swelling in the submental to submandibular areas (Fig. 4.17 a). Patients complain of difficulty swallowing and speaking (“muffled speech”). High fever is also present. The downward spread of infection can lead to dyspnea with acute respiratory distress, and descending infection through the fascial compartments of the neck can incite a life-threatening mediastinitis. Imaging is necessary to define the extent of the oral floor abscess (often this cannot be done by physical examination alone due to local pain and induration). The principal options are ultrasonography and computed tomography (Fig. 4.17 b, c). Fig. 4.17 Oral floor abscess (Ludwig’s angina) a b c Abscess Abscess a Typical clinical presentation, with erythematous swelling about the oral floor. b, c Sequential axial computed tomography scans show the abscess, which originates from the oral floor (b) and extends downward (c). Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 94. 4 Lips and Oral Cavity Differential diagnosis: See 4.9. Treatment: The treatment of choice is incision and drainage of the abscess via the intraoral and transcervical route. Concomitant antibiotic therapy should be appropriate for a mixed spectrum of aerobic and anaerobic organisms. Lingual Abscess Overt or covert mucosal injuries to the tongue can become infected, resulting in a lingual abscess (Fig. 4.18). The diagnosis is established unequivocally by the clinical appearance of the tongue. Treatment is surgical and consists of incision and drainage of the abscess with concomitant antibiotic therapy. Candidiasis Candidiasis of the oral mucosa (synonym: thrush) occurs in persons with weakened host resistance due to radiation or cytostatic therapy, diabetes mellitus, long-term antibiotic use, corticosteroid inhalations, leukosis or leukopenia due to a different cause, or HIV infection. 4.10 4.9 Differential diagnosis of oral floor abscess The differential diagnosis of a suspected oral floor abscess should include an abscess of the submandibular or sublingual glands as well as actinomycosis, in which subcutaneous infection by the bacterium Actinomyces israelii can cause an indurating infiltration of the fatty tissue in the oral floor region. The complaints differ from the symptoms of an oral floor abscess in that actinomycosis is less painful and tends to form an external fistula. Symptoms: Clinical examination of the oral cavity reveals whitish, firmly adherent plaques that can be scraped from the mucosa, leaving an erythematous, bleeding surface (Fig. 4.14, p. 82). Treatment: Oral candidiasis is treated with topical antifungal agents such as nystatin solution or amphotericin-B lozenges. Every case should be treated, for otherwise the infection could spread to deeper portions of the alimentary tract (candida esophagitis) causing severe dysphagia, decreased food intake, and rapid weight loss. Syphilis Clinical features: Although lesions of the oral and oropharyngeal mucosa can occur in all stages of syphilis, the manifestations in the primary and secondary stages are most important for the differential diagnosis of mucosal lesions in these regions. Three weeks pass until the primary lesion appears. The sites of predilection for extragenital primary lesions, after the perianal region, are the oral cavity and oropharynx. Besides the lips and buccal mucosa, the tonsil (unilateral) and tongue are most commonly affected. The primary chancre is painless and appears as an initially papular lesion that gives way to an erosive or ulcerative eruption. Concomitant regional lymphadenopathy (bubo) is frequently present and is also painless. The secondary stage begins about 6 weeks after the primary lesion appears, as the disease becomes generalized due to hematogenous spread of the micro-organisms. The most commonly affected sites are the skin and mucous membranes. The mucosal syphilids (mucous plaques) are a dangerous source of infection, as they are teeming with infectious organisms. The syphilitic enanthema in the secondary stage typically consists of patchy, reddish lesions on the hard and soft palate and buccal mucosa. An even more common finding is specific angina. In contrast to the unilateral tonsillar changes in the primary stage, both palatine tonsils are inflamed and covered with grayish-white coatings. A sweetly fetid breath odor is also present. A particularly severe form of secondary syphilis is malignant syphilis, which occurs predominantly in immunosuppressed and especially HIV-infected patients. The tertiary stage may develop within a period of 3–5 years. Lesions of the oral and oropharyngeal mucosae are less common at this stage, but gummata (syphilitic granulomas) are occasionally found on the soft palate and uvula and also on the tonsil (unilateral). The tonsillar gumma appears as a sharply circumscribed ulcer with a greasy coating on its base and may initially be mistaken for a primary lesion, but the latter is almost always associated with painless regional lymphadenopathy. Interstitial glossitis is another, rare intraoral manifestation of tertiary syphilis. Differential diagnosis: If specific angina is suspected, the differential diagnosis should include diphtheria, in which the mucosal lesions spread to involve the soft palate and uvula. It is important to differentiate interstitial glossitis from the innocuous fissured tongue (see Fig. 4.19, p. 87). Diagnosis: Identification of the causative organism from the primary lesion can be accomplished with dark-field microscopy (the only reliable test in the early primary stage). Serologic tests such as the Treponema pallidum hemagglutination (TPHA) test or fluorescent treponemal antibody absorption (FTA-ABS) test are not positive until 3 weeks after the infection is acquired. A good follow-up test is the cardiolipin complement binding reaction (CBR), a modification of the Wassermann reaction whose titers correlate with the patient’s response to therapy. Treatment: Penicillin G (600,000 IU daily for 14 days) is the drug of choice for all stages of the disease. It is replaced by erythromycin in patients allergic to penicillin. Syphilis serology should be retested at the conclusion of treatment. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 85
  • 95. 86 II Oral Cavity and Pharynx Fig. 4.18 Lingual abscess a Superficial Tongue Lesions Lesions in the surface of the tongue may reflect systemic diseases and thus provide important clues to the patient’s general state of health. Besides harmless morphologic variants and localized inflammatory lesions, therefore, medical disorders should always be considered in the differential diagnosis of these changes. Hunter’s Glossitis Synonyms: atrophic glossitis Hunter’s glossitis is an atrophic inflammatory condition of the tongue base. It is an accompanying feature of pernicious anemia. Common symptoms are burning of the tongue, dry mouth, and altered sense of taste. Clinically, the tongue presents a typical smooth, shiny appearance with partial atrophy of the filiform papillae. b 4.11 Geographic tongue Geographic tongue (synonym: benign migratory glossitis) is marked by areas of desquamation of the filiform papillae on the dorsal surface of the tongue. The affected areas are irregularly shaped but are clearly demarcated relative to surrounding areas. The disease is harmless, and histologic examination shows signs of inflammation. Generally, the only symptom is an occasional burning sensation. Treatment is unnecessary. 4.12 a Clinical examination reveals a tense, dorsal swelling on the right side of the tongue. b A dorsal lingual abscess has formed around a foreign body used for tongue piercing. Black hairy tongue Features: Black hairy tongue (synonym: lingua villosa nigra) is based on a hyperkeratosis of the filiform papillae, imparting a furry appearance to the tongue (Fig.). Pathogenesis: The papillary elongation may result from failure of desquamation of the cornified layers or an excessive formation of keratin. Etiology: Various precipitating mechanisms have been discussed. Besides antibiotic and corticosteroid use, they mainly include chronic mucosal irritation from oral hygiene procedures or nicotine abuse as well as metabolic disorders (e.g., diabetes mellitus), vitamin deficiency, and wasting diseases. Treatment: Many cases are adequately managed by eliminating the causal factors or underlying disease. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 96. 4 Lips and Oral Cavity Fig. 4.19 Fissured tongue Typical appearance, with conspicuous furrows in the dorsal surface of the tongue. Treatment: The cause of the angioedema is a key factor in selecting the appropriate treatment. The treatment of choice for angioedema not induced by a C1-INH deficiency is symptomatic treatment with corticosteroids or epinephrine (especially in the form of the disease induced by ACE inhibitors). In the form that is induced by a C1-INH deficiency, direct replacement with a C1-inhibitor concentrate should be provided in acutely life-threatening cases with swelling of the tongue and larynx. Antihistamines and cortisone preparations are of little or no benefit in this form of angioedema. Immunologic Diseases Fissured Tongue Fissured tongue, characterized by the presence of numerous furrows on the dorsal surface of the tongue, is a harmless hereditary condition that affects approximately 10–15 % of the population. Lingual fissures may also be a sign of Melkersson–Rosenthal syndrome (see p. 294). Clinically, the tongue presents a characteristic appearance (Fig. 4.19). The differential diagnosis should include interstitial glossitis in tertiary syphilis (see 4.10, p. 85). Systemic lupus erythematosus, see 4.13. Pemphigus vulgaris, see 4.14. Behcet’s disease, see 4.15. ¸ Erythema multiforme, see 4.16. Lichen planus, see 4.17. Fixed Drug Eruption A fixed drug eruption is a delayed (type IV) allergic reaction that occurs at the same cutaneous or mucosal sites (e.g., the extremities, soles of the feet, palms of the hands, external genitalia, oral mucosa) following repeated drug use. Particularly with mucosal involvement, the disease is characterized by superficial erosions that may resemble an HSV infection due to their scalloped margins. The eruption may be induced by analgesics, anti-inflammatory agents (e.g., pyrazolone, Angioedema Definition: Angioedema denotes a transient, frequently pronounced vascular reaction which, in the head and neck region, can lead to swelling of the face, lips, tongue, and larynx. Pathogenesis: This disease occurs as one feature of an anaphylactic or anaphylactoid reaction. Drugs such as acetylsalicylic acid and angiotensin-converting enzyme (ACE) inhibitors are known to precipitate an attack. With ACE inhibitors, bradykinin appears to have a major pathogenic role. By contrast, the forms caused by a C1-esterase inhibitor (C1-INH) deficiency are much less common. Angioedema due to C1-INH deficiency may be hereditary or acquired. Clinical manifestations: The disease is characterized by sometimes massive facial swelling that is most pronounced in the periorbital region but also affects the lips, tongue, tongue base, and laryngeal area. Massive tongue swelling in particular can cause acute obstruction of the upper airways. The hereditary form is additionally characterized by swelling of the extremities and episodes of abdominal pain. 4.13 Systemic lupus erythematosus (SLE) Systemic lupus erythematosus is a chronic inflammatory systemic disease of the vascular connective tissue with cutaneous involvement and the potential involvement of almost all the organs. The etiopathogenesis of the disease is not yet fully understood. Besides genetic factors (familial incidence in 10% of cases), causal significance has been attributed to hormonal changes (symptoms worsen during estrogen therapy and pregnancy), viral involvement, ultraviolet radiation exposure, and various drugs (e.g., isoniazid, sulfonamide, phenytoin, penicillamine). Signs and symptoms: The oral mucosa is involved in 40% of cases. The lesions appear as edematous erythematous areas, erosions, or ulcerations covered by fibrinous exudate and located on the hard palate, buccal mucosa, and tongue. In rare cases the oral lesions precede other cutaneous and organ manifestations of the disease (e.g., polyarthritis, serositis, renal involvement, central nervous system involvement, hematologic changes). Diagnosis: Besides further clinical evaluation by a dermatologist, special laboratory tests are necessary to establish the diagnosis (see textbooks of dermatology). Treatment is geared toward the course of the disease and should be directed by the dermatologist. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 87
  • 97. 88 II Oral Cavity and Pharynx 4.14 Pemphigus vulgaris Pathophysiology: Pemphigus vulgaris is an autoimmune disease characterized by the formation of antibodies directed against adhesion proteins in the epidermis. These antibodies can be detected in affected mucocutaneous areas and in the serum. The etiology is uncertain. Besides a genetic disposition, the disease has been attributed to ultraviolet radiation exposure and various medications (e.g., phenylbutazone, indomethacin, ibuprofen, tuberculostatic drugs). The disease may also occur spontaneously, however, and it occasionally coexists with other autoimmune diseases (e.g., myasthenia gravis). Clinically, 50% of patients with pemphigus vulgaris show involvement of the oral mucosa with bullous eruptions or saliva-macerated bullae that can make eating extremely difficult. 4.15 Behcet’s disease ¸ Behcet’s disease occurs predominantly in eastern Mediterra¸ nean countries (especially Turkey) and in Japan but is becoming more prevalent in Western urban areas as a result of immigration. Etiology: A viral etiology has been suggested in addition to an autoimmune mechanism. The major features of the disease are oral aphthae, aphthous genital ulcers, and hypopyoniritis. The minor features are polyarthritis, gastrointestinal symptoms, and vascular lesions. 4.16 Diagnosis relies mainly on the immunologic detection of pemphigus antibodies; elevated titers correlate with an exacerbation of symptoms. The diagnosis is most quickly established by the histologic or immunohistologic analysis of affected mucosal areas (see textbooks of dermatology). Treatment: Initial treatment consists of systemic corticosteroids, whose use has led to a significant decline in the mortality of the disease. The addition of immunosuppressants is frequently indicated and can reduce the necessary corticosteroid dose. The most widely recommended local measures are oral rinses with anti-inflammatory or anesthetic solutions. Prognosis: Untreated, the disease may lead to death within a period of months or years, generally due to secondary complications such as sepsis or bronchopneumonia. The diagnostic criteria for Behcet’s disease are either the pres¸ ence of the three major features or the presence of two major and two minor features. Treatment depends on disease severity and includes the use of corticosteroids. Cytostatics and immunosuppressants may also be required. Oral mucosal lesions can be treated locally with mouth rinses (chamomile) or pyoktanin (2%). Erythema multiforme (EM) Etiology and pathogenesis: Erythema multiforme has a multifactorial etiology. Known precipitating causes are viral infections such as HSV infections, hepatitis B, mumps, and measles. The main bacterial agents are streptococci infecting the upper respiratory tract. The disease may also occur in the setting of diphtheria or syphilis. Other causes are drug side effects (sulfonamides, pyrazolone derivatives, barbiturates, penicillins, phenothiazines). Systemic diseases such as polyarteritis nodosa, Wegener granulomatosis, systemic lupus erythematosus, and various malignancies (lymphoma, carcinoma) also have causal significance. Signs and symptoms: A minor form of EM, marked initially by bulla formation on the oral mucosa and lips and later by erosive lesions (see Fig. 4.12 b, p. 81), is distinguished clinically from a major form (Stevens–Johnson syndrome). Major EM runs a very severe course and may develop following a herpes infection or in response to certain drugs. Besides erythematous areas on the extremities and buttock, conspicuous mucosal erosions appear predominantly on the lips, oral mucosa, and pharynx. These lesions are very painful and interfere with eating. There may also be ocular involvement in the form of conjunctivitis, keratitis, iritis, or uveitis. Systemic signs consist of generalized weakness, headache, and high fever. Severe cases may develop renal and cardiopulmonary disorders ranging to renal failure or toxic circulatory collapse. Treatment: Due to the painful involvement of the oral mucosa, adequate food and fluid intake should be stressed (and may necessitate parenteral nutrition). Milder forms of the disease may respond satisfactorily to local treatments (rinsing with chamomile solution, local anesthetics if required). Corticosteroids are the agents of choice for the severe forms, accompanied by the administration of a broad-spectrum antibiotic to prevent superinfection. Patients with frequent bouts of severe, postherpetic EM may benefit from long-term prophylaxis with acyclovir. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 98. 4 Lips and Oral Cavity 4.17 Lichen planus (LP) The etiology of lichen planus is unknown. Besides an immune pathogenesis in the setting of viral diseases (e.g., hepatitis B and C), there appears to be an association with certain medications (e.g., antimalarial drugs, organ arsenic compounds, gold salts). A psychosomatic mechanism is also likely, since lesions often appear following severe emotional trauma or other stressful situations. Signs and symptoms: The disease often affects the skin and mucosae concomitantly, with mucosal involvement occurring in 25–70% of patients. Lesions are particularly common on the oral mucosa (fig.) and the vermilion border of the lips. Diagnosis can be difficult due to the variable clinical manifestations of the disease. Oral lesions most typically appear as reticular white markings on the mucosa of the cheek (fig.) and tongue (Wickham’s phenomenon—requires histologic differentiation from leukoplakia!). But painful ulcerations may also occur (erosive LP), requiring differentiation from the lesions of pemphigus vulgaris, systemic lupus erythematosus, and stage II syphilis. Treatment: A variety of treatments have been recommended for LP ranging from antibiotics and tuberculostatics to antimalarial drugs. Most therapies tried to date have been unconvincing because they were not applied in a controlled-study framework. Corticosteroids are of symptomatic benefit, and aromatic retinoid and isotretinoin combined with corticosteroids are recommended for the treatment of mucosal lesions. Oral rinses with anti-inflammatory and local anesthetic solutions are recommended mainly for very painful, erosive intraoral lesions. 4.18 The prognosis of LP is guarded in terms of a complete recovery. It is common for oral mucosal lesions to persist for years, especially in the erosive form of the disease. Since it is now believed that LP is a potentially premalignant disease, regular follow-ups are also essential. Burning mouth syndrome (BMS) Burning mouth syndrome (BMS) is a symptom complex characterized by a burning sensation and other soreness in the oral cavity, often with an absence of objective mucosal findings. Although the tongue is most commonly affected (“burning tongue”), involvement of the hard palate, alveolar ridge (especially in denture wearers), and other regions of the oral cavity (buccal mucosa, oral floor, mucosal surfaces of the lips) has also been described. Concomitant xerostomia and dysgeusia are occasionally reported. BMS is most prevalent in postmenopausal women. Causes: •Local: – Dentures – Candidiasis – Geographic tongue – Allergic mucosal reactions (e.g., to sorbic acid, zimtaldehyde, nicotinic acid) – Toxic mucosal reactions (e.g., to nickel sulfate or mercury) – Radiotherapy •Systemic: – – – – – – – – – Iron-deficiency anemia Vitamin B12 deficiency Vitamin B1, B2 and B6 deficiency Folic acid deficiency Sjögren disease Menopause Diabetes mellitus Human immunodeficiency virus infection Drug side effects (angiotensin-converting enzyme inhibitors) •Psychogenic: – Depression – Cancerophobia – Emotional stress phenylbutazone, phenazone), antibiotics (penicillin, tetracyclines, erythromycin), chemotherapeutic agents, sulfonamides, and by certain hypnotics (e.g., barbiturates) and laxatives (phenolphthalein). Treatment consists of avoiding the suspicious substances. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 89
  • 99. 90 II Oral Cavity and Pharynx 4.5 Tumors of the Lips and Oral Cavity Benign tumors of the lips and oral cavity, while rare, can occur as neoplasms of the various epithelial and mesenchymal tissues in this region. Among the precancerous lesions, leukoplakia is particularly important because of its morphologic similarity to carcinoma in situ. Malignant tumors of the lips and particular- ly the oral cavity have become more prevalent in past decades as a result of alcohol and nicotine abuse and today are counted among the most frequent head and neck malignancies along with pharyngeal and laryngeal cancers (see 5.3–5.5, pp.108–111 and 17.7, pp. 368–378). Benign Tumors Fig. 4.20 Benign tumors of the oral cavity Benign tumors of the lips and oral cavity can arise from all epithelial and mesenchymal tissues in the head and neck region but are relatively rare. Besides papillomas (Fig. 4.20 a) and pleomorphic adenomas (Fig. 4.20 b), various mesenchymal tumors can occur such as fibromas, lipomas, rhabdomyomas, leiomyomas, and chondromas. There are also hemangiomas and lymphangiomas, which are congenital in most cases. Treatment: Treatment is generally surgical and is indicated for patients who describe symptoms and in cases in which it is necessary to exclude a malignant tumor. Hemangiomas and lymphangiomas are a special case. Due to the high rate of spontaneous remission during the first years of life, conventional surgical treatment or laser surgery is advised only if the tumor persists beyond that period, provided the patient does not have serious symptoms such as dyspnea or dysphagia that would necessitate earlier surgical intervention. Radiotherapy is no longer advocated for these tumors due to the potential for adverse sequelae (malignant transformation, growth disturbance). a Papilloma b Pleomorphic adenoma Precancerous Lesions Leukoplakia is the most common precancerous lesion of the lips and oral cavity (Fig. 4.21). Many of these lesions are asymptomatic and are detected incidentally. Exogenous irritants such as denture pressure or alcohol/nicotine abuse have been most strongly implicated as causal factors. Given their morphologic resemblance to carcinoma in situ and invasive carcinoma and their potential for malignant degeneration, leukoplakic lesions should always be investigated by biopsy. The treatment of choice is complete surgical removal of the neoplasm. Bowen’s disease of the oral mucosa, a chronic inflammatory disease caused by an intraepidermal carcinoma, is rare by comparison. Its morphologic features are similar to those of leukoplakia. a Papilloma of the uvula. b The bulge in the palate is caused by a pleomorphic adenoma arising from the palatal salivary glands. Malignant Tumors Malignant Tumors of the Lips Malignant tumors of the lips (T categories Table 4.2, p. 93) are almost invariably squamous cell carcinomas and most commonly affect the lower lip (approximately 90% of cases). They occur predominantly in pipe smokers. Prolonged, intense sun exposure is considered a cofactor. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 100. 4 Lips and Oral Cavity Fig. 4.21 Leukoplakia of the oral mucosa a b Malignant Tumors of the Oral Cavity Squamous cell carcinomas also predominate in the oral mucosa and are variable in their clinical appearance (Fig. 4.24). Approximately 90 % of patients have a long history of nicotine and alcohol abuse, and nearly 75 % of malignant tumors form in the drainage area of the oral cavity—i.e., the trough between the base of the alveolar ridge and the border of the tongue (Figs. 4.24 a, 4.25 a). Symptoms: Symptoms vary with the location and extent of the tumor and may consist of painful swallowing, blood-tinged saliva, and a fetid breath odor. Some tumors are completely asymptomatic, however. c Typical whitish plaques at the oral commissure (a), on the tongue (b), and on the anterior part of the oral floor (c). Symptoms and diagnosis: Early tumors often appear clinically as “intractable” ulcerations in the vermilion border of the lip (Figs. 4.22 a, 4.23 a) but may also consist of large, exophytic lesions (Fig. 4.22 b). Whenever a tumor is suspected, a biopsy should be taken to confirm the diagnosis. Differential diagnosis: Differentiation is mainly required from keratoacanthoma and a primary syphilis chancre (see 4.10, p. 85). Basal cell carcinoma (see Fig. 3.48, p. 61) involves the vermilion border of the lip only by secondary spread. Treatment: The treatment of choice is almost always surgical excision followed by a local primary closure or plastic repair of the defect using various reconstructive techniques (Fig. 4.22 c–g and Fig. 4.23 b–d). As a rule, even extensive tissue defects can be repaired using regional flap techniques. Carcinomas of the lip have an inherently low rate of metastasis to regional lymph nodes, but a neck dissection should be performed in patients with category 2 or higher tumors (see 16.5, p. 332). Diagnosis: Visual inspection can raise the suspicion of a malignant neoplasm. This should be followed by bimanual palpation, since many tumors infiltrate deeper tissues and the visual impression of superficial findings can be misleading. The clinical examination also includes palpation of the regional cervical lymph nodes to exclude metastases. Imaging procedures (ultrasound, computed tomography, magnetic resonance imaging) are generally necessary only for extensive masses, as many tumors can be adequately evaluated clinically owing to their exposed location. But with more advanced lesions, imaging is valuable for defining the depth of tumor infiltration and assessing the involvement of adjacent structures (bone). It is also an important tool for excluding regional cervical lymph-node metastases. Treatment: The treatment of choice in most cases is surgical removal of the primary tumor. The resulting defect is either closed primarily or reconstructed using pedicled flaps (see Fig. 4.25) or microvascular free transfers (e.g., a radial forearm flap). A unilateral or bilateral neck dissection (see p. 334) may be necessary, depending on the location and T category of the primary tumor (see Table 4.2, p. 93). Radiation to the tumor site and lymph areas is frequently indicated following surgery. Primary radiotherapy or combined radiochemotherapy may be considered as alternatives for T3 and T4 tumors. Prognosis: The prognosis of oral malignancies depends on the location and stage of the disease. The five-year survival rate varies accordingly, ranging from 0% to 80%. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 91
  • 101. 92 II Oral Cavity and Pharynx Fig. 4.22 Malignant tumors of the lower lip d e Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 102. 4 Lips and Oral Cavity Fig. 4.23 Malignant tumor of the upper lip a b c d a Ulcerated carcinoma of the upper lip, extending to the nasal base. b, c The resection defect is closed primarily by mobilizing a flap from the nasolabial fold. d One year later, the operative site is healed and free of irritation. Table 4.2 T classification of malignant tumors of the lip, oral cavity, and oropharynx Largest tumor dimension T1 T2 T3 T4 ≤ 2 cm > 2 cm and < 4 cm ≥ 4 cm but still superficial Tumor of any size that invades deeper structures (e.g., bone) The clinical appearance of T1 (a) and T2 squamous cell carcinomas (b), which present different morphologic features. c The diagram illustrates a technique for reconstructing a postresection defect in the lower lip. d The flap is mobilized from the upper lip and transposed into the lower lip defect. e Appearance after flap inset and closure of the donor defect in the upper lip. f Good flap healing is seen 6 weeks after the operation. A “commissure plasty” can be performed at this stage to extend the obliterated left oral commissure. g Appearance 3 months after the first operation. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 93 3
  • 103. 94 II Oral Cavity and Pharynx Fig. 4.24 Malignant tumors of the oral cavity 4.19 a b Malignant tumors of the oral cavity in patients infected with human immunodeficiency virus (HIV) HIV-positive patients have a disproportionately high incidence of malignant tumors because of their weakened immune status. Most of these lesions in the oral cavity are Kaposi sarcomas. A smaller percentage are various types of B-cell lymphoma. Kaposi sarcomas were first seen in association with HIV infection in the early 1980s. They are present in approximately 20% of affected homosexual and bisexual men but occur in less than 5% of HIV-infected individuals from other risk groups. The tumor has a variable appearance, depending on its location in the oral cavity. The hard palate is considered a site of predilection in this region (Fig. a). Fig. b illustrates a Kaposi sarcoma of the tongue. a c b The typical clinical appearance of squamous cell carcinoma of the oral floor (a), buccal mucosa (b), and soft palate (c). Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 104. 4 Lips and Oral Cavity Fig. 4.25 Surgical treatment of oral floor carcinoma a b d e f g a The typical location of an oral floor carcinoma in the drainage area of the oral cavity between the alveolar ridge and border of the tongue. After resection of the tumor, which has infiltrated the tongue (b), a pedicled myofascial flap (here a myofascial pectoralis major flap; see also Fig. 3.12, p. 38) is outlined beneath the skin of the chest, mobilized, swung into the tissue de- c fect, and sutured into place (c–e). f One month later, granulation tissue is still present in the previous tumor defect that was reconstructed with the myofascial flap. g The texture of the mucosa appears almost normal 21⁄2 months after the operation. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 95
  • 105. 5 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 106. II Oral Cavity and Pharynx 4 5 6 Lips and Oral Cavity The Salivary Glands Pharynx and Esophagus 5.1 Anatomy, Physiology and Immunology of the Pharynx and Esophagus 98 Nasopharynx, Oropharynx, and Hypopharynx 98 Parapharyngeal Space 100 Esophagus 100 Physiology of Swallowing 101 Structure and Function of the Tonsillar Ring 101 Phonation and Articulation 103 5.2 Methods of Examining the Pharynx 104 Mirror Examination and Endoscopy 104 Imaging Procedures 105 5.3 Diseases of the Nasopharynx Adenoids 108 Benign Tumors 108 Malignant Tumors 109 5.4 Diseases of the Oropharynx 112 Injuries and Foreign Bodies 112 Acute Inflammations 113 Chronic Inflammations 119 Peripheral Obstructive Sleep Apnea Syndrome (OSAS) 120 Tumors 122 5.5 Diseases of the Hypopharynx and Esophagus 124 Injuries and Foreign Bodies 124 Diverticula 126 Tumors of the Hypopharynx 128 108 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 107. 98 II Oral Cavity and Pharynx 5.1 Anatomy, Physiology and Immunology of the Pharynx and Esophagus The pharynx is a tubular, fibromuscular space extending from the skull base to the inlet of the esophagus (upper esophageal sphincter). Anatomically and clinically, the pharynx consists of a nasal part (nasopharynx), an oral part (oropharynx), and a laryngeal part (hypopharynx). The entire pharynx is bounded externally by several muscle systems, which perform diverse functions and are continuous distally with the muscles of the esophageal wall. The primary function of the pharynx and esophagus is to coordinate the act of swallowing, which is regulated by a complex interaction of various cranial nerves and peripheral muscular and connective-tissue structures located in the oral cavity, pharynx, and esophagus. The pharynx also contains the tonsillar ring, a series of lymphoepithelial organs that are important in the immune response to infection. Finally, portions of the pharynx function as a variable resonance chamber for modulating vocal sounds. Nasopharynx, Oropharynx, and Hypopharynx anterior wall is formed by the back of the larynx, which protrudes into the hypopharynx and forms two lateral mucosal pouches (piriform sinuses), which rejoin at the level of the esophageal inlet. Anatomical Extent Nasopharynx: This highest part of the pharynx extends from the bony skull base to an imaginary horizontal line at the level of the velum (Fig. 5.1). It communicates with the nasal cavity via the choanae and with the middle ear via the orifice of the eustachian tube. The nasopharynx is bounded superiorly by the floor of the sphenoid sinus and pharyngeal roof. Also in this region is the pharyngeal tonsil, which forms part of the tonsillar ring (see below). Medial to the eustachian tube orifice, the tubal cartilage forms a projecting lip called the torus tubarius. The concavity behind it is termed the pharyngeal recess (Rosenmüller fossa) (see Fig. 5.8 b, p.105). The nasopharynx is bounded posteriorly by the curve of the first cervical vertebra, with its overlying prevertebral cervical fascia and prevertebral musculature. Oropharynx: The oral cavity communicates via the faucial isthmus (Fig. 4.1, p. 71) with the oropharynx, which extends inferiorly from the lower boundary of the nasopharynx to the upper margin of the epiglottis (see Fig. 5.1). It is bounded anteriorly by the tongue base and lingual tonsil (Fig. 4.4, p. 73) and posteriorly by the second and third cervical vertebrae with their prevertebral fascia. It is bounded laterally by the faucial pillars (tonsillar pillars, see 4.1, pp. 70–75), which flank the palatine tonsils. Hypopharynx: The lowest pharyngeal segment is the hypopharynx, which extends from the superior border of the epiglottis to the inferior border of the cricoid cartilage plate of the larynx (Fig. 5.1), where it joins with the esophagus. Lying posterior to the hypopharynx are the third through sixth cervical vertebrae. Its Mucosal Lining The mucosa that lines the nasopharynx consists of several rows of ciliated epithelium. At the oropharynx this gives way to a stratified, nonkeratinized squamous epithelium, which also lines the hypopharynx. Pharyngeal Musculature The muscular boundaries of the pharynx are formed by the constrictor pharyngis muscle group. The highest of these muscles, the constrictor pharyngis superior, begins at the level of the nasopharynx just below the tough, fibrous pharyngobasilar fascia, which in turn is suspended from the bony skull base. Just below the superior constrictor muscle are the overlapping constrictor pharyngis medius and inferior muscles, the latter of which joins distally with the esophageal musculature (Fig. 5.2). While most of the constrictor pharyngis muscle fibers run obliquely, the lowest portions of the constrictor 5.1 Weak points in the wall of the hypopharynx Three muscular weak points exist in the lower posterior wall of the hypopharynx. The first is the Killian triangle, located between the constrictor pharyngis inferior and the uppermost fibers of the cricopharyngeus muscle. The second area of weakness is the Killian–Jamieson region between the oblique and transverse fibers of the constrictor pharyngis. The third is the Laimer triangle, which is bounded above by the cricopharyngeus and below by the uppermost fibers of the esophageal musculature (see also Fig. 5.2). The Killian triangle is a particularly common site for the formation of hypopharyngeal diverticula. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 108. 5 Pharynx and Esophagus Fig. Anatomy of the pharynx Anatomy of the nasopharynx (blue), oropharynx (yellow), and hypopharynx (green) shown in midsagittal section. Nasopharynx Supraglottic space (laryngeal vestibule) Oropharynx Hypopharynx Glottis Food way Airway for nasal breathing Subglottic space Fig. Musculature of the pharynx and esophagus Various muscles contribute to the wall structure of the pharynx and esophagus. Constrictor pharyngis superior Constrictor pharyngis medius Constrictor pharyngis inferior Killian triangle Killian-Jamieson region Laimer triangle Uvula Stylopharyngeus muscle Palatopharyngeus muscle Cricopharyngeus muscle Esophageal musculature pharyngis inferior (cricopharyngeal part) run directly horizontally, creating anatomical weak spots in the pharyngeal wall (Laimer and Killian triangles, 5.1). These weak spots are sites of predilection for the development of pulsion (Zenker) diverticula in the hypopharynx (see Fig. 5.28, p.127). Three additional pairs of external muscles are distributed to the pharyngeal wall and assist in controlling vertical movements of the pharynx: the stylopharyngeus, the salpingopharyngeus, and the palatopharyngeus (Fig. 5.2). Neurovascular Supply The pharynx receives its blood supply from the territory of the external carotid artery (branches of the facial artery, maxillary artery, ascending pharyngeal artery, lingual artery, and superior thyroid artery). The veins of the pharynx drain into the internal jugular vein. The lymphatic drainage of the upper portions of the pharynx is through the retropharyngeal lymph nodes, while the lower portions drain to the parapharyngeal or deep cervical nodes. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 99
  • 109. 100 II Oral Cavity and Pharynx Nerve supply: The muscles and mucosa of the pharynx receive their motor and sensory innervation from the pharyngeal plexus, which in turn receives fibers from the glossopharyngeal and vagus nerves. The plexus itself is located on the outer aspect of the constrictor pharyngis medius muscle. Parapharyngeal Space The parapharyngeal space encompasses an anatomically well-defined region with the shape of an inverted pyramid whose base is formed by the inferior surface of the petrous bone and whose apex is at the lesser horn of the hyoid bone. The parapharyngeal space is divided anatomically into two parts, the retropharyngeal space and the lateral pharyngeal space. The latter in turn is subdivided by the common connective-tissue sheath of the muscles arising from the stylohyoid process (stylopharyngeal aponeurosis) into a prestyloid and a retrostyloid part. The prestyloid part communicates with the parotid compartment. It contains the lateral and medial pterygoid muscles, lingual nerve, optic ganglion, and maxillary artery. Its lower part is directly adjacent to the tonsillar compartment. The retrostyloid part of the lateral pharyngeal space is traversed by neurovascular bundles made up of the internal carotid artery, internal jugular vein, and lower cranial nerves (IX–XII). The retropharyngeal space contains smaller arterial and venous vessels and, most notably, the retropharyngeal lymph nodes that drain the nasopharynx. Esophagus The esophagus begins at the upper esophageal sphincter, located at the level of the C6 and C7 vertebrae (inferior border of the cricoid cartilage). The esophagus terminates at the gastric cardia in the plane of the T10 vertebra (Fig. 5.3 a). The three physiologic constrictions of the esophagus are clinically important due to the tendency for ingested foreign bodies to become lodged at those levels (Fig. 5.3 b): • Upper constriction: in the area of the esophageal inlet between the cricoid cartilage and the cricopharyngeal part of the constrictor pharyngis inferior muscle • Middle constriction: where the aortic arch crosses over the tracheal bifurcation • Lower constriction: where the esophagus pierces the diaphragm The wall structure of the esophagus adheres to the pattern of the gastrointestinal tract as a whole, consisting of several layers: • The mucosa, composed of stratified, nonkeratinized squamous epithelium Fig. Anatomy of the esophagus a b 0 Thyroid cartilage Cricoid cartilage Epiglottis Cricopharyngeus muscle Esophagus Cricoid cartilage Upper esophageal constriction Trachea Midesophageal constriction Heart Aorta Trachea Aorta Sternum Piriform recess Thyroid cartilage Cricopharyngeus muscle 16 23 Diaphragm Diaphragm Lower esophageal constriction Cardia Gastric fundus Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 38 40 [cm] a The esophagus extends from C6/C7 to the gastric cardia at the level of the T10 vertebra. b The three physiologic constrictions of the esophagus and their relationship to surrounding structures. The numerical scale shows distance in centimeters from the upper incisor teeth.
  • 110. 5 Pharynx and Esophagus • The submucosa • The muscularis, consisting of inner circular and outer longitudinal muscle fibers: – Upper fourth of the esophagus: striated fibers – Second fourth: mixed striated and smooth fibers – Lower half: smooth fibers The adventitia • Neurovascular Supply Blood supply: The cervical part of the esophagus receives most of its blood supply from the inferior thyroid artery (and a lesser amount from branches of the subclavian and vertebral arteries). The thoracic esophagus is supplied by the aorta and intercostal arteries, and the abdominal esophagus by the left gastric artery and left inferior phrenic artery. Venous blood in the neck is drained by the inferior thyroid vein. Thoracic and abdominal drainage is to the azygos and hemiazygos veins and esophageal veins. Lymphatic drainage is to the lymph nodes of the posterior mediastinum and pulmonary hilum. Nerve supply: The upper, cervical part of the esophagus is supplied with branches from the recurrent nerve and the lower part with unnamed branches from the vagus nerve. Below the tracheal bifurcation is the esophageal plexus, formed by the two vagus nerves. Physiology of Swallowing Normal swallowing requires a coordinated interaction of various anatomic structures in the oral cavity, pharynx, larynx, and esophagus. From a functional standpoint, the voluntarily initiated oral phase of swallowing is distinguished from an “involuntary” pharyngeal phase and esophageal phase, which are controlled through reflex mechanisms (Fig. 5.4). During the oral phase of swallowing, food is broken down and moistened to form a bolus that is moved toward the oropharynx. This is accomplished mainly by pressing the food against the hard palate with the tongue (Fig. 5.4, ➀). The pharyngeal phase begins when the bolus comes into contact with receptors in the throat (especially on the tongue base), eliciting an involuntary swallowing reflex (➁). The afferent impulses for this reflex travel through the glossopharyngeal and vagus nerves, while the efferent neurons that supply the pharyngeal muscles arise from cranial nerves V3, VII, IX, X, and XII. nied by a reflex adduction of the vocal cords ➄, allowing the food to pass through the piriform sinuses toward the esophagus while bypassing the larynx ➅. The esophageal phase of swallowing begins with a primary peristaltic wave, which is reflexly initiated in response to movement of the bolus through the pharynx (cranial nerves IX, X) ➆. Secondary peristalsis is additionally triggered in the esophagus by the pressure of the bolus against the esophageal wall ➇. Through the coordinated action of these mechanisms, the bolus is transported into the stomach within 7–10 seconds. Structure and Function of the Tonsillar Ring Anatomy The tonsillar ring (Waldeyer’s ring) is composed of a series of lymphoepithelial “organs” called the tonsils. This tissue is structurally similar to lymph nodes but lacks afferent lymphatic vessels. The tonsils are named for their location, consisting of a pharyngeal tonsil, the paired palatine tonsils, and the unpaired lingual tonsil at the base of the tongue. Additionally, smaller condensations of lymphoepithelial tissue are found in the pharyngeal recess (Fig. 5.8) and in the “lateral bands” (tubopharyngeal folds) on the posterior wall of the oropharynx and nasopharynx. The epithelium of the tonsils also varies by location. While the pharyngeal tonsil is covered mainly by multiple rows of ciliated epithelium, the palatine and lingual tonsils are covered by stratified, nonkeratinized squamous epithelium. Structure of the Palatine Tonsil The palatine tonsil has special immunologic importance among the tissues of the tonsillar ring owing to its distinctive morphology. Its surface is invaginated by crypts—fold-like tissue indentations that are lined by porous epithelium and substantially increase the surface area of the tonsil. This arrangement facilitates contact between inspired or ingested antigens and the subepithelial lymphatic tissue. The extensive nerve supply highlights the complexity of swallowing as well as the potential vulnerability of this process. While the involuntary swallowing reflex is triggered during the pharyngeal phase, the velum is elevated to close off the nasopharynx ➂. The larynx is also sealed off by elevation of the epiglottis ➃. This is accompaProbst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 101
  • 111. 102 II Oral Cavity and Pharynx Fig. Physiology of swallowing a Oral phase b Pharyngeal phase Bolus c Esophageal phase Bolus Bolus The circled numbers refer to the text (p.101) which describes the oral, pharyngeal, and esophageal phases of swallowing. Within the lymphatic tissue, primary follicles are formed during embryonic development and differentiate into secondary follicles after birth (Fig. 5.5 a). The secondary follicles mainly contain B lymphocytes at various stages of differentiation, along with scattered T lymphocytes (Fig. 5.5 b–d). Besides the lymph follicles, there are also extrafollicular areas with B and T lymphocytes that enter the lymphatic tissue through the postcapillary venules. Functional Importance of the Tonsils in the Immune System The palatine tonsil in particular is considered to be an “immune organ” that plays a significant role in the defense against upper respiratory infections. By analogy with comparable lymphoepithelial tissue masses in the bronchi and intestinal tract, the lymphatic tissue in the tonsillar ring is also termed the mucosa-associated lymphatic tissue (MALT) of the upper respiratory tract. Accordingly, this tissue has the ability to mount specific immune reactions in response to various antigens. The activity of this lymphatic organ is especially pronounced during childhood, when immunologic challenges from the environment induce hyperplasia of the palatine tonsils (Fig. 5.6). Following this “active phase” of immune initiation, which lasts until about 8–10 years of age, the lymphatic tonsillar tissue becomes less important as an immune organ, and there is a corresponding decline in the density of lymphocytes in all regions of the tonsils. While the tonsils become less important immunologically with ageing, the tonsillar tissue continues to perform immune functions even at an advanced age, although this should not alter the decision to remove the tonsils if a valid indication for tonsillectomy exists (see Chronic Tonsillitis, p.119). While the tonsils are “learning” their immune function during childhood, extreme tonsillar hyperplasia (“kissing tonsils”) may develop, leading to functionally significant narrowing of the faucial isthmus, with eating difficulties and obstructed breathing. Especially Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 112. 5 Pharynx and Esophagus Fig. Histology and immunohistochemistry of the tonsils Fig. Tonsillar hyperplasia a Mantle zone Germinal zone b The size and activity of the germinal centers are maximal at approximately 6–8 years of age, reflecting the immunologic activity of the palatine tonsil. They decline steadily thereafter. Tonsillar hyperplasia develops in many children during this “active immunization phase.” c when recumbent, these children may experience significant respiratory dysfunction, with periods of apnea. They also have an increased long-term risk of developing cor pulmonale. Consequently, there should be little hesitation in recommending tonsillectomy, even in small children. Phonation and Articulation Besides the oral cavity (see 4.1, Basic Anatomy and Physiology of the Lips and Oral Cavity, p. 70), the pharynx also functions as a variable resonance chamber for phonation and articulation. d a The histologic section shows the characteristic epitheliumcovered surface invaginations in the palatine tonsil (crypts). The secondary follicles in the lymphatic tissue, which are essential for tonsillar immune function, feature a light-colored germinal zone and a dark mantle zone with mature lymphocytes. b–d Immunohistochemical sections of various antibody-labeled cells in the pharyngeal tonsillar tissue (ABC method with hemalum counterstain). b B lymphocytes (CD22-labeled) outnumber other lymphocytes and are located mainly in the mantle zone. c T lymphocytes (CD3-labeled) are not only distributed throughout the follicle, but are also found in the interfollicular region and epithelium. d Section showing KP1-labeled macrophages. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 103
  • 113. 104 II Oral Cavity and Pharynx 5.2 Methods of Examining the Pharynx Clinical examination of the pharynx is an essential part of any otolaryngologic examination and relies on various techniques. Besides the classic mirror examination, diagnostic endoscopic procedures have been increasingly utilized in recent years. Imaging procedures have also assumed major importance in the investigation of various pharyngeal disor- ders. This trend is due largely to the advent of computed tomography and magnetic resonance imaging, while conventional radiographs have become largely obsolete in the investigation of diseases of the pharynx. On the other hand, conventional radiographs are still an essential tool for the investigation of many esophageal disorders. Mirror Examination and Endoscopy ular teeth and advanced past the uvula to the posterior wall of the pharynx (Fig. 5.8). Nasopharynx The location of the nasopharynx can make it very difficult to access and examine, especially for beginners. Before the advent of endoscopy, the only technique available for examining the nasopharynx was posterior rhinoscopy (Fig. 5.7). The establishment of endoscopic techniques has dramatically improved the diagnostic evaluation of the nasopharynx. Endoscopy: Nasopharyngeal endoscopy may be performed using a transoral or transnasal technique. The latter technique is described fully in 2.1 (pp.16–18) and permits the nasopharynx to be examined from the front. It can also provide detailed views of the eustachian tube region, the pharyngeal recess, and other difficult-to-reach sites (see p. 98). Transoral endoscopy is basically a postrhinoscopic technique that provides the examiner with an excellent overview of the nasopharynx. Transoral endoscopic technique: With the tongue pulled forward (to enlarge the space between the soft palate and posterior pharyngeal wall), the endoscope is introduced into the oral cavity over the left mandib- Fig. Oropharynx Most structures of the oropharynx can also be evaluated during the examination of the oral cavity. The technique is shown in Fig. 4.6, p. 76. The palatine tonsils are evaluated for their symmetry, mobility, and for the presence of any coatings or ulcerations. A laryngeal mirror or telescopic laryngoscope (see 17.2, pp. 346–350) should be used to examine the tongue base and the lateral walls of the oropharynx. Hypopharynx Clinical examination of the hypopharynx (mirror examination, endoscopy) is performed concurrently with the examination of the larynx (see pp. 346–350). Esophagus The esophagus can be examined by means of flexible or rigid endoscopy. Flexible esophagoscopy can be performed under local anesthesia, is generally well tolerated, and allows for concomitant examination of the stomach and duode- Posterior rhinoscopy The tongue is carefully depressed with a tongue blade, and then a small, prewarmed mirror is introduced between the soft palate and posterior pharyngeal wall. The mirror should not touch the mucosa to avoid evoking a gag reflex. Structures that can be evaluated with this technique include the posterior ends of the turbinates, the choanae, the posterior margin of the vomer, and the various structures of the nasopharynx (see Fig. 5.8). Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 114. 5 Pharynx and Esophagus num. It is the technique generally preferred by internists. Rigid esophagoscopy can also be performed under local anesthesia in principle, but it is more comfortable for the patient and examiner to conduct the procedure under general endotracheal anesthesia. Rigid esophagoscopy provides a better overview, particularly when looking for foreign bodies, because the advancing rigid scope tends to flatten out the mucosal lining, making it easier to detect trapped foreign objects. Fig. Transoral endoscopy of the nasopharynx a Imaging Procedures Conventional Radiographs Posterior end of turbinate b In the area of conventional radiography, the oral contrast examination is the most valuable technique for diagnosing hypopharyngeal (see Fig. 5.28) and esophageal diverticula, tumors, stenoses, and disorders of esophageal motility. Various contrast media can be used (e.g., barium, Gastrografin, Ultravist, Isovist), depending on the nature of the investigation and any preexisting disorders. If there is a risk or suspicion of a perforation, barium should not be used. Eustachian tube orifice Torus tubarius Pharyngeal recess Posterior margin of vomer c Another conventional radiographic technique, used mainly in patients with equivocal swallowing disorders, is high-speed cineradiography. This technique can be used to evaluate the different phases of swallowing with high temporal resolution (approximately 50 images per second). Computed Tomography and Magnetic Resonance Imaging a The tip of the endoscope has been positioned between the soft palate and the posterior wall of the pharynx in an anatomical specimen. b Normal view through a 90 endoscope, showing the posterior ends of the turbinates, the posterior margin of the vomer, the eustachian tube orifice, and the torus tubarius. c The same area viewed with a 120 endoscope. 8 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 8 The modern sectional imaging modalities of computed tomography (CT) and magnetic resonance imaging (MRI) have significantly advanced the diagnosis of pharyngeal tumor masses as well as certain inflammatory processes in this region. MRI (Fig. 5.9) has proven particularly effective for the soft-tissue discrimination of tumors in relation to surrounding structures, while CT (Fig. 5.10) is the method of choice for confirming or excluding osseous involvement. 105
  • 115. 106 II Oral Cavity and Pharynx Fig. Magnetic resonance imaging of the pharynx: normal findings Nasopharynx a Nasopharynx: axial, without CM Masseter muscle Intrinsic tongue muscles b Oropharynx: axial, with CM Oropharynx Jugular vein Parotid gland Medial pterygoid muscle Genioglossus m. Oropharynx Longus colli m. Medial pterygoid muscle Masseter m. Parotid gland Torus tubarius Eustachian tube c Oropharynx: axial, with CM Tongue base Medial pterygoid muscle Parotid gland Sphenoid sinus d Oropharynx: coronal, without CM Nasopharynx Soft palate Oropharynx Sphenoid sinus e Oropharynx: coronal, with CM f Oropharynx: sagittal, with CM Nasopharynx Sphenoid sinus Nasopharynx Lateral pterygoid muscle Intrinsic tongue muscles Medial pterygoid muscle Soft palate Oropharynx Intrinsic tongue muscles Tongue base Epiglottis Mandible Oral floor musculature Masseter muscle Mandible Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. Genioglossus muscles Geniohyoid muscle
  • 116. 5 Pharynx and Esophagus Fig. Computed tomography of the pharynx: normal findings a Nasopharynx Nasopharynx Eustachian tube Prevertebral musculature b Oropharynx Palatine tonsils Lateral pterygoid Oromuscle pharynx Medial pterygoid muscle The T1-weighted magnetic resonance images are labeled to indicate the image plane (axial, coronal, or sagittal) and whether the image was obtained with or without contrast medium (CM). Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. Genioglossus muscles 107 3
  • 117. 108 II Oral Cavity and Pharynx 5.3 Diseases of the Nasopharynx Diseases of the nasopharynx can have strikingly different causes at different ages. While adenoids are most common in children, tumors predominate in adults. Because lesions of the nasopharynx are difficult to examine and may produce nonspecific symptoms, malignant tumors in particular are apt to go undetected for some time. Modern endoscopic techniques using a high-intensity light source, together with the new sectional imaging modalities, have brought significant improvements, particularly in the early detection of nasopharyngeal lesions. Adenoids tympanometry, see p.185; if necessary, otoacoustic emissions, see p.189). Synonyms: polyps, adenoid vegetations “Adenoids,” the common term for hyperplasia of the pharyngeal tonsil, is a very widespread condition in children 3–6 years of age. The proliferation of lymphatic tissue in this region is so common in children that it can hardly be considered an abnormal condition, and nearly all children have some degree of adenoid hypertrophy due to the immunologic activity of that tissue. As a result, enlarged adenoids should be considered abnormal and treated accordingly only if they are causing symptoms. Not infrequently, the presence and severity of adenoidal symptoms depend on the relationship between the size of the nasopharynx and that of the adenoids. Clinical manifestations: Common symptoms of adenoids are chronic nasal airway obstruction (“mouth breathing,” Fig. 5.11 a), nasal discharge (“runny nose”), snoring, anorexia, and a hyponasal voice (rhinophonia clausa). Also, many small patients have frequently recurring infections of the nose and paranasal sinuses with otitis media and chronic impairment of eustachian tube ventilation, caused for example by adenoid tissue obstructing the tubal orifices. Prolonged conductive hearing loss (see 9.1, pp.198–201), especially during the first 3–4 years of life, can lead to delays in speech development. Finally, chronic mouth breathing can lead to maxillary deformity and dental malalignment. Many of these small patients also have enlarged tonsillar lymph nodes at the mandibular angle (Fig. 5.11 a). Diagnosis: Besides posterior rhinoscopy or endoscopy (see pp.17–18 and 104–107), the diagnostic workup includes microscopic examination of the tympanic membrane (otoscopy, see p.166). Often this will show retraction of the tympanic membrane or a middle ear effusion resulting from chronic impairment of eustachian tube ventilation, with negative pressure in the middle ear. Additionally, hearing should be tested in adenoid patients (pure-tone audiogram, see p.178; Treatment: The treatment of abnormally enlarged adenoids basically consists of surgical removal of the adenoids under general endotracheal anesthesia (adenotomy, adenoidectomy). In patients with concomitant middle ear effusion, paracentesis should be performed in the same sitting or a ventilation tube should be inserted for drainage (see p. 240). Benign Tumors Juvenile Angiofibroma Epidemiology: Benign tumors of the nasopharynx are rare. The most common of these is juvenile angiofibroma, which accounts for less than 0.05% of all ear, nose, and throat (ENT) tumors and occurs exclusively in boys 10–18 years of age (Fig. 5.12). Symptoms: Typical symptoms are obstructed nasal breathing, recurrent epistaxis, headache, impaired eustachian tube ventilation with middle ear effusion, and conductive hearing loss due to obstruction of the eustachian tube orifice. Diagnosis: The typical endoscopic appearance is that of a well-circumscribed, vascularized mass (Fig. 5.12 a) with superficial vascular markings, situated in the nasopharynx or posterior part of the nasal cavity. If there is clinical suspicion of an angiofibroma, a biopsy should not be performed due to the risk of heavy bleeding. The primary workup should include MRI or CT, which can accurately define tumor extension into surrounding structures (Fig. 5.12 b). Digital subtraction angiography (DSA) is useful for identifying tumor-feeding vessels (Fig. 5.12 c). Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 118. 5 Pharynx and Esophagus Fig. Adenoids a b c Posterior margin of vomer a Children with enlarged adenoids are “mouth breathers” due to nasal airway obstruction and exhibit a typical facial expression called “adenoid facies.” The arrows point to the enlarged lymph nodes at the mandibular angle. b Postrhinoscopic endoscopy shows the typical appearance of the hyperplastic pharyngeal tonsil (*), which is covered with viscous secretions and almost completely fills the nasopharynx (contrast with normal finding in Fig. 5.8 b). c The transnasal view shows hyperplastic adenoid tissue (*) partially obstructing the choanae. Treatment: The treatment of choice is surgical removal of the tumor. Preoperative embolization of the feeding vessels (usually the maxillary artery) should be performed to reduce the intensity of intraoperative bleeding (Fig. 5.12 d). Etiology: The Epstein–Barr virus (EBV) appears to have a key role in the etiology of undifferentiated lymphoepithelial carcinoma. Malignant Tumors Epidemiology: Carcinomas of squamous-cell origin account for the great majority of malignant nasopharyngeal tumors. A basic distinction is drawn between squamous cell carcinomas and lymphoepithelial carcinomas (Schmincke tumor). Much less common tumors of this region are adenocarcinoma, adenoid cystic carcinoma, malignant melanoma (Fig. 5.13), sarcoma, lymphoma, and plasmacytoma. Symptoms: Early symptoms of nasopharyngeal malignancies are unilateral conductive hearing loss with middle ear effusion. Any persistent middle ear effusion of long duration in an adult patient with no prior history of middle ear disease is suspicious for a tumor and should be investigated accordingly. Cervical lymph-node metastasis, usually involving the nodes at the mandibular angle, is another common initial finding. Features of advanced disease include nasal airway obstruction, recurrent epistaxis, headaches, and cranial nerve palsies. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 109
  • 119. 110 II Oral Cavity and Pharynx Fig. a Juvenile angiofibroma Inferior turbinate b Tumor Nasal septum Tumor c a Endoscopy reveals a spherical, well-circumscribed tumor in the posterior portions of the right nasal cavity. b Axial T1-weighted MRI after contrast administration demonstrates an enhancing mass in the nasopharynx. d c Digital subtraction angiography shows a well-vascularized tumor (arrows). d After embolization of the feeding vessels, the tumor is no longer visible. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 120. 5 Pharynx and Esophagus Fig. Malignant melanoma Fig. Nasopharyngeal carcinoma a Tumor Posterior surface of soft palate Right tubal orifice Tumor Posterior wall of pharynx Endoscopic view of a malignant melanoma in the nasopharynx. b Diagnosis: The primary study is endoscopy of the nasopharynx (Fig. 5.14 a, b). Nasopharyngeal malignancies can have a variety of appearances ranging from a smooth, well-circumscribed tumor surface to mucosal ulcerations. Inferior turbinate Nasal septum Tumor Some of these tumors are initially submucosal and are easily missed at endoscopy. Otomicroscopy reveals unilateral tympanic membrane retraction and a middle ear effusion as a result of impaired eustachian tube ventilation. Given the EBV association of many nasopharyngeal cancers, the EBV antibody titer should be determined (this shows an elevated IgA, contrasting with the elevated IgM/ IgG that is found in infectious mononucleosis). MRI or CT is useful for defining tumor extent (Fig. 5.14 c). Nasal floor c Tumor Treatment: The treatment of choice for most nasopharyngeal carcinomas is primary high-voltage radiotherapy, because most of these tumors are very radiosensitive and the unfavorable tumor location and rapid invasion of the skull base preclude curative surgery in many cases. a Postrhinoscopic endoscopy demonstrates a mass that has obstructed the nasopharynx. b In the transnasal endoscopic view, the tumor completely fills the choanae (only the right side is shown here). c The corresponding axial T1-weighted magnetic resonance image after contrast administration shows the tumor and its extension into surrounding structures. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 111
  • 121. 112 II Oral Cavity and Pharynx 5.4 Diseases of the Oropharynx The most common diseases of the oropharynx are inflammatory processes. Tumors, especially malignancies, are far less common in this region but should still be considered in the differential diagnosis, especially when certain risk factors are present (heavy smoking, alcohol abuse). Lesions of the oropharynx can also contribute to the development of sleep-related breathing disorders, particularly obstructive sleep apnea. Injuries and Foreign Bodies Foreign Bodies Scalds and Corrosive Injuries Foreign bodies in the oropharynx are most commonly located in the tonsils and at the tongue base. Typical foreign objects are fish bones (Fig. 5.15) and bone fragments, usually with an obvious prior history of oral ingestion. Most patients describe well-localized pain on swallowing. Treatment: The foreign material should be removed as soon as possible due to the risk of superinfection. Etiology: The accidental drinking of hot liquids by children can cause severe scalding of the lips, oral cavity, and oropharynx. Corrosive injuries are more common in adults due to the ingestion of caustic liquids with suicidal intent. Symptoms: The dominant clinical symptoms are severe pain, especially on swallowing, and increased salivation. Diagnosis: Initially the mucosa appears erythematous on mirror examination. Subsequent blistering may occur, followed by the formation of a whitish fibrin coating. Further tests are aimed at excluding injuries at lower levels of the alimentary tract and in the mediastinum. A chest radiograph should always be obtained (to check for mediastinal widening due to esophageal perforation). An early, careful endoscopic examination can be performed so that the extent of the esophageal injury can be accurately assessed. Treatment: The initial treatment for scalds and corrosive injuries is to rinse the oral cavity with cold water. If the lips are affected, they should be treated with a corticosteroid-containing ointment. Patients with more severe injuries can additionally be treated with systemic corticosteroids, antibiotics, and analgesics. A nasogastric feeding tube should be placed in patients with severe dysphagia who are unable to swallow. Fig. Foreign bodies in the oropharynx Uvula a Correct placement of the tube should be checked radiographically before the initial feeding, because the tube may perforate an esophagus that is affected by severe mucosal changes. b Epiglottis a Clinical appearance of a fish bone lodged in the right tonsil (arrows). b A fish bone lodged in the tongue base just above the vallecula (arrows). Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 122. 5 Pharynx and Esophagus Acute Inflammations 5.2 Rapid streptococcal test This rapid immunoassay makes use of colloid-labeled specific antibodies, which are placed onto reaction strips along with the pharyngeal smear. A color change in the “result window” indicates the presence of streptococcal group A antigen. The specificity and sensitivity of the various rapid tests available on the market range from 80% to 90%, making them useful tools in deciding whether to administer antibiotics. Note that a correlation exists between the test result and clinical findings—i.e., asymptomatic patients with a positive rapid test should not be placed on antibiotics. Conversely, a culture should be taken in cases where there is clinical suspicion of streptococcal tonsillitis but the rapid test is negative. Acute Tonsillitis Synonym: streptococcal angina Definition, etiology: Acute tonsillitis is an acute bacterial inflammation of the palatine tonsils that is generally caused by group A β-hemolytic streptococci. Rare cases may be caused by staphylococci, Haemophilus influenzae, or pneumococci. Symptoms: This disease is particularly common in children and adolescents and presents initially with high fever and severe pain on swallowing, which often radiates to the ear. Other symptoms are swollen tonsillar lymph nodes and muffling of speech due to oropharyngeal swelling. Clinical suspicion of streptococcal tonsillitis Diagnosis: Mirror examination: Both tonsils are swollen, bright red, and coated (Fig. 5.16). Inflammatory parameters: The blood count shows leukocytosis, and the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are elevated. Bacteriologic testing: A bacterial culture is rarely taken from throat smears because it usually takes 2–3 days to obtain a definitive result, by which time treatment should already be initiated. It is better to perform a rapid immunoassay, which can identify the causative organism as a group A streptococcus in just 10 minutes ( 5.2). Fig. Rapid test Positive Negative Antibiotic therapy Bacterial culture Acute tonsillitis a a Typical appearance of the palatine tonsils, which are bright red, swollen, and coated. b b The tonsils in this patient were so swollen that they caused respiratory distress, necessitating an immediate tonsillectomy. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 113
  • 123. 114 II Oral Cavity and Pharynx 5.3 Complications and sequelae of streptococcal tonsillitis Lingual tonsillitis In rare cases, the lingual tonsils may become inflamed and greatly swollen, and there may be concomitant edema involving the tongue base and laryngeal introitus. Endoscopic findings (Fig.) include marked hyperplasia of the lingual tonsils, which appear cylindrical with a stippled surface. These patients may experience brief periods of progressive respiratory distress, requiring intubation. Patients with lingual tonsillitis should be hospitalized for observation and should receive high doses of antibiotics. Streptococcal gingivostomatitis In rare cases, tonsillitis may be followed or accompanied by streptococcal gingivostomatitis, characterized by diffuse inflammation and redness of the gingival mucosa and the formation of gingival abscesses. These lesions may also be seen at other sites on the oral mucosa and on the lips. Sequelae of streptococcal tonsillitis Rarely, a delayed-type antigen-antibody reaction can give rise to poststreptococcal diseases involving the kidneys (acute glomerulonephritis), major joints (acute rheumatic fever), or heart (rheumatic endocarditis). Besides appropriate medical therapy, the treatment of choice is tonsillectomy under antibiotic coverage. Treatment: The standard treatment for streptococcal tonsillitis is a 10–14-day course of penicillin V. This regimen should be continued for at least 7 days to avoid late complications (see below). Macrolides or oral cephalosporins can be used in patients allergic to penicillin. Analgesics are also administered for pain relief. Complications: See 5.3 and Tonsillogenic Complications on p.118. 5.4 Complications of scarlet fever A feared complication is necrotizing scarlet fever tonsillitis, which will cause extensive necrotic areas in the pharynx and oral cavity unless adequately treated. Septic complications can also arise, manifested by extensive soft-tissue infections and a toxic-shock-like syndrome. As in all infections with βhemolytic streptococci, late sequelae can develop after an initial period of apparent recovery (rheumatic fever, diffuse hemorrhagic glomerulonephritis, and rheumatoid arthritis) (see 5.3). Scarlet Fever The tonsillitis in scarlet fever is also caused by infection with group A β-hemolytic streptococci. These are highly virulent bacterial strains that produce the scarlet fever exotoxin. Clinically, patients present with a rash that begins on the trunk. The area around the mouth is spared (“perioral pallor”). A pathognomonic feature is a bright red tongue with a glistening surface and hyperplastic papillae (“raspberry tongue,” Fig. 5.17). The tonsils are greatly swollen with a deep red color. Occasionally there is an enanthema of the soft palate with hemorrhagic areas. The diagnosis is established by the overall clinical picture combined with a positive rapid streptococcal test (see 5.2). Medical therapy relies on penicillin, as in acute tonsillitis. Additionally, the oral cavity should be rinsed with mild antiseptic solutions, and analgesics should be given for pain. Fig. Raspberry tongue Typical clinical appearance of the tongue in scarlet fever. The bright red coloration and prominent papillae create a raspberry-like appearance. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 124. 5 Pharynx and Esophagus Plaut–Vincent Angina This inflammatory disease is caused by fusiform rods and spirochetes and presents clinically with unilateral dysphagia and a fetid breath odor with very little malaise. Mirror examination reveals a unilateral, fibrincoated ulcer on the palatine tonsil. Differential diagnosis: tonsillar carcinoma. The causative organisms can be detected by the direct microscopic examination of a gram-stained smear. Treatment: Local measures (cautery with 10% AgNO3 or 5 % chromic acid) are usually satisfactory, but should be supplemented by antibiotics (penicillin) in patients with more severe complaints. Diphtheria Epidemiology: Diphtheria was controlled for a time by active immunization, but lately its incidence has been rising due to low vaccination numbers, especially in immigrants from Eastern Europe, and secular fluctuations in the virulence of the toxin. All instances of the disease must be reported to health officials. Causative organism: The causative organism is Corynebacterium diphtheriae, which is transmitted by droplet inhalation or skin-to-skin contact. The incubation period is 1–5 days. Pathogenesis: The bacterium produces a special endotoxin that causes epithelial cell necrosis and ulcerations. Clinical manifestations: Two main forms are distinguished based on their clinical presentation: • Local, benign pharyngeal diphtheria • Primary toxic, malignant diphtheria The disease begins with moderate fever and mild swallowing difficulties. The clinical picture becomes fully developed in approximately 24 hours, characterized by severe malaise, headache, and nausea. Diagnosis: Mirror examination of the pharynx reveals typical grayish-yellow pseudomembranes that are firmly adherent to the tonsils and may spread to the palate and pharynx. The underlying tissue bleeds when the coatings are removed. A slightly sweet breath smell is also characteristic. The diagnosis is confirmed by the overall clinical impression, combined with smear findings. Treatment: First, the patient should be isolated. Whenever diphtheria is suspected, even before it is con- firmed by smear results, diphtheria antitoxin (200– 1000 IU/kg body weight) should be administered by intravenous or intramuscular injection. Allergy to the antitoxin should be excluded (with a skin test) before it is administered. Penicillin G should also be administered. Discharge from the hospital is contingent upon test results: three smears taken at 1-week intervals must all be negative. Two percent of patients continue to carry the bacterium and should undergo tonsillectomy. Complications: Dangerous complications, which occur mainly in association with the primary toxic malignant form, are toxic myocarditis (which may terminate fatally in 10–14 days) and interstitial nephritis. The more severe the diphtheria, the earlier these complications may arise. Electrocardiography and urinalysis follow-ups should be continued for at least 6 weeks after the onset of the disease. Tuberculosis Epidemiology: Oral or oropharyngeal manifestations of tuberculosis most commonly occur in the setting of advanced organ tuberculosis. Although these lesions are very rare (0.2 % of patients with organ tuberculosis), they should be considered in the differential diagnosis since the incidence of tuberculosis has been on the rise. It is even less common to see oropharyngeal involvement by a primary complex or in the setting of miliary tuberculosis. Clinical manifestations: Primary complex: A primary tuberculous complex in the tonsillar and cervical lymph-node region is most common in children who have become infected by drinking cow’s milk contaminated with tubercle bacilli. The primary complex in these cases consists of a typical ulcerative lesion of the oral mucosa and tonsil, associated with regional cervical lymphadenopathy. The swelling in the neck leads most patients to seek medical attention. Organ tuberculosis with ulcerative mucocutaneous lesions occurs mainly in regions that may come into contact with secretions containing infectious organisms, resulting in the formation of ulcerative mucosal lesions that are sometimes necrotic. (Other forms of organ tuberculosis can affect the lung, bowel, etc.) Morphologically, the lesions may appear as mucosal ulcerations on the lips and dorsum of the tongue or as slightly raised, nodular eruptions on the palate. Skeletal involvement is also occasionally seen due to hematogenous spread. In this case “cold abscesses” may form about the cervical spine (Fig. 5.18), causing the posterior wall of the pharynx to bulge forward and Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 115
  • 125. II Oral Cavity and Pharynx Fig. “Cold abscess” of the cervical spine in tuberculosis skin test is also performed to assess the reactivity of the organism to tubercle bacilli. Calcifications detected by ultrasound in enlarged cervical lymph nodes are pathognomonic for tuberculosis. If the result is equivocal, a cervical lymph-node biopsy should be taken for a histologic and bacteriologic tissue analysis. Treatment: Inpatient antituberculous polychemotherapy is required, consisting either of a triple regimen (isoniazid, ethambutol, rifampicin) or a quadruple regimen with pyrazinamide added. Acute Viral Pharyngitis Axial CT scan after contrast administration shows a marked protrusion (*) of the posterior wall of the oropharynx. It also reveals sites of bone destruction in the cervical vertebral body behind the oropharynx (arrows). Fig. Peritonsillar abscess Etiology, symptoms: Acute viral pharyngitis, which is often caused by influenza or parainfluenza viruses, typically presents clinically with sudden onset of fever, sore throat, and headache. There may also be coughing and catarrhal symptoms (e.g., rhinitis, sinusitis). Concomitant cervical adenopathy may also be present. Diagnosis: The pharyngeal mucosa appears red and coated on mirror examination. If a bacterial etiology is suspected, a rapid streptococcal test can be performed (see 5.2, p.113). Treatment is supportive and consists mainly of analgesic agents. Cold compresses to the neck can also help to relieve pain. The patient should drink copious amounts of warm liquid to ease complaints. Infectious Mononucleosis Synonyms: Pfeiffer’s glandular fever, kissing disease Inspection reveals typical unilateral erythema, swelling, and protrusion of the left tonsil and of the soft palate on the left side. mimicking the features of a retropharyngeal or parapharyngeal abscess (see below). Miliary tuberculosis: Involvement of the oral mucosa can result from hematogenous spread, appearing as multiple pinhead-size papules, some hemorrhagic, that form on the oral mucosa. Diagnosis: The diagnosis is established by the detection of acid-fast rods in smears, sputum, bronchial secretions, gastric juice, or biopsy material. The diagnostic workup should include biplane chest radiographs to check for pulmonary involvement. The tuberculin Causative organism: Infectious mononucleosis is caused by infection with the Epstein–Barr virus (EBV). It predominantly affects adolescents and young adults. The incubation period is 7–9 days. Clinical manifestations: Although infectious mononucleosis is a systemic illness, it is common to encounter tonsillitis as the initial or cardinal symptom. Besides systemic symptoms such as fatigue, anorexia, and moderate temperature elevation (38–39 C), patients complain of severe pain on swallowing, headache, and limb pains. 8 116 Diagnosis: Clinical examination: The tonsillar and nuchal lymph nodes, axillary nodes, and inguinal nodes are palpably enlarged. Often there is concomitant enlargement of the spleen and liver. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 126. 5 Pharynx and Esophagus Fig. Infectious mononucleosis 5.5 Rare tonsillogenic complications Tonsillogenic sepsis Tonsillogenic sepsis has become rare in the antibiotic era. It most commonly affects patients with weakened host resistance. In these cases, bacteria enter the bloodstream by the hematogenous or lymphogenous route, and the bacteremia can lead to full-blown sepsis. At clinical examination, the tonsils are bright red and swollen, with fibrin coatings. On mirror examination, the tonsils are found to be bright red, swollen, and covered with a grayish fibrin coating (Fig. 5.20). Laboratory tests: The blood count initially shows leukopenia, followed later by leukocytosis (20,000/μL) with 80–90 % atypical lymphocytes (lymphomonocytoid cells, Pfeiffer cells). EBV serology (especially IgM and IgG) is another important test. The enzyme-linked immunosorbent assay (ELISA) can confirm infectious mononucleosis by quantitatively detecting antibodies against the various EBV antigens (virus capsid antigen, early antigen, Epstein–Barr nuclear antigen). Rapid mononucleosis tests are also available but are less sensitive and specific than ELISA. The serum hepatic enzymes should be determined to exclude concomitant involvement of the liver or spleen. Upper abdominal ultrasound and an electrocardiogram are also recommended. Retropharyngeal and parapharyngeal abscess An inflammation or abscess may arise from the prevertebral or parapharyngeal lymph nodes or by hematogenous spread as the result of a minor foreign-body injury or upper respiratory inflammation. This abscess is called a retropharyngeal or parapharyngeal abscess, depending on whether it is located between the spinal column and posterior pharyngeal wall or lateral to the pharyngeal wall. The clinical hallmarks are severe pain on swallowing with progressive dysphagia, muffled speech, and possible trismus and dyspnea. Diagnosis: The mirror examination shows pronounced swelling in the oropharynx or hypopharynx, usually at a prevertebral or parapharyngeal location. The swelling may also spread to the larynx. The blood count indicates leukocytosis with a left shift and elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) values. An imaging study should be performed (Fig.: postcontrast axial CT scan of a right parapharyngeal abscess) to define the extent of the abscess and exclude the spread of infection through the fascial compartments of the neck to the mediastinum (see p. 331). Treatment consists of surgical incision and drainage of the abscess under general endotracheal anesthesia. Retropharyngeal abscess is generally approached by the transoral route. Sometimes it is better to drain a parapharyngeal abscess through an external approach. The surgery is performed under antibiotic coverage, taking into account the mixed spectrum of aerobic and anaerobic causative organisms. Cortisone should also be administered in patients with significant dyspnea. Some patients require prolonged intubation. Treatment: Treatment centers on the symptomatic relief of pain and fever. The agents of choice for pain relief are acetaminophen or ibuprofen. Aspirin products should not be used, as they could cause bleeding problems if tonsillectomy is required. Antibiotics (penicillin V) should be given only if signs of bacterial superinfection are present. Ampicillin and amoxicillin should be avoided because they frequently induce a pseudoallergic rash (Fig. 5.21). In cases of infectious mononucleosis that run a severe course with persistent fever, respiratory distress or stridor, a tonsillectomy can expedite recovery by eliminating the focus of greatest viral proliferation. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. Abscess 117
  • 127. 118 II Oral Cavity and Pharynx Fig. Pseudoallergic rash in infectious mononucleosis a b A pseudoallergic rash developed in this patient following treatment with ampicillin. Complications: Complications are rare and consist mainly of myocarditis, hemorrhage, nephritis, hepatitis, meningitis, or encephalitis. Tonsillogenic Complications Peritonsillar abscess: Peritonsillar abscess is a unilateral inflammatory process that involves not only the tonsillar parenchyma but also the peritonsillar tissue—i.e., the abscess spreads past the tonsil to involve the connective tissue between the parenchyma and pharyngeal musculature. The clinical features are pronounced unilateral redness and swelling of the soft palate (Fig. 5.19), muffled speech, and possible trismus. This is frequently accompanied by uvular edema, but the swelling may also spread to the tongue base and lateral pharyngeal wall, causing respiratory complications. The treatment of choice is removal or incision of the affected tonsil under antibiotic coverage, bearing in mind that most patients harbor a mixed spectrum of aerobic and anaerobic organisms. Other complications: see 5.5. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 128. 5 Pharynx and Esophagus Chronic Inflammations plaints. Chronic Pharyngitis Chronic Tonsillitis Etiology: Chronic pharyngitis is often a result of longterm exposure to various noxious agents (nicotine, alcohol, chemicals, gaseous irritants). It can also occur as a result of chronic mouth breathing due to nasal airway obstruction (e.g., deviated septum) or as an accompanying feature of chronic sinusitis. Pathogenesis: Like infections confined to the tonsillar crypts, recurrent inflammations of the tonsils and peritonsillar tissue can lead to permanent structural changes with scarring. Bacteria that grow on cellular debris in poorly drained crypts can perpetuate a smoldering inflammation, chronic tonsillitis. In this condition the palatine tonsils provide a “focus” that can sustain a variety of diseases in other parts of the body (rheumatic fever, glomerulonephritis, iritis, psoriasis, inflammatory heart disease, pustulosis palmaris and plantaris, erythema nodosum). Symptoms: The main clinical manifestations are a drythroat sensation with frequent throat clearing and the drainage of a viscous mucus. Some patients have a dry cough and a foreign-body sensation in the pharynx. Diagnosis: The history will often direct attention to possible noxious agents. On mirror examination, the pharyngeal mucosa appears red and “grainy” due to the hyperplasia of lymphatic tissue on the posterior pharyngeal wall (hypertrophic form: Fig. 5.22). The pharyngeal mucosa may also have a smooth, shiny appearance in some cases (atrophic form). A thorough nasal examination should be performed to exclude nasal airway obstruction as the cause of chronic pharyngitis, giving particular attention to possible septal deviation or turbinate hyperplasia. The middle meatus should also be examined endoscopically (see 1.3, Anatomy of the Ostiomeatal Unit, p. 7). Treatment: Any agents causing the pharyngitis should be avoided. Also, an herbal product such as sage or chamomile can be used in a steam inhalation to moisten the airways. In patients with nasal airway obstruction due to septal deviation or turbinate hyperplasia, a surgical procedure can be performed to improve com- Fig. Chronic pharyngitis Symptoms: Chronic tonsillitis may cause recurrent episodes of pain or may run an asymptomatic course. The most frequent complaints are lethargy, poor appetite, a bad taste in the mouth, and a fetid breath odor. Diagnosis: Mirror examination often reveals small, firm, immobile tonsils with associated peritonsillar redness. Occasionally a purulent liquid can be expressed from the crypts. Tonsillar smears are found to contain group A β-hemolytic streptococci. Palpation: The tonsillar lymph nodes at the mandibular angle may be enlarged. Laboratory tests: An elevated ESR and CRP and a left shift in the differential blood count are present as signs of the inflammatory process. An antistreptolysin titer of approximately 400 IU/mL or higher is considered pathologic. Treatment: The treatment of choice is tonsillectomy, which is performed under general endotracheal anesthesia with the head hyperextended. The tonsil is exposed by incision of the anterior faucial pillar, shelled out along the connective-tissue plane between the parenchyma and pharyngeal muscle, and detached at its inferior pole. Heavy postoperative bleeding may occur on the day of the tonsillectomy, during the first week after the operation, or even later in rare instances. The typical appearance of a granulating inflammation involving the posterior wall of the pharynx (hypertrophic form). Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 119
  • 129. II Oral Cavity and Pharynx Peripheral Obstructive Sleep Apnea Syndrome (OSAS) Table 5.1 Signs in the patient’s history that are suggestive of (obstructive) sleep apnea Obstructive sleep apnea syndrome (OSAS), like snoring, is a type of sleep-related breathing disorder that can have serious health effects and social consequences. The history can provide important clues to the presence of OSAS (Table 5.1). Etiology and pathogenesis (Fig. 5.23): There is a tendency for the velum, oropharynx, and/or hypopharynx to collapse during sleep, narrowing the pathway for airflow and causing periods of apnea or hypopnea that can last up to 2 minutes. This leads to frequent arousals from sleep and gasping for air, preventing a normal sleep pattern. Besides disturbing the sleep–wake rhythm, OSAS can have longer-term effects due to a reduction in blood oxygen levels, with a potential for significant damage to the cardiopulmonary system. Factors that narrow the pharyngeal airway or lead to decreased muscle tone (Table 5.2) can promote or intensify the disease process. Symptoms: Typical symptoms of OSAS are morning lethargy and daytime fatigue, with a tendency to fall Fig. • Loud, irregular snoring • Periods of apnea during sleep (witnessed) • Unusual daytime sleepiness or fatigue • Restless sleep • Intellectual deterioration (poor concentration and impaired memory) • Personality changes • Loss of libido, impotence • Nycturia, enuresis Source: adapted from Günther, see p. 430. asleep during the day. Witnesses additionally report irregular snoring with periods of apnea followed by “gasping” and loud snoring. Obesity is usually present as an accompanying condition. Diagnosis: Mirror examination may demonstrate an elongated uvula, a narrow velopharyngeal passage, and a bulky soft palate with a small oropharyngeal lumen. It is also common to find a hyperplastic tongue base and hyperplasia of the palatine tonsils. The nasal Pathophysiology, effects, and clinical manifestations of obstructive sleep apnea Onset of sleep Muscle tone ↓ (oral floor, tongue, pharynx, auxiliary respiratory muscles) Pharyngeal cross-section↓ Pharyngeal compliance ↓ Apnea Bradycardia, arrhythmia Pulmonary vasoconstriction ↓ Negative pressure (oropharynx, trachea, thorax) Airway resistance pO2 ↓ pCO2 ↓ ↓ Systemic vasoconstriction Erythropoiesis Central arousal Return to sleep Sudden cardiac death ? Pulmonary hypertension ? Systemic arterial hypertension pH ↓ ↓ 120 Loss of deep sleep, fragmented sleep Resumption of breathing Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. Polycythemia Daytime fatigue, drowsiness, intellectual deterioration
  • 130. 5 Pharynx and Esophagus Table 5.2 Factors and conditions that promote snoring and apnea Classification Pharyngeal obstruction Common factors • Overweight, obesity • Adenoids • Tonsillar hyperplasia • Tumors in the oral cavity, pharynx, larynx, neck Nasal obstruction Decreased muscle tone Treatment: General treatment measures consist of weight reduction, abstinence from alcohol and nicotine, and avoiding big meals, especially at night. It is also important to establish a regular sleep–wake cycle and avoid the use of sedatives. One nonsurgical treatment option is the Esmarch splint, an occlusive splint that advances the lower jaw. By moving the tongue base and adjacent pharynx forward, this device widens the airway in the unstable portion of the oropharynx. In patients with severe grades of OSAS or an unsuccessful trial with an occlusive splint, the unstable portions of the airway can be “pneumatically splinted” by means of transnasal continuous positive pressure ventilation; this keeps the tissues from collapsing during sleep and obstructing airflow. A nasal continuous positive airway pressure (CPAP) mask for this purpose is custom-fitted at the sleep laboratory. Surgical treatment options are tailored to the specific pathology causing the apnea. • Dysgnathia • Acromegaly • Turbinate hyperplasia • Septal deviation • Nasal polyps • Deformities of the external nose • Tumors of the nose • Alcohol • Nicotine • Drugs (sedatives, hypnotics, muscle relaxants) Other Confirming the diagnosis: The current gold standard for confirming OSAS and differentiating it from other sleep-related breathing disorders is polysomnography. Conducted as an inpatient procedure in a sleep laboratory, it measures thoracic and abdominal respiratory excursions, transcutaneous Po2, and records an EEG in addition to the usual screening parameters. • Sleep deprivation • Shift work • Hypothyroidism • Sex (males predominate) • Genetic predisposition: familial occurrence • Sleeping in a supine position airway should also be examined for possible septal deviation, turbinate hyperplasia, or other abnormalities. Flexible transnasal endoscopy can be used to perform a functional test (Müller maneuver) that is helpful in assessing the degree of oropharyngeal obstruction at the level of the soft palate. Technique: The patient sits in an upright or 45 reclined position. With the endoscope in place, the examiner compresses the patient’s nostrils and instructs the patient to inhale the residual intraoral air while keeping the mouth closed. Result: The negative inspiratory pressure during the Müller maneuver produces various collapse effects in the pharynx when OSAS is present, and these effects can be observed endoscopically. When a healthy patient performs this maneuver, it causes very little decrease in the cross-sectional area of the pharyngeal lumen. Objective measuring techniques: Screening: Reports given by the patient and witnesses can be objectified by recording O2 saturation, respiratory sounds, and heart rate on an outpatient basis during sleep. However, these screening devices alone (e.g., the Madaus Electronic Sleep Apnea Monitor, MESAM) cannot provide an accurate sleep evaluation, since they do not at present include an electroencephalography (EEG) channel. Surgical treatment requires very careful patient selection, because many patients will derive little or no benefit from the operation. The result of the Müller maneuver can be helpful in selecting patients for a surgical procedure on the soft palate. An established procedure is the uvulopalatopharyngoplasty (UPPP) with tonsillectomy, in which redundant mucosa is resected from the posterior pillars and the remaining mucosa is tightened by suturing it to the anterior pillars. At least part of the uvula is also resected in most cases. The operation may employ conventional instruments or a laser technique (laser-assisted uvulopalatoplasty, LAUP). Some patients will also require adjuvant intranasal surgery (septoplasty, septorhinoplasty, turbinate reduction). Differential diagnosis: The differential diagnosis should include various disorders that are associated with snoring or with the hypersomnia that is typical of obstructive sleep apnea (Table 5.3). 8 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 121
  • 131. 122 II Oral Cavity and Pharynx Table 5.3 Differential diagnosis of sleep apnea • Occasional or habitual nonobstructive snoring • Upper airway resistance syndrome • Narcolepsy • Underlying heart disease with Cheyne–Stokes respiration (e.g., heart failure) • Nocturnal bronchial asthma • Periodic hypersomnia, hypersomniac form of endogenous depression • Insomnia • Chronic alcohol and drug abuse Source: adapted from Günther, see p. 430. Tumors Benign Tumors and Precancerous Lesions The occurrence, incidence, clinical features, and treatment of these lesions are covered in 4.5, Benign Tumors and Precancerous Lesions of the Oral Cavity (p. 90). Malignant Tumors The overwhelming majority of malignant tumors of the oropharynx are squamous cell carcinomas. Approximately 80% are located in the palatine tonsils or tongue base. Less common sites are the soft palate and posterior wall of the pharynx. Etiology: In most patients, chronic nicotine and alcohol abuse have a major etiologic role in the development of oropharyngeal cancers. Symptoms: Cancers at some sites in the oropharynx may remain clinically silent for some time. Otherwise the symptoms depend on the location and extent of the tumor. Besides dysphagia and odynophagia, the symptoms may include blood-tinged saliva and a fetid breath odor. Advanced stages (Fig. 5.24 a) often produce trismus, signifying that the tumor has invaded the surrounding musculature (pterygoid muscles). Diagnosis: Inspection: Tonsillar carcinomas may appear as exophytic lesions (Fig. 5.24 a) or may show an ulcerating, infiltrating type of growth. Occasionally they are not grossly visible (microcarcinomas of the tonsils), and the first presenting symptom of the disease is cervical lymph-node metastasis. CT and MRI (Fig. 5.24 b–d) are useful for defining the extent of tumor growth and detecting the invasion of surrounding structures. Treatment: The treatment of choice for most cases is surgical tumor removal. The resulting tissue defect may be closed primarily with local pedicled flaps or by using microvascular free tissue transfers, depending on the size and location of the defect (see Fig. 4.25, p. 95). A neck dissection (see p. 334) may be necessary on one or both sides, depending on the location and stage of the primary tumor (see Table 4.2, p. 93). Postoperatively, radiation should usually be delivered to the tumor site and lymphatic pathways. Alternatives for the treatment of advanced tumors (T3, T4) are primary radiotherapy or combined radiation and chemotherapy. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 132. 5 Pharynx and Esophagus Fig. Tonsillar carcinoma a b Tumor c Tumor a Visual inspection reveals an exophytic mass arising from the left tonsil. b, c T1-weighted axial MR images before (b) and after contrast administration (c) show that the tumor (*) has deeply infiltrated the lingual muscles. d Tumor d The corresponding fat-suppression sequence more clearly delineates the tumor from its surroundings. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 123
  • 133. 124 II Oral Cavity and Pharynx 5.5 Diseases of the Hypopharynx and Esophagus The diseases of the hypopharynx that have the greatest clinical importance are foreign bodies, hypopharyngeal diverticula, and especially malignant tumors, which frequently do not produce symptoms until they have reached an advanced stage. The ENT physician is not often confronted with diseases of the esophagus. The majority are caused by injuries and foreign bodies. Congenital malformations such as brachyesophagus and tracheoesophageal fistulas are managed by a thoracic or pediatric surgeon, while esophageal tumors are treated by a general surgeon or abdominal surgeon. Injuries and Foreign Bodies cannot be confirmed by imaging studies, esophagoscopy should be performed using careful technique. Caustic Ingestion Etiopathogenesis: Caustic ingestion in children is almost always accidental, caused by drinking an alkaline or acidic liquid that has not been properly stored. Most such injuries in adults result from attempted suicide. While acids cause a coagulation necrosis with the denaturation of proteins, alkalis cause a colliquative necrosis with liquefaction of the necrotic tissue. Strictures caused by scarring are common sequelae of this type of injury. There is a long-term risk of cancer developing in esophageal strictures caused by caustic ingestion. Symptoms: Acute cases present with severe pain in the mouth and pharynx and possibly in the retrosternal and epigastric areas. Drooling is also present. Patients with an esophageal perforation may also present with subcutaneous emphysema in the neck or a pneumomediastinum (see Fig. 5.27, p.127), and mediastinitis may supervene. Symptoms such as high fever and retrosternal or interscapular pain in these cases are accompanied by typical shock symptoms with an elevated pulse rate, a fall in blood pressure, cold sweats, and pallor. Generalized symptoms of intoxication such as renal and liver failure, electrolyte imbalance, and hemolysis generally do not appear until 1– 2 days after the caustic injury. In the long term, patients may develop an esophageal stricture with progressive dysphagia. Diagnosis: Acute evaluation begins with a mirror examination of the oral cavity, oropharynx, hypopharynx, and larynx. The mucosa initially appears erythematous and edematous and later may show epithelial defects and a whitish fibrin coating. It is also important to obtain radiographs of the chest and abdomen to exclude a perforation of the esophagus or stomach. If the diagnosis The extent of the injuries to the oral and pharyngeal mucosa does not necessarily reflect the severity of corrosive damage to the esophagus, which may be very severe despite a normal appearance of the oral and pharyngeal mucosae. Follow-up: Caustic injuries to the esophagus require long-term follow-up with imaging studies and periodic esophagoscopy. Treatment: Acute: The first priority is to treat the patient for shock. It is important to stabilize the airway, replace fluids, correct electrolyte imbalances, relieve pain, and provide sedation. Treatment should also include high doses of corticosteroids as well as antibiotics to prevent superinfection. Fig. Conservative treatment of esophageal strictures An esophageal stricture is treated with a dilator passed over a guide wire. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 134. 5 Pharynx and Esophagus The therapeutic value of “neutralizing” agents (e.g., magnesium oxide for acid ingestion, citric or acetic acid for alkali ingestion) is questionable because the tissue damage occurs on immediate contact with the corrosive substance, and some time passes before the neutralizing agent can be administered. Long-term: Some esophageal strictures can be treated by dilation. In cases with severe caustic injury, early dilation should be started just one week after the injury. The dilator should never be introduced blindly but should always be passed over a guide wire (Fig. 5.25). If a stricture cannot be expanded by dilation, the stenotic segment should be resected. It may then be necessary to perform a gastric pull-up or interpose a free segment of jejunum with microvascular anastomosis, depending on the length of the esophageal segment that has been removed. Foreign Bodies Etiology and pathogenesis: Foreign bodies typically become lodged in the hypopharynx or in the upper constriction of the esophagus (see Fig. 5.3, p.100). Most patients are small children who have swallowed coins, nuts, or toy parts, but in many cases they are older patients who have decreased sensation in the hard palate (e.g., due to a maxillary denture). Objects typically swallowed by adults are fish bones or larger bone fragments (Fig. 5.26 a), pieces of meat (Fig. 5.26 b), and denture parts. Symptoms: Typical symptoms are a feeling of pressure, a “pricking” sensation, or pain in the hypopharynx or retrosternal area. Dysphagia may also be present, depending on the size and location of the foreign body. Diagnosis: Inspection and palpation will disclose any cutaneous emphysema caused by perforation of the hypopharynx or esophagus (sharp object!). This is followed by indirect mirror examination of the hypopharynx. If this fails to locate the foreign body, diagnostic imaging should also be performed. The imaging procedure of choice depends on the nature of the foreign body suggested by the patient’s history. If a radiopaque foreign body is believed to be lodged in the hypopharynx or upper esophageal constriction, the soft tissues of the neck should be imaged with a lateral radiograph (Fig. 5.26 a). Otherwise, an oral contrast examination (with a water-soluble medium) should be performed (Fig. 5.26 b). An abdominal plain film can also show evidence of a foreign body in some cases (Fig. 5.26 c). Treatment: The sun should never rise and set on a foreign body. Whenever an ingested foreign body is suspected, rigid esophagoscopy should be performed without delay to retrieve the foreign object. With a foreign body that has skewered and cannot be removed endoscopically, it may be necessary to expose the object through an external approach. This may require a transcervical incision or thoracotomy, depending on the location of the foreign body. Rupture of the Esophagus Synonym: Boerhaave syndrome Boerhaave syndrome refers to a spontaneous rupture in the left posterolateral portion of the terminal esophagus just above the esophageal hiatus caused by forceful vomiting or retching. The condition is most common in patients with habitual vomiting and in alcoholics. Symptoms: The classic symptoms occur immediately after the rupture and consist of very severe retrosternal or epigastric pain that may be accompanied by the features of an acute abdomen. Patients may also exhibit hematemesis, dyspnea, and progressive shock symptoms. Diagnosis: First, an anteroposterior chest radiograph should be obtained in the standing or left lateral decubitus position. This will disclose a pneumomediastinum or possible air crescent below the diaphragm caused by air leakage from the ruptured esophagus. Neither of these signs is always evident in the chest radiograph, however, and so CT should be performed if there is lingering suspicion of a rupture (Fig. 5.27). Another option is oral contrast radiography of the esophagus, making certain to use only a water-soluble contrast medium (Gastrografin). If imaging procedures do not furnish a definitive diagnosis, the patient should undergo endoscopy. The treatment of choice is immediate surgical intervention by thoracotomy with primary closure of the defect and pleural repair, leaving a drain in the pleura or mediastinum. The surgery must be performed under antibiotic coverage. Since there is always a danger of perforation, barium should never be used in oral contrast examinations (risk of foreign-body reaction or pneumonia). Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 125
  • 135. 126 II Oral Cavity and Pharynx Fig. Various foreign bodies in the hypopharynx and esophagus a b c a Lateral radiograph of the cervical soft tissues shows a radiopaque foreign body (arrows) in the hypopharynx, corresponding to a sharp-edged bone fragment. b Oral contrast examination with a water-soluble medium (Gastrografin) in the anteroposterior and lateral projections shows a nonradiopaque foreign body (lodged piece of meat) surrounded by an irregular pool of contrast material. c The radiopaque foreign body in the abdominal plain film is a knife, which has become lodged between the lower third of the esophagus and the stomach. Diverticula The treatment of esophageal diverticula is described in standard textbooks of surgery. Two types are distinguished: pulsion diverticula, in which the mucosa herniates through a weak point in the muscular coat due to a rise of intraluminal pressure; and traction diverticula, which usually form at parabronchial sites due to scar traction following hilar lymphadenitis and involve all layers of the esophageal wall. Hypopharyngeal Diverticulum Synonym: Zenker diverticulum Epidemiology: The hypopharyngeal (Zenker) diverticulum is the most common diverticulum of the esopha- Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 136. 5 Pharynx and Esophagus geal inlet. Most patients are middle-aged or older, with a 3 : 1 preponderance of males over females. Pathogenesis: The herniation of esophageal mucosa (pulsion diverticulum) classically occurs at “weak points” in the posteroinferior hypopharyngeal wall located above the cricopharyngeal part of the constrictor pharyngis inferior muscle (see 5.1, p. 98, and Fig. 5.2, p.104). Many patients present with a long history of reflux esophagitis. Fig. Boerhaave syndrome Tracheal bifurcation Mediastinal and precordial air In rare cases, a carcinoma may be the cause of a hypopharyngeal diverticulum. Symptoms: Classic symptoms are dysphagia and the regurgitation of undigested food, especially in the morning and while lying down. Patients also complain of pronounced halitosis caused by food residues trapped in the diverticulum. Smaller diverticula are sometimes manifested only by a foreign-body sensation or may be completely asymptomatic. Diagnosis: Mirror examination or indirect laryngoscopy (see 17.2, pp. 346–349) will occasionally show the pooling of saliva in the piriform sinus, but only an imaging procedure can establish the diagnosis. An oral contrast examination of the esophagus is best for defining the diverticulum (Fig. 5.28). If reflux esophagitis is suspected (belching, heartburn, possible epigastric pain and dysphagia), the imaging study should be supplemented by ambulatory 24-hour pH-metry and esophageal manometry ( 5.6). Aorta Esophagus Axial CT scan of a pneumomediastinum resulting from a spontaneous rupture of the terminal esophagus. Fig. Hypopharyngeal diverticulum: radiographic appearance a b * * 5.6 pH and esophageal manometry With the development of special pH electrodes and modern data-storage capabilities, it is now possible to perform pH recordings and long-term manometry in the esophagus on an ambulatory basis over a 24-hour period. Indications: This study is used to differentiate primary from secondary reflux in patients with reflux esophagitis, investigate motility disorders (achalasia, esophageal spasms), and investigate causes in clinical syndromes such as globus sensation and noncardiac chest pain. The procedure is also used to evaluate response to medical therapy, sphincter dilation, antireflux surgery, and myotomy. Treatment: The treatment of choice is surgery, using either an endoscopic or external approach. Endoscopic approach: The endoscope is advanced through the mouth toward the esophageal introitus. The muscular septum formed by the cricopharyngeus is transected using either conventional technique or a CO2 laser (Fig. 5.29), thereby reintegrating the diverticular pouch into the hypopharynx or esophagus. The endoscopic technique is particularly suitable for Oral contrast study of the esophagus shows pooling of contrast medium in the diverticular pouch (*) in the anteroposterior (a) and lateral (b) projections. older patients with a high surgical risk, as the procedure is well tolerated and of relatively short duration. External approach: An alternative is to resect the diverticulum through an external transcervical ap- Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 127
  • 137. 128 II Oral Cavity and Pharynx Fig. Hypopharyngeal diverticulum: endoscopic treatment Esophagus a Muscular septum At surgery, the muscular septum is identified endoscopically and (in this case) divided with a CO2 laser. Diverticular pouch b proach (Fig. 5.30). In this technique the cricopharyngeus is exposed and divided through a cervical incision, and the diverticular pouch is removed. A postoperative radiograph should always be taken to assess the integrity of the esophagus (Fig. 5.31). Tumors of the Hypopharynx Benign Tumors Benign tumors of the hypopharynx are considered a rarity. They may present clinically with dysphagia, regurgitation, or retrosternal pain. The diagnosis is established with an incisional biopsy taken endoscopically under general endotracheal anesthesia. Treatment consists of surgical removal, depending on the tumor size. Esophagus Malignant Tumors Table 5.4 T stages of hypopharyngeal carcinoma T stage Definition T1 Tumor confined to one site (piriform sinus, postcricoid region, posterior wall of hypopharynx) T2 Tumor extension to multiple sites or an adjacent site, no fixation to surrounding structures T3 Tumor extension to multiple sites or an adjacent site, with fixation to surrounding structures (larynx, upper esophagus, oropharynx) T4 Tumor extension beyond the hypopharynx, with massive invasion of surrounding structures (larynx, cervical soft tissues, other nearby organs) Fig. Histologically, almost all of these tumors are squamous cell carcinomas. As with oral and oropharyngeal carcinomas, there is an etiologic link to chronic alcohol and nicotine abuse. Symptoms: Most malignant tumors of the hypopharynx are diagnosed at an advanced stage because earlier lesions do not produce symptoms. Initial complaints tend to be nonspecific, depending on tumor size and location (Table 5.4), and consist of dysphagia and a fetid breath odor. Later there may be Removal of a diverticulum through an open cervical approach a The cervical soft tissues are divided, exposing the diverticulum and the cricopharyngeal part of the constrictor pharyngis inferior muscle, before (a) and after (b) division of the muscular septum. The diverticular pouch is then removed, and the hypopharynx is closed with external sutures. b Diverticulum Diverticulum Cricopharyngeus Cricopharyngeus Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 138. 5 Pharynx and Esophagus pain radiating to the ear. Hoarseness and possible dyspnea signify tumor extension to the larynx. In many cases, cervical lymph-node metastasis is noted as the earliest sign of disease. Fig. Hypopharyngeal carcinoma a Sternocleidomastoid muscle Diagnosis: Besides the mirror examination or indirect laryngoscopy (see 17.2, p. 346), the diagnostic workup should include endoscopic examination under general endotracheal anesthesia, as this is the best way to evaluate tumor extent. A biopsy can also be taken in the same sitting for histologic confirmation. Additionally, sectional imaging modalities can help to define the tumor size and check for involvement of adjacent structures while also evaluating the cervical lymphnode status (Fig. 5.32 a). Treatment: Treatment depends on tumor size but usually consists of local surgical excision with a concomitant neck dissection (see p. 334). Many malignant tumors of the hypopharynx have already spread to the larynx, making it necessary to perform a laryngectomy in the same sitting (see 17.7, pp. 368–377). The tissue defect is closed primarily whenever possible. This cannot be done with extensive hypopharyngeal resections due to the high risk of stricture formation, and larger defects should be reconstructed by means of a free jejunum transfer with microvascular anastomosis. Surgery should be followed by radiation to the tumor site and lymphatics. Alternative treatments for advanced hypopharyngeal cancers are primary radiotherapy and combined radiation and chemotherapy. Fig. Carcinoma Lymph-node metastasis b Epiglottis Carcinoma Diverticulum after endoscopic removal Postoperative radiograph after endoscopic cricopharyngeal myotomy (see Fig. 5.29) shows no evidence of a diverticular sac. Divided cricoid cartilage plate a The axial CT scan demonstrates a mass that is completely filling the right hypopharynx. The arrows point to an ipsilateral lymph-node metastasis below the sternocleidomastoid muscle. b The surgical specimen includes a posteriorly incised larynx, which has been resected along with the left piriform sinus. The left piriform sinus has been completely obliterated by an extensive squamous cell carcinoma infiltrating the larynx. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 129
  • 139. 6 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 140. II Oral Cavity and Pharynx 4 5 6 Lips and Oral Cavitys Pharynx and Esophagus 6.5 Noninflammatory Diseases and Injuries to the Salivary Glands 142 Sialolithiasis 142 Sialadenosis 142 Injuries 143 6.6 Inflammatory Diseases of the Salivary Glands (Sialadenitis) 144 Acute Sialadenitis 144 Chronic Sialadenitis 145 6.7 Tumors of the Salivary Glands Benign Tumors 148 Malignant Tumors 149 The Salivary Glands 6.1 Clinical Anatomy of the Salivary Glands Classification 132 Parotid Gland 132 Submandibular Gland 132 Sublingual Gland 133 6.2 Functional Morphology and Physiology of the Salivary Glands 134 Histologic Structure 134 Composition of the Saliva 134 Physiologic Functions of Saliva 135 6.3 Clinical Examination, Imaging Studies, and Biopsy of the Salivary Glands 136 Clinical Examination 136 Imaging Studies 137 6.4 132 Overview: Diagnosis and Management of Salivary Gland Swelling 140 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 148
  • 141. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. -erc ,roolf laro eht fo snoitrop roiretsop dna laugnilbus eht stcennoc tnemtrapmoc raludnalg eht ,tnemegnar -ra siht fo esuaceB .aicsaf lacivrec retuo eht fo revoc rednu eerged elbairav a ot enogirt eht tsap sdnetxe dnalg eht fo trap retuo ehT .elcsum dioyholym eht fo redrob roiretsop eht dnuora dneb depahs-U a sekam dnalg ehT .elbidnam eht dna elcsum cirtsagid eht fo strap peed owt eht neewteb enogirt ralubidnam -bus eht ni seil dnalg ralubidnambus ehT :noitacoL dnalG ralubidnambuS .sniahc ladon raluguj peed dna ralubidnambus eht ot sedon hpmyl raludnalgirep dna raludnalgartni lareves hguorht si dnalg ditorap eht fo eganiard citahpmyL .niev raluguj lanretni eht otni niard taht slessev suon -ev dna )yretra laicaf esrevsnart ,yretra laropmet laicif -repus( yretra ditorac lanretxe eht fo sehcnarb era sep eht ot laideM .ymotceditorap laretal a dellac si sunires -na sep eht ot laretal dnalg eht fo noitrop eht fo lavom -er lacigruS .detalosi dna knurt sti ta deifitnedi si evren Submandibular gland Sublingual process Submandibular duct Sublingual gland Caruncle Masseter muscle Buccinator muscle Parotid gland with small accessory gland and parotid duct laicaf ehT .dnalg ditorap eht fo yregrus gnirud kram -dnal tnatropmi na sedivorp noisividbus lacimotana sihT .noitrop laidem dna laretal a otni dnalg eht gni -dividbus ,suniresna sep eht ta suxelp a otni sehcnarb evren laicaf eht ,dnalg ditorap eht gniretne retfA .segde desiar ylthgils htiw ecifiro na gnimrof ,ralom reppu dno -ces eht etisoppo snepo tI .asocum laccub dna elcsum rotaniccub eht secreip dna elcsum eht fo redrob ro -iretna eht dnuora sdniw tI .)1.6 .giF( elcsum retessam eht revo drawrof sessap dna driht roirepus roiretna sti ni dnalg ditorap eht sevael ,gnol mc 6 yletamixorp -pa ,tcud yrotercxe sihT :)tcud nesnetS( tcud ditoraP .)631 .p ,5.6 .giF ees º,romut grebeciª( ecaps laegnyrahparap dna assof enitalapogyretp eht drawot sromut dna snoitammalfni fo daerps eht gni -tatilicaf ,yllaidem dna ylroirefni esned ssel si tI .dnalg eht fo gnillews etuca si ereht nehw niap ereves esuac nac dna elbisnetsid ylroop si eluspac ehT .flesti dnalg ditorap eht htiw dna niks eht htiw sdnelb tub reyal eus -sit etercsid a ton si ,eussit suorbif esned fo desopmoc ,eluspacoduesp suoenatucbus ehT :eluspac suorbiF .elcsum cirtsag -id eht fo ylleb roiretsop eht dna elcsum diotsamodielc -onrets eht htiw tcatnoc ni seil ti ,eluspacoduesp suo -enatucbus a ni deddebmE .diotsam eht dna elbidnam eht fo sumar lacitrev eht neewteb assof ralubidnam -orter eht otni sdnecsed dnalg ditorap ehT :noitacoL dnalG ditoraP .suocum yltnanimoderp si taht avilas a eterces yehT .asocum laegnyrahp eht ni sdnalg laegnyrahp dna ,eugnot eht ni sdnalg laugnil ,etalap eht fo asocum eht ni sdnalg enitalap ,spil eht fo asocum eht ni sdnalg laib -al fo tsisnoc esehT :)2.6 .giF( sdnalg yravilas roniM · .noiterc -es suoresocum a secudorp osla :dnalg laugnilbuS · .noiterc -es suoresocum a secudorp :dnalg ralubidnambuS · .noiterces suores a secudorp ylniam ti ,dnalg yravilas tsegral ehT :dnalg ditoraP · :tcart evitsegidorea reppu eht tuohguorht detubirtsid sdnalg yravilas ronim ,yratilos derdnuh lareves dna )1.6 .giF( sdnalg yravilas rojam fo sriap eerht era erehT rof laitnesse si ymotana dnalg yravilas fo egdelwonk A .sdnalg yravilas ronim dna rojam eht fo ymotana tnav -eler yllacinilc eht weiver lliw ew ,noitcudortni na sA .tnemtaert etairporppa gnidivorp dna sdnalg yravilas eht fo sesaesid gnisongaid dna gnidnatsrednu noitacifissalC .giF sdnalg yravilas rojaM sdnalG yravilaS eht fo ymotanA lacinilC 1.6 xny rahP dna ytivaC larO II 231
  • 142. 331 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .stcud llams sa asocum laro eht otni yltcerid nepo yam ro tcud ralubidnambus eht otni niard yam stcud yrotercxE .)3.6 .giF( elbidnam eht fo ecafrus laidem eht gnola detubirtsid dna tcud ralubidnambus eht ot laretal ,elcsum dioyholym eht no roolf laro eht fo trap suocumbus ,roiretna eht ni seil dnalg laugnilbus ehT dnalG laugnilbuS .tcud ralubidnam -bus dna dnalg laugnilbus eht fo ymotana cihpargopot laroartnI Caruncle Lingual frenulum .)433 .p ees( demrofrep si noitcessid kcen a nehw dnalg ralubidnambus eht evomer ot yras -secen yllausu si ti ,siht fo esuaceB .ytivac laro dna ecaf eht morf eganiard eviecer osla hcihw ,dnalg eht fo noit -rop roirefnioretsop dna laretal eht ni sedon hpmyl ot si dnalg ralubidnambus eht fo eganiard citahpmyl ehT .dnalg eht fo trap roiretsop eht dnuora pool niev dna yretra laic -af ehT .dnalg eht ot laidemorefni snur evren lassolgop -yh ehT .noilgnag ralubidnambus eht ot sehcnarb setu -birtsid ti erehw ,ydob dnalg eht evoba tsuj snur taht uneg a smrof osla tub tcud yrotercxe eht ot desoppa yl -esolc ylno ton si evren laugnil ehT :slessev dna sevreN .elcnurac laugnilbus eht ta snepo dna )3.6 .giF( evren laugnil eht revo sessorc tI .asocum eht htaeneb draw -rof snur dna roolf laro eht fo enalp laugnilbus eht ot dnalg eht fo ssecorp laugnilbus eht htiw sessap dnalg ralubidnambus eht fo ,gnol mc 5 yletamixorppa ,tcud yrotercxe ehT :)tcud notrahW( tcud ralubidnambuS .)roolf laro eht fo sitilullec ro ssecs -ba( noitcefni fo daerps eht rof etuor laitnetop a gnita Sublingual gland Submandibular duct (Wharton duct) 2.6 .)341 .p ,stsyc dnalg y ravilaS , tcud ralubidnambuS .giF ees( snoitammalfni tnerruc -er ot esopsiderp nac yehT .seitilamronba deriuqca ,ralimis morf noitaitneref fid eriuqer stcud y rotercxe eht fo snoitam -roflam latinegnoc esehT Lingual nerve :saisatce dna stsyc citenegsyD .sdnalg tnarreba eseht morf poleved yam sromut dnalg y ravilaS .rae elddim eht ni ylerar dna avignig ro kcen laretal eht ni yltneuqerf tsom rucco yehT .lanoitcnuf -non era dna metsys tcud a evah ton od taht aidromirp dnalg 1.6 .giF y ravilas cipotoreteh era sdnalg y ravilas tnarrebA .) ees( dnalg ditorap eht ot dedneppa dnuof ylnommoc tsom era yehT .lanoitcnuf ylluf era dna metsys tcud eht htiw etacinummoc taht sdnalg y ravilas rojam eht fo segadneppa era sdnalg y ravilas y rosseccA .elcsum retessam eht ot roiret Pharyngeal glands -na detacol dnalg ditorap a sa hcus ,dnalg y ravilas depoleved yllamron esiw rehto na fo noitacol lamronba eht ot srefer aip -otsyD :sdnalg yravilas tnarreba dna yrossecca ,saipotsyD .mrof yam stsyc dna ,sdnalg ralubidnambus eht stcef -fa ylnommoc tsom aiserta tcuD .erar osla era sdnalg y ravilas Palatine glands laudividni gnitcef fa snoitamroflaM .erar ylemertxe si sdnalg y ravilas eht lla fo aisalpA :aiserta tcud ,aisalpopyh ,aisalpA snoitamroflaM .tnempoleved fo keew dn22 eht yb tnetap emoceb stcud y rotercxe ehT .aidrom Labial glands -irp edon-hpmyl edulcni yam dna eussit raludnalg eht setag -erges amyhcnesem gnidnuorrus ehT .tnempoleved cino - y rbme fo skeew ythgie dna htruof eht neewteb tugerof eht ni seussit lamredotce morf esira sdnalg y ravilas rojam ehT ygoloyrbmE sdnalg yravilas roniM sdnalG y ravilaS ehT .giF seilamona dna ,snoitamroflam ,ygoloyrbmE 1.6 6
  • 143. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .)1.6 elbaT( noiterces gnitser eht naht retaerg semit 5±4 yletam snicum suocum ylevitaleR suores eroM semyzne wef ,snicuM rewef ,semyznE stnetnoC ycnetsisnoC sdnalg y ravilas ronim dna eht morf ylniaM eht morf ylniaM dna ralubidnambus dnalg ditorap -ixorppa si noiterces detalumits siht ,dnalg ditorap eht nI .noiterces yravilas fo etar eht esaercni yltnacifingis nac ,.cte ,sllems ,stnemevom gniwehc detaicossa eht dna gnitae ylralucitrap ,srotcaf lanretni dna lanretxE .suelcun yrotavilas eht fo ytivitca cisab eht ot setaler ylbaborp ,noiterces gnitser eht dellac ,noitcudorp siht ,ilumits lanretxe fo ecnesba eht nI .avilas fo tnuoma niatrec a ecudorp yltnatsnoc sdnalg yravilas ehT avilaS eht fo noitisopmoC sdnalg laugnilbus noiterces gnitseR noiterces detalumitS nigirO noiterces detalumits susrev noiterces gnitseR 1.6 elbaT .seitreporp sti gniretla ylthgils ylno elihw avilas eht stropsnart ylniam hcihw ,metsys tcud ralubolretni eht yb dewollof ,diulf eterces ylevitca dna ylkciuq nac hcihw ,stcud detairts eht emoc txeN .noit -artnecnoc etylortcele eht etaluger dna snicum eterces stcud detalacretni trohs ehT .avilas yramirp eht fo yc -netsisnoc dna stnetnoc eht seifidom ylevitca tub met -sys tropsnart evissap a ton si metsys tcud yravilas ehT metsyS tcuD yravilaS .noitca elitcartnoc a hguorht stnetnoc sti edurtxe nac dna sunica eht sdnuorrus taht erutcurts ekilbew a mrof hcihw ,sllec lailehtipeoym edulcni inica ehT Striated duct Fluid )sdnalg laug -nilbus dna ralubidnambus eht ,.g.e( sdnalg dexiM · )sdnalg enitalap eht ,.g.e( nicum ecudorp ylniam hcihw ,sdnalg suocuM · )dnalg ditorap eht ,.g.e( semyzne ecudorp ylniam hcihw ,sdnalg suoreS · :demrof era taht snicum dna semyzne fo stnuoma evit -aler eht no desab dehsiugnitsid era sepyt cigolotsih lareveS .snicumolais dna )esalyma gnidulcni( semyzne sniatnoc hcihw ,avilas yramirp eht ecudorp inica ehT Intercalated duct Mucins Electrolytes Serous Mucous inicA raludnalG Acini Primary saliva Myoepithelial cells Axon .srebif evren dna ,eussit citahpmyl ,slessev citahpmyl dna doolb ,eussit evitcennoc sniat -noc taht amyhcnesem raludnalg a ni deddebme era metsys tcud eht dna inica ehT .)4.6 .giF( stcud yravilas fo metsys a ot detcennoc inica raludnalg :elpicnirp larutcurts nommoc a no desab era sdnalg yravilas llA -curts cigolotsih nommoc eht wonk ot tnatropmi osla si ti ,noitcnuf dnalg yravilas fo sredrosid dnatsrednu oT .noitcnufsyd yroterces rof smret lacinilc eht dna ,avil -as eht fo snoitcnuf cigoloisyhp eht ,sdnalg eht fo erut erutcurtS cigolotsiH .giF sdnalg yravilas eht fo erutcurts cisaB sdnalG yravilaS eht fo ygoloisyhP dna ygolohproM lanoitcnuF 2.6 xny rahP dna ytivaC larO II 431
  • 144. 531 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .stnialpmoc emoselbuort yrev htiw detaicossa yltneuqerf si tI .)senarbmem suocum rehto dna avitcnujnoc eht gnivlovni yllanoitidda( emordnys accis ro )htuom yrd( aimotsorex demret eb yam noit -avilasopyh decnuonorp morf gnitluser noitidnoc ehT )easocum latineg ,avitcnujnoc( .melborp gnisrun tnacifingis a emoceb yam dna yslap larber -ec htiw nerdlihc ni nommoc ylralucitrap si aehrrolaiS .desaercni ylirassecen ton si avilas eht fo ytitnauq eht ,aehrrolais nI .)3.6 elbaT( rehtona eno morf detaitne -reffid ylraelc syawla ton era dna wolf yravilas desaerc -ni ot deilppa era smret lareveS .ailyhcsyd si sred -rosid eseht rof mret lareneg ehT .avilas eht fo ytitnauq dna ytilauq eht ni segnahc ot dael nac noitpmusnoc dna ,tropsnart ,noiterces dnalg yravilas fo sredrosiD sredrosiD yroterceS senarbmem suocum rehto ailaisA noiterces y ravilas fo ecnesbA aimotsoreX asocum laro eht fo sseny rD emordnys acciS dna asocum laro eht fo sseny rD ainepolais :mynonyS 2.6 elbaT ees :sesuaC avilas fo wolf desaerceD noitavilasopyH )noitcurtsbo laegahpose ,romut laegny rahp( noitcurtsbo lacinahceM · )yslap larberec ,sivarg ainehtsaym ,sisylarap rablub ,esaesid snosnikraP( sesaesid cigolorueN · :ot eud .ecnat -ropmi cisnerof fo eb nac ,ti fo tnednepedni tub met -sys OBA eht ot ralimis era seitreporp cinegitna esohw ,snietorpocylg denimreted yllaciteneg fo noitercxe ehT .)VIH( suriv ycneicifedonummi namuh ,seibar ,suriv -eikcasxoc ,surivolagemotyc ,rraB±nietspE ,B sititapeh ,sitileymoilopÐavilas eht aiv dettimsnart eb nac taht sesuriv fo dna )eniroulf ,enidoi( snoi niatrec fo noiterc -xe eht si ecnatropmi lacinilc fO .avilas eht ni detercxe eb nac secnatsbus suonegoxe dna suonegodne htoB noitercxE seitlucif fid gniwollaws yb desuaC )gnirebbols ,gniloord( htuom msilaytp :mynonyS 2.6 elbaT ees :sesuaC aehrrolaiS eht morf avilas fo wolf evissecxE redrosiD smotpmyS ailyhcsyD y ravilas fo secnabrutsid lareneG noitavilasrepyH avilas fo wolf desaercnI noitcudorp ro noiterces noiterces yravilas fo sredrosid rof smreT 3.6 elbaT .seirac latned dna esaesid mug fo noitnev -erp eht ni tnatropmi osla si avilas fo noitcudorp ehT .)AgI ylniam( snil -ubolgonummi dna )sesadixorep ,sesadimarum ,emyz -osyl( semyzne fo noiterces eht seod sa ,elor a syalp )noitagirri( gnisnaelc lacinahceM .ytivac laro eht fo ueilim cinagroni dna lacigoloiborcim eht no ecneulfni rojam a evah avilas fo noitisopmoc dna ytitnauq ehT snoitcnuF evitcetorP scitehtsena lacipot ,)stnasserpeditna ,.g.e( sgurd evitcaohcysp ,)enipreser ,enidinolc ,.g.e( ,enillyhpoeht ,eraruc ,senimatsihitna enief fac stnega evisnetrepyhitna .dnalg ditor -ap eht yb ylniam decudorp si taht emyzne gnittilps -hcrats a ,esalyma-a si emyzne evitsegid lautca ehT .gniwollaws etatilicaf ot sulob eht etacirbul avilas eht ni snietorpocylg ehT .etsat fo noitpecrep eht ni gnidia ,stneutitsnoc doof sevlossid dna seifislume avilas ehT citemimohtapmysaraP stnega cigrenilohcitnA ,enipracolip ,.g.e( stnega -alopocs ,eniporta ,.g.e( avilaS fo snoitcnuF cigoloisyhP ,)enitocin ,eniracsum srekcolb-ahpla ,)enim stnega citemimohtapmys ,)enimalotnehp ,.g.e( noitsegiD dna noitirtuN ,)loneretorposi ,.g.e( srekcolb ateb ,ediroulf ,edimorb ,enidoi ,)lolonarporp ,.g.e( snosiop ,sdica ,sdooF ,sdnalg eht fo noitammalfnI ,)dael ,cinesra ,y rucrem( ,sumsaram ,noitardyhed ycnangerp ,aesuan erusopxe noitaidar noitavilasrepyH noitavilasopyH noitalumitS noisserpeD noitcudorp avilas ecneulfni taht srotcaF 2.6 elbaT sdnalG y ravilaS ehT .esalyma-a fo noitaluger eht ni yllaicepse ,srot -pecer cigrenerda-1b dna -a aiv noitcnuf lortnoc a esic -rexe osla ilumits citehtapmys tuB .ilumits cigrenilohc -citehtapmysarap yb ylniam dellortnoc si avilas fo noitcudorp ehT .)2.6 elbaT( redneg dna ,ega ,noitirtun ,ekatni diulf ,etamilc sa hcus srotcaf suoremun yb ecne -ulfni ot tcejbus ,Lm 0001 ot 005 morf si sdnalg yrav -ilas eht lla yb deterces avilas fo emulov yliad latot ehT 6
  • 145. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .dnalg ralubidnambus eht fo noitaplap launamiB Sublingual gland Submandibular gland Lymph node roolf laro eht fo noitaplaP .giF .)ºromut grebeciª( noiger rallisnot eht ni eglub a ecudorp yam dnalg ditorap eht fo snoit rop peed eht gnivlovni romut A .nosirap -moc edis-ot-edis a ni detnemucod dna detset eb syawla dluohs noitcnuf evren laicaf ,segnahc citsalp -oen yllaicepse ,dnalg ditorap eht ni segnahc htiW .dnalg ditorap eht fo snoitrop peed eht fo gnillews ot eud tnenimorp raeppa yam noiger rallis -not ro laegnyrahparap ehT :)5.6 .giF( noiger rallisnoT .)degnit-doolb ,tnelurup ,tneluccolf ,tnes -ba ro raelc avilas( sgnidnif lamron dna ,noitammalf -ni ,noitcurtsbo neewteb gnitaitnereffid rof retemar -ap tnatropmi na si ,egassam raludnalg ot esnopser ni ro suoenatnops rehtie ,avilas fo wolf ehT .gnillews dna ssender rof detaulave era )stcud nesnetS dna not -rahW( stcud yrotercxe eht fo secifiro ehT :ytivac larO .noit -aplap dna noitcepsni ot elbissecca ylisae ti gnikam ,elcsum retessam eht setavitca sihT .rehtegot swaj eht ezeeuqs tneitap eht gnivah yb detaitnereffid ylisae si tub dnalg ditorap eht fo tnemegralne cimim nac aisalprepyh retessaM .elbisiv ton si dnalg ditorap lam -ron A .niht si niks gniylrevo eht fi enogirt ralubidnam -bus eht ni dnalg ralubidnambus eht fo ruotnoc talf eht ylno slaever noitcepsni lausiv ,yllamroN :lanretxE .detset eb os -la dluohs noitcnuf rotom evren laicaF .noiger rallisnot dna ytivac laro eht htiw gnola )noiger ralubidnambus dna raluciruairep( yllanretxe detcepsni era sdnalg ehT noitcepsnI Tonsil Mandible Parotid gland Tumor Facial nerve Mastoid dnalg ditorap eht fo romut peeD .giF .tnemtaert rof sisab eht sedivorp ti sa ,tnatropmi ylralucitrap si sis -ongaid cigolotsih ehT .seiduts enil-dnoces sa elbaliava era )IRM( gnigami ecnanoser citengam dna )TC( yhp )531 .p ,3.6 elbaT ees( emordnys accis ro ,aehrrolais ,noitavilasopyh dna noitavilasrepyH · ytivac laro dna sdnalg eht gnivlovni )yparehtoid -ar( seipareht ro ,serudecorp lacigrus ,sessenlli roirP · )531 .p ,2.6 elbaT ees ;sgurd cituep -arehtohcysp ,sgurd evisnetrepyhitna( snoitacideM · sdnalg yravilas eht no tceffe cimetsys a evah nac hcihw ,)sutillem setebaid ,.g.e( sredrosid cilobatem yllaicepse ,sesaesid cimetsyS · :ot nevig eb dluohs noitnetta ralucitraP yrotsiH noitanimaxE lacinilC -argomot detupmoc ;yhpargonosartlu si noitagitsevni rehtruf rof ytiladom enil-tsrif ehT .noitanimaxe lacinilc deliated a no desab citsalpoen ro yrotammalfni sa deif -issalc eb nac esaesid dnalg yravilas a ,sesac ynam nI sdnalG yravilaS eht fo yspoiB dna ,seidutS gnigamI ,noitanimaxE lacinilC 3.6 xny rahP dna ytivaC larO II 631
  • 146. .noitammalfni etuca fo ecneserp eht ni detacidniartnoc si yhpargolaiS .noitammalfni cinorhc dna ,sisonedalais ,stcud yrot -ercxe eht fo seilamona ,stcud yrotercxe eht ni senots llams fo noitceted eht edulcni snoitacidni elbissop stI .IRM dna ,ypocsodneolais ,dnuosartlu fo ytilibaliava eht dna )noitasavartxe ,noitamrof ssecsba ,noitcefni( snoitacilpmoc laitnetop ot eud ,revewoh ,yadot demrof -rep ylerar si yhpargolaiS .sdnalg ralubidnambus dna ditorap eht fo smetsys tcud eht fo weiv deliated tsom eht sevig noitaziretehtac retfa stcud yrotercxe eht fo noitanimaxe tsartnoc cihpargoidaR :yhpargolaiS .)weiv roolf laro( tcud notrahW eht ni enots yravilas detcepsus a htiw stneitap ni ylno eu -lav citsongaid fo era shpargoidar nialp ,nosaer siht roF .ezis ni mm 3±2 tsael ta erusaem dna tnetnoc muiclac tneiciffus a evah tsum iluclac ,shpargoidar no elbisiv eb oT .serutcurts desopmirepus fo esuaceb gnidraw -er modles era dnalg ditorap dna ,dnalg ralubidnam -bus ,roolf laro eht fo shpargoidar nialP :shpargoidaR .yspoib noitaripsa eldeen-enif htiw denib -moc eb nac tI .desu erudecorp gnigami tsrif eht si noit -animaxe dnuosartlu eht yllareneG .)7.6 .giF( iluclac dna ,sedon hpmyl ,sromut ,)noitcafeuqil tuohtiw ro htiw( sessecorp yrotammalfni ,amyhcnerap raludnalg lamron gnoma etaitnereffid nac tI .sdnalg yravilas eht gnitagitsevni rof yduts gnidrawer dna detarelot-llew a eb ot devorp sah dnuosartlU :noitanimaxe dnuosartlU seidutS gnigamI .denimaxe eb osla dluohs sedon hpmyl lacivrec dna ,raludnalgirep ,raludnalgartni ehT .detaplap eb tonnac dnalg laugnilbus lamron A .seussit gniylrednu dna niks eht ot evitaler ytilibom dna ,ssenrednet ,sruotnoc ecafrus ,ycnetsisnoc rieht gnissessa dna sretemitnec ni seitilamronba yna fo ezis eht gniton ,)6.6 .giF( ylla -unamib detaplap era stcud yrotercxe eht dna ,sdnalg laugnilbus eht fo gnillews a ,sdnalg ralubidnam -bus ehT .elbaplap ylerab si dnalg ditorap lamron A noitaplaP .tcud not rahW eht Wharton duct 731 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. Tumor Mandible Masseter muscle b Parotid gland tumor Salivary stone Mylohyoid muscle .dnalg ditorap eht ni rom -ut detacramed-lleW b detalid dna detcurtsbo Submandibular gland sah ,wodahs citsuoca latsid a stsac hcihw ,enots ehT .tcud not rahW eht ni enots y ravilas egraL a a Salivary stone sdnalg yravilas eht fo noitanimaxe dnuosartlU sdnalG y ravilaS ehT 7.6 .giF 6
  • 147. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .wol si ytivitisnes sti tub ,aisehtsena lacol rednu mrofrep ot ysae dna efas si erudecorp sihT .sisongaid cigolotsih a dleiy yam pil rewol eht ni dnalg yravilas ronim a fo yspoib eht ,)sitinedalais laileht -ipeoym ,.g.e( esaesid dnalg yravilas dezilareneg htiW .noitces nezorf evitarepoartni na htiw denibmoc dnalg eht fo lavomer lacigrus sevlovni sihT .eluspac sti htiw gnola devomer yletelpmoc eb dluohs romut eht ,)041 .p( ngineb ylekil tsom si romut eht fI .sromut dnalg yrav -ilas ngineb rof detacidniartnoc si yspoib lanoisicnI .yrujni evren laicaf fo ksir tneserp-re -ve eht ot eud ,dnalg ditorap eht ni yllaicepse ,dediova eb dluohs yspoib lanoisicni na ,esiwrehtO .yslap evren laicaf htiw stneitap ni dna snoisel evitareclu rof efas ylevitaler si yspoib lanoisicni nA .ssecorp yrotammalf -ni cinorhc a fo noitagitsevni eht rof detnarraw eb yam sdnalg yravilas eht fo yspoib lanoisicni na ,sesac erar nI :noitces nezorf evitarepoartni dna yspoib lanoisicnI .BANF ni ton tub seispoib eroc ni smelborp laitnetop era kcart eldeen eht gnola noitanimes -sid llec romut dna ,gnideelb ,yrujni evren laicaF .yadot desu eb regnol on dluohs ,decitcarp ylediw ecno ,yspoib eroC .euqinhcet citpesa suolucitem seriuq -er erudecorp eht yhw si hcihw ,etis erutcnup eht fo noitcefni yradnoces si BANF fo noitacilpmoc niam ehT .ecnadiug dnuosartlu rednu detaripsa eb nac snoisel detautis ylpeed eroM .sisylana cigoloiretcab rof lairetam hsinruf osla nac tI .gnillews dnalg yravilas fo noitagitsevni evitarepoerp eht ni erudecorp detarelot-llew ,ksir-wol a sa flesti dehsilbatse sah )BANF( yspoib noitaripsa eldeen-eniF yspoiB .yspirtohtil resal yb ro pool a htiw enots a fo lavomer eht ro noitalid sa hcus demrofrep eb osla nac serudecorp lanoitnevretnI .sesonets dna ,iluclac ,sgulp suocum etartsnomed nac hcihw ,ypoc -sodne gnirud detagirri si tcud ehT .eallipap eht fo noit -alid retfa aisehtsena lacol rednu decudortni era hcihw ,sepocsodne laiceps htiw detcepsni eb osla nac )stcud notrahW dna nesnetS( stcud yrotercxe rojam ehT ypocsodneolaiS .)c±a 9.6 .giF( sromut dnalg yravilas fo sisongaid eht ni TC ot roirepus si IRM .)8.6 .giF( dnalg ditorap eht fo snoitrop peed eht evlovni ro seiradnuob dnalg eht dnecsnart taht sessam dna sromut ot seilppa ylralucitrap sihT .IRM ro TC yb detagitsevni eb tsum sgnidnif dnuosartlu dna ,noitap -lap ,yrotsih eht morf desongaid yletauqeda eb tonnac taht sdnalg yravilas eht fo snoisel tsoM :IRM dna TC .)noitartsinimda tsartnoc ret fa wod -niw eussit-tfos( etalap drah eht fo level eht ta nacs laixA .gniward evitalerroc a htiw ,dnalg ditorap t fel eht ni ssecsba na fo nacs TC Posterior Internal jugular vein External carotid artery Sternocleidomastoid muscle Internal carotid artery Abscess Right parotid gland Left parotid gland Tonsil Pterygoid muscle Mandible Maxilla Masseter muscle Right Anterior Left dnalg ditorap eht fo ssecsbA .giF xny rahP dna ytivaC larO II 831
  • 148. sdnalG y ravilaS ehT 6 dnalg ditorap eht fo romuT Anterior Left Parotid gland tumor .giF Maxillary sinus Nasopharynx External auditory canal Mastoid and middle ear Cerebellum Posterior Right b Anterior Left Maxillary sinus Parotid gland tumor Nasopharynx External auditory canal Cerebellum Mastoid Posterior Right c Left Internal carotid artery Parotid gland tumor Sphenoid sinus Parotid gland Submandibular gland Submandibular gland c eht fo level eht ta ) ( egami lanoroc a dna ,lanac y rotidua lanret .sunis dionehps -ap tfel eht fo amoignahpmyl a fo segami ecnanoser citengaM a( ) dethgiew-1T laixA .sgniward evitalerroc htiw ,dnalg ditor b( dethgiew-2T dna -xe eht fo level eht ta segami tsartnoctsop ) Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 931 Right a
  • 149. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .sromut tnan -gilam dna ngineb gnihsiugnitsid ni lufpleh era taht sngis rof kool ot tnatropmi si tI .eludon elbaplap a htiw gnillews laretalinu ,sselniap ssel ro erom a yb yllac -inilc detsefinam era sromuT .romut a fo esac eht ni yl -ralucitrap ,noitarepo fo emit eht ta edam yllanoisacco si dnalg yravilas nellows a fo sisongaid evitinifed ehT .11.6 .giF ni nwohs sa seiduts cificeps erom ,lanoitidda rof deen eht etacidni ro sisongaid a dleiy yllausu lliw noitamrof -ni sihT .elpmaxe rof ,noisel dilos dna tsyc a neewteb gnitaitnereffid ,gnillews eht eziretcarahc yletarucca erom dna metsys tcud eht ni segnahc etartsnomed nac tI .noitanimaxe lacinilc eht wollof ot erudecorp citson -gaid txen eht si noitanimaxe dnuosartlu na ,yllareneG .noitcefni na ot gnidael ,sisats yravilas desuac sah romut evitcurtsbo na erehw noitautis eht si elur siht ot noitpecxe erar tahwemos A .stset doolb enit -uor ni segnahc on ecudorp yllareneg sdnalg yravilas eht fo sromuT .noitammalfni fo evitseggus si )PRC( nietorp evitcaer-C ro )RSE( etar noitatnemides etycor -htyre ,tnuoc llec doolb etihw detavele nA .romut a dna noitammalfni neewteb gnihsiugnitsid ni lufpleh osla era stset yrotarobal dradnatS .01.6 .giF ni deniltuo era sisongaid laitnereffid a gnikam ni devlovni spets lac -inilc ehT .drager siht ni tnatropmi ylralucitrap si rom -ut tnangilam a fo noicipsus lacinilc ehT .gnitset reht -ruf rof sisab a sa sisongaid laitnereffid a hsinruf ylla -usu lliw noitanimaxe lacisyhp dna yrotsih deliated A .aisalpoen ro ,noitammalfni ,noitcurtsbo tcud fo tluser a eb yam sdnalg yravilas erom ro eno fo gnillews ehT .giF smotpmys lanoitidda oN · eussit gnidnuorrus eht gnitartlifni romut fo sngis oN · elbavom yleerf si taht eludon esnet ro tfos ,sselniaP · )sraey ot shtnom( htworg wolS · :romut ngineb a gnitseggus sngiS .romut eht fo sisongaid laitnereffid eht ot seulc hsinruf osla nac romut dnalg yravilas a fo noitacol ehT tnemegralne edon-hpmyL · )21.6 .giF ,yslap evren laicaf( sevren ro ,niks ,elcsum gnitartlifni romut fo ecnedivE · eludon dexif ,lufniaP · )shtnom ot skeew( htworg dipaR · :romut tnangilam a gnitseggus sngiS .sdnalg yravilas rehto eht ni sromut fo flah yletam -ixorppa htiw derapmoc ,tnangilam era dnalg ditor -ap eht ni sromut fo % 02 tuoba ylnO .dnalg ralubidnam -bus eht htiw esac eht netfo ssel si sihT .romut a seifin -gis netfo yrev dnalg ditorap eht fo gnillews dezilacol A .sdnalg yravilas rehto ni % 01 dna ,dnalg ralubid -nambus eht ni % 01 yletamixorppa ,dnalg ditorap eht ni rucco sromut dnalg yravilas fo tnecrep ythgiE .romut tnangilam a seifingis syawla tsomla dnalg ditorap eht ni romut a htiw detaicossa yslap evren laicaF gnillews cinorhc dna etucA .)151±841 .pp ,7.6 osla ees( ecitcarp ni detanidrooc ylevitceffe eb nac snoitpo citsongaid suoirav eht woh swohs sihT .)931±631 .pp ,3.6 ees( elor tnatropmi na evah yspoib dna ,sei -duts gnigami ,noitanimaxe lacinilc ,yrotsih eht hcihw ni snoitaredisnoc citsongaid laitnereffid ot sdael gnil -lews sihT .sdnalg eht fo gnillews laretalib ro laretalinu yb detsefinam netfo era sdnalg yravilas eht fo sesaesiD gnillewS dnalG yravilaS fo tnemeganaM dna sisongaiD :weivrevO 4.6 xny rahP dna ytivaC larO II 041
  • 150. .ycnangilam a edulcxe yltnedifnoc ton seod BANF no sllec tnangilam fo ecnesba eht ,emit emas eht tA .revewoh ,noitceser evren laicaf sa hcus erudecorp lacidar a yfitsuj ton seod tI .ecno ta detaitini eb dluohs stset etairporppa dna ,romut tnangilam a fo ecneserp lautca eht htiw noitalerroc hgih a sah sllec tnangilam fo noitceted evitisop ehT .sromut fo % 08 yletamixorp -pa ni sisongaid cigolotyc etarucca na dleiy lliw BANF .tnangilam si romut eht taht doohilekil eht retaerg eht ,dnalg yravilas eht re -llams eht :sromut dnalg yravilas rof bmuht fo eluR .romut eht yb ev ren eht fo noisavni gniyfingis ,yslap ev ren laicaf htiw dnalg ditorap thgir eht fo amonicrac diomredipeocuM b 141 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. a .giF sesaesid dnalg yravilas fo noitagitsevni eht rof trahcwolF .giF romut dnalg yravilas a ot eud yslap evren laicaF sdnalG y ravilaS ehT 6
  • 151. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .sdnalg yravilas detceffa eht fo noitavrenni cimonotua dered -rosid si esuac ylekil tsom ehT .sllec ranica degralne yb deziretcarahc redrosid yroterces a si sisonedalaiS sredrosid gnitae rehto dna asovren aixeronA · ycneicifed nietorP · sutillem setebaiD · seicneicifed nimatiV · msilohocla cinorhC · :htiw noitaicossa ni rucco nac sisonedalaiS :sisenegohtaP .detceffa ylnommoc tsom si dnalg ditorap ehT .esuac nwonknu yltneuqerf ,cimetsys a yb desuac sdnalg yravilas rojam eht fo gnillews lacirtemmys ,yrotammalfninon a ot srefer sisonedalaiS :noitinifeD sisonedalaiS .detacidni ylerar si ymotceditorap A .)stnega yrotammalfni-itna ,ekat -ni diulf desaercni( tsrif deirt si ypareht evitavresnoC .taert ot tluciffid erom era dnalg ditorap eht ni senotS .)sevaw kcohs dnuosartlu( yspirtohtil laeroprocart -xe ro )sevaw kcohs dnuosartlu ro maeb resal a gni -su( noitatnemgarf cipocsodne yb devomer eb nac dnalg eht raen ro tcud eht ni detacol senots yravilaS · .desicxe eb dluohs dnalg degamad yllacinorhc a dna dnalg ralubidnambus eht fo senots raludnalgartnI · .)noitazilaipusram( asocum eht ot muileht -ipe tcud eht erutus dna ,enots eht tcartxe ,tcud yrot -ercxe eht esicni ot tneiciffus si ti ,senots latsid htiW · .lacigrus yllareneg si tnemtaerT :tnemtaerT .roolf laro eht fo ylralucitrap ,ssecsba dna noitcefni :snoitacilpmoC .erar yrev era samolucrebut edon-hpmyl deificlac dna ,erar era shtilobelhP .sisongaid laitnereffid tneuq -erf tsom eht si ,romut ro erutned a yb sa ,tcud yroterc -xe eht fo noitcurtsbo lanretxE :sisongaid laitnereffiD .serutcurts desop -mirepus yb derucsbo era dna deificlac ylroop era yeht esuaceb shpargoidar no enifed ot tluciffid ylralucit -rap era dnalg ditorap eht ni iluclaC .sgnidnif dnuosart -lu lacoviuqe htiw sesac erar eht ni ylno yrassecen si siht tub ,tcud notrahW eht fo trap latsid eht ni senots etartsnomed nac hpargoidar roolf laro nA .dnalg ralubidnambus eht ni gnirrucco esoht ylralucitrap ,euqapoidar era senots eht fo % 07 yletamixorppA .gni -wodahs citsuoca lacipyt htiw metsys tcud eht fo noit -alid slaever dnuosartlU .dnalg ralubidnambus eht fo metsys tcud eht ni elbaplap netfo era senotS :sisongaiD .)541 .p ,sitinedalaiS etucA ees( motpmys yradnoces ro yramirp a sa tneserp yam hcihw ,dnalg dna tcud yrotercxe eht fo noitcefni ot dael nac sisats ehT º.romut yravilasª decudni-sisats a eb osla yam erehT .)ºciloc enots yravilasª( niap ereves yb deinapmocca netfo ,dnalg detceffa eht fo gnillews a eticni ilumits yrotatsug rehto dna gnitaE :smotpmyS .sdnuopmoc cinagroni fo noitatipicerp eht ot dna sisats yravilas desaercni ot dael nac noit -acificlacorcim A .)snicum( stnetnoc yravilas cinagro dehcirne morf mrof taht ºsgulpª fo noitacificlac yradno -ces eht morf tluser senots yravilaS :sisenegohtapoitE .dnalg laugnilbus ro sdnalg yravilas ron -im eht ni rucco egatnecrep rellams A .dnalg ditorap eht ni % 02 yletamixorppa dna ,dnalg ralubidnam -bus eht ni rucco senots yravilas fo % 08 ot % 07 morF .sesac lla fo % 01±6 yletamixorp -pa ni tneserp si )enots yravilas dna ,senotsllag ,senots yraniru( sisaihtil dezilareneG .tcud niam eht ni de -tacol era senots yravilas fo % 07 ot % 06 morF :noitacoL .1 : 2 fo oitar a yb gni -tanimoderp selam htiw ,detceffa ylnommoc tsom era sedaced htruof dna driht eht ni stludA :ygoloimedipE .dnalg yravilas a fo met -sys tcud yrotercxe eht ni noitamrof enotS :noitinifeD esaesid enots yravilas :mynonyS sisaihtilolaiS .seirujni dna ,sisonedalais ,sisaihtilolais era tnatrop -mi tsom ehT .sromut dna snoitammalfni yramirp naht rehto sesaesid dnalg yravilas htiw slaed sihT sdnalG yravilaS eht ot seirujnI dna sesaesiD yrotammalfninoN 5.6 xny rahP dna ytivaC larO II 241
  • 152. 341 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .ecifiro tcud eht morf egakael ro noitpros -baer yb detanimile ylkciuq eb dluohs ria eht dna ,yras -secennu si tnemtaert cificepS .noitaplap yb elbatcet -ed ylerar si amesyhpme suoenatuC .dnalg ditorap eht fo noiger eht ni niap tneisnart yb dekram si tI .noollab a gnitalfni ro ,ssalg gniwolb ,tnemurtsni lacisum a gni -wolb nehw ro noitalitnev ksam elbicrof gnirud rucco yam hcihw ,ytivac laro eht ni erusserp evitisop hgih a morf stluser tI .amuart ditorap fo esac laiceps a deredis -noc si tcud nesnetS eht otni ria fo yrtne edargorter ehT .yrassecen ylerar si siht tub ,yspoib raludnalg yb demrifnoc yllacigolotsih eb nac sisongaid ehT .sgni -dnif lacinilc lacoviuqe htiw sesac ni detacidni eb yam yspoib noitaripsa eldeen-enif ro IRM ,TC .noitanima -xe lacinilc no deton yllacipyt si sdnalg yravilas eht fo gnillews sselniap ,lacirtemmys ,laretalib A :sisongaiD .gnitae ot detalernu si taht gnillews lacirtem -mys yllausu ,sselniap a sesuac esaesid ehT :smotpmyS ditorapomuenP .desivda si tnemtaert ylrae ro etaidemmI .592 .p ,2.41 ees :seirujni evren laicaF .muitso-oen a gnitaerc ,asocum eht ot pmuts tcud eht erutus ot si noitpo rehtonA .retehtac citsalp enif a revo demrof -rep eb dluohs sisomotsana dne-ot-dne lacigrusorcim a ,elbissop revenehW .dnalg eht fo driht roiretna eht ot amuart morf tluser nac yrujni tcud A :seirujni tcuD .)yruj -ni evren laicaf fo ksir( dleif derucsbo na ni dediova eb dluohs noitagil ro ,gnippilc ,noitalugaoC .noisserpmoc yramirp yb deganam eb yllausu nac dna gninetaerht -efil ton si dnalg ditorap eht ni gnideelB :gnideelB .derolpxe yl -lacigrus eb dluohs yrujni dnalg yravilas nepo yrevE .evren laicaf ro met -sys tcud yrotercxe eht gnivlovni seirujni morf enola amyhcnerap raludnalg eht ot seirujni hsiugnitsid ot tnatropmi si tI .dnalg ralubidnambus eht naht noitac -ol detcetorp ssel a seipucco hcihw ,dnalg ditorap eht tceffa ylnommoc tsom seirujni tnulb ro prahs tceriD amuarT tnulB ro gnitarteneP seirujnI .deriuq -er si sisonedalais rof ypareht cificeps oN .esuac gni -ylrednu eht drawot detcerid si tnemtaerT :tnemtaerT .stneitap regnuoy ni yltnanimoderp rucco dna laretalib eb ot dnet yeht ;snoitcefni )VIH( suriv ycneicifed -onummi namuh ni nommoc ylralucit rap si tsyc fo epyt sihT .llaw tsyc eht ni eussit citahpmyl slaever noitanimaxe cigol -otsiH .dnalg ditorap eht ni ylniam rucco erofereht dna selcil -lof hpmyl morf etanigiro ylbaborp stsyc lailehtipeohpmyL .etalap eht no detacol si ssam eht nehw yllaic -epse ,sdnalg y ravilas ronim eht fo romut elbissop a edulc -ni osla dluohs sisongaid laitneref fid ehT .pil rewol eht fo asocum eht ni yltnanimoderp rucco smrof htoB .gninil laileht -ipe na htiw )stsyc noitneter =( stsyc eurt ot esir evig snoit -curtsbo tcuD .tsycoduesp a gnimrof ,eussit eht otni epacse :sdnalg yravilas ronim eht fo stsyc noitneter dna selecocuM ot avilas wolla yam sdnalg y ravilas ronim ot seirujnI .noitcefni yb detacilpmoc eb yam yehT .dnalg ditorap eht ni yltnanimoderp rucco stsyc tcud yravilaS .nerdlihc ni ylralucit rap ,demalf -ni emoceb yam dnalg ditorap eht fo stsyc citenegsyD .lavomer lacigrus fo stsisnoc tnemtaerT .detcefni emoceb os -la yam tI .gniwollaws dna hceeps htiw seitlucif fid esuac dna ytilibom eugnot tcirtser nac ezis tneicif fus fo alunar A .).giF ,gorf a fo cas ria lacov dednapxe eht ot ecnalbmeser sti ret fa º,gorf elttilª( alunar a dellac si noitacol siht ta tsyc A .stcud yrotercxe sti dna dnalg laugnilbus eht ni ylnommoc tsom rucco stsyc citenegsyD .stsyc deriuqca ,yradnoces morf dehsiugnitsid eb tsum dna ytilamronba latnempoleved a morf gnitluser stsyc y ramirp era esehT .dnalg eht fo yhportrepyh yttaf htiw ytisebo dna aisalprepyh retes -sam era seitilibissop tneuqerf sseL .dedulcxe eb tsum sitinedalais cinorhc fo smrof llA :sisongaid laitnereffiD sdnalG y ravilaS ehT :stsyc citenegsyD :deretnuoc -ne eb yam smrof suoiraV .snoitammalfni cinorhc dna srom -ut morf noitaitneref fid eriuqer sdnalg y ravilas eht fo stsyC stsyc dnalg yravilaS 2.6 6
  • 153. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .romut a ro ,sisaihtilolais ,ssecsba ro noitcef -ni cinegotned a ,sititorap tnerrucer cinorhc era dere -disnoc eb ot snoitidnoc tneuqerf sseL .sititorap evitar -uppus etuca dna sitinedahpmyl lacivrec morf deriuq -er ylniam si noitaitnereffiD :sisongaid laitnereffiD .cte ,spord nomel htiw noitalumits yravilas dna ,ekatni diulf desaercni ,sciseg -lana fo gnitsisnoc ,evitroppus si tnemtaerT :tnemtaerT era snoitacilpmoc tneuqerf ssel tub suoireS .nommoc ylevitaler si sitigninem suores yb deinapmocca noitan -imaxe diulf lanipsorberec lamronba nA :snoitacilpmoC .)esu reporp htiw etar noitcetorp % 69( margorp noitaniccav spmum a si erusaem evitneverp tseb ehT :sixalyhporP .devlovni eb osla yam seiravo dna saercnap ehT .sesac tsom ni laretalinu si dna rucco osla yam ssenfaeD .sitihtnirybal dna ,sitihcro ,sticifed evren lainarc tnenamrep htiw sitilahpecneogninem .sisoelcunonom elb -meser taht smotpmys cimetsys sesuac dna stneitap desim -orpmoconummi ni srucco ylnommoc tsom noitcefni eht efil fo segats retal nI .ssol gniraeh laruenirosnes sa hcus ,sevles -meht sdnalg y ravilas eht morf etarapes smotpmys suoirav ecudorp yam ro esruoc tnelis a nur yam noitcefni eht ,yllat -anirep deriuqca net fO .avilas eht ni dehs si dna sngis y rotam -malfni on htiw dnalg y ravilas eht stcef fa yllausu suriv ciport -olais ehT .)esaesid noisulcni dnalg y ravilas( surivolagemot - yc yb desuac si sitinedalais lariv nommoc tsom dnoces ehT sitinedalais surivolagemotyC 3.6 · sisolucrebuT · sisocymonitcA · silihpyS :)4.6 ( sitinedalais suotamolunarg suoitcefnI 4.6 ;emordnys tdrofreeH( llec dioilehtipE · ) )emordnys nergöjS( lailehtipeoyM · :sitinedalais enummI sitinedalais noitaidaR )romut renttüK( sitinedalais gnisorelcs ,dnalg ralubidnambus eht fo sitinedalais tnerrucer cinorhC sititorap tnerrucer cinorhC sitinedalais cinorhC · sititorap evitaruppus etucA · sitinedalais )etylortcele( evitcurtsbO :lairetcaB azneulfni ,sesuriv azneulfniarap ,surivohce ,suriveikcasxoC · · spmuM · 3.6 ( surivolagemotyC ) :lariV .sisongaid eht sehsilbatse esaesid eht fo tesno eht retfa skeew 3±2 sretit ydobitna fo esir dlof-ruof A .sesac luf -tbuod ni ylno yrassecen si gnitset cigoloreS .noitatnes -erp lacinilc eht no desab si sisongaid ehT :sisongaiD .skeew 2±1 ni evloser dluohs noitcef -ni ehT .elirbefa era stneitap fo % 03 yletamixorppa dna ,tneserp si revef dlim a ylno yllausU .tnelurupnon era snoiterces eht dna ,nellows ylthgils dna denedder era secifiro tcud ehT .sdnalg ralubidnambus eht dna ,dnalg ditorap etisoppo eht ,sedon hpmyl lacivrec eht fo gnil -lews yb retal syad lareves dewollof ,yllaitini detceffa si dnalg ditorap eno netfO .)ºskeehc retsmahª( amede yhguod a htiw sdnalg ditorap eht fo gnillews etuca ,luf -niap ,esuffid htiw tneserp yllacipyt sesaC :smotpmyS .ytinummi gnolefil srefnoc noitcefni eht dna ,esruoc tnelis a nur sesac fo tnecrep ytfiF .syad )01 ( 81 si doirep noitabucni ehT .etuor suonegotameh eht yb detcefni era sdnalg yravilas rojam ehT .nois -simsnart telpord yb daerps si noitcefni eht dna ,avil -as eht ni dehs si suriv ehT .sesurivoxymarap fo ylimaf eht morf ,suriv spmum eht si msinagro evitasuac ehT .sititor -ap suoitcefni ,sititorap cimedipe :smynonyS .nerdlihc ni ylevisulcxe ton tub yltnanimoderp srucco hcihw ,)woleb ees( spmum fo msinagro evitasuac eht si tI .suriv spmum eht si negohtap lariv nommoc tsom ehT .suriv ycneicifedonummi namuh eht dna ,suriv azneulf -ni ,suriveikcasxoc ,)3.6 ( surivolagemotyc era sesuac eraR .sdnalg yravilas eht fo snoitammalfni lariv etuca fo esuac eht sa deifitnedi neeb evah smsinagro suoiraV sitinedalaiS etucA sitinedalais fo sepyT 4.6 elbaT spmuM ,sitinedalaiS lariV etucA sitinedalais etucA .erusopxe noitaidar gnizinoi ro ,sesaesid enummiotua ,snoitcefni lairetcab ,snoitcefni lariv yb desuac eb yam yehT .cinorhc ro etuca eb yam hcihw ,sitinedalais fo smrof suoirav eht sweiver 4.6 elbaT .dnalg eritne eht fo gnillews esuffid ot sdael yllausu dnalg yravilas a fo noitammalfni ehT )sitinedalaiS( sdnalG yravilaS eht fo sesaesiD yrotammalfnI 6.6 xny rahP dna ytivaC larO II 441
  • 154. 541 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .yrujni evren laicaf fo ksir tnacifingis a seirrac dna sesac eseht ni tluciffid si hcihw ,ymotceditorap a eriuqer yam stneitap tludA .nerdlihc ni detacidni yl -etinifed si hcaorppa evitavresnoc A .sititorap lairetcab etuca sa emas eht detaert era snoitabrecaxE :tnemtaerT .noitamrof ssecs .noitamrof ssecsbA :snoitacilpmoC -ba htiw sititorap evitaruppus etucA ssecsba ditoraP .nemow ni yltnanimoderp srucco sitinedala -is enummI .yspoib lanoisicni na etatissecen yam dna stluda ni tluciffid eb nac sitinedalais enummi nommoc ssel eht morf noitaitnereffiD :sisongaid laitnereffiD .)stnemges tcud lanimret dna inica eht fo aisatce htiw stcud yroterc -xe( nrettap ºeert yfaelª a etartsnomed nac yhpargol -ais ,detacidni ylerar hguohT .skcatta neewteb deniat -bo si margonos lamron a yllareneG .esruoc lacinilc dna yrotsih eht morf edam si sisongaid ehT :sisongaiD .smotpmys fo noituloser detaicossa na htiw ,esaec yllanif dna eldniwd ot noitcudorp avilas sesuac am -yhcnerap eht fo gnirracs evitaretilbo hcihw ni esruoc detcartorp yrev a ekat yam stluda ni sesaC .ytreb -up gnirud evloser yllausu smotpmys eht ,nerdlihc nI .detarudni eb yam dnalg ditorap eht tub smotpmys evitcejbus on sah tneitap eht ,skcatta neewteB .slavretni gniyrav ta rucer skcatta ehT .tneserp yltneuqerf si sumsirT .tnelurup ro ,ralunarg ,yklim si avilas ehT .lufniap yrev eb yam hcihw ,dnalg ditorap eht fo gnillews )laretalib ylerar( gnitanretla ro laretalinu a si ereht yllausU :smotpmyS .rotcaf gnisopsiderp a eb ot deveileb si aisatcet -cud latinegnoC .niatrecnu si ,stluda ni rucco osla tub doohdlihc ni nommoc era hcihw ,dnalg ditorap eht fo snoitcefni lairetcab tnerrucer fo sisenegohtap ehT sititoraP tnerruceR cinorhC )641 .p ,4.6 osla eeS( sitinedalaiS cinorhC .evren laicaf eht fo sehcnarb eht ot lellarap desicni eb dluohs dnalg ditorap eht ,spoleved ssecs -ba na fI .eneigyh laro doog dna ,noitalumits yravilas ,noitardyh ,)stnega yrotammalfni-itna ladioretsnon( sciseglana ,scitoibitna htiw tnemeganam lacidem ot llew sdnopser esaesid eht yllareneG :tnemtaerT sdnalG y ravilaS ehT .giF .)dnalg ralubidnambus eht fo sitinedalais htiw yllaicepse( sitinedahpmyl ro ssecsba raluciruairep a htiw sitito ral -ucnuruf si esuac tneuqerf ssel A .sgnidnif ralimis ecud -orp nac noitcefni cinegotned A :sisongaid laitnereffiD .ytivitisnes cito -ibitna enimreted ot yllacigoloiretcab detset eb dluohs egrahcsid ehT .ssenlli roirp gnidnopserroc a htiw stneitap ni egrahcsid evitaruppus dna sgnidnif elbap -lap lacipyt eht morf edam si sisongaid ehT :sisongaiD .tneserp eb yam sumsirT .ylsuoenatnops niard yam ro ecifiro dnalg eht morf desserpxe eb nac sup ro diulf dibrut A .nellows dna der era secifiro tcud yr -otercxe ehT .)31.6 .giF( noitcafeuqil eussit ot eud tnaut -culf emoceb yam dnalg eht dna ,denedder eb yam dnalg eht revo niks ehT .dnalg detceffa eht fo gnillews esuffid ,lufniap a htiw stneserp tneitap ehT :smotpmyS .eneigyh latned dna laro roop ro ,sesnefed tsoh denekaew ,sutillem setebaid sa hcus sitinedalais lairet -cab rof noitidnoc gnisopsiderp lareneg a si ereht ylla -usU .wolf yravilas desaerced htiw tneitap a ni noitcef -ni lairetcab gnidnecsa na si nrettap lacipyt ehT .rucco osla smsinagro rehto dna ,sulihpomeaH ,iccocotpertS .suerua succocolyhpatS si msinagro evitasuac niam ehT .erut -an ni cinegotned ro )erutned gnittif ylroop ,sisaihtilol -ais( evitcurtsbo yllausu si esuac eht ,detceffa si dnalg ralubidnambus eht nehW .stneitap detardyhed ,de -tatilibed ni dnalg ditorap eht stceffa ylnommoc tsom noitcefni evitaruppus sihT :sisenegohtap dna ygoloitE sitinedalais evitaruppus etuca :mynonyS sitinedalaiS lairetcaB etucA 6
  • 155. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. -ni na ekat ot lufpleh netfo si tI .yrassecen ylerar si tub )nrettap ºeert sselfaelª( metsys tcud erab eht setarts -nomed yhpargolaiS .detceted eb yllareneg nac )sei -dobitna ditorap( muilehtipe tcud-yrotercxe tsniaga seidobitna cimsalpotyC .RSE detavele na sa hcus noit -ammalfni fo sngis cificepsnon wohs stseT :sisongaiD .seirac latned dna ,as -ocum laro eht fo snoitcefni ,ssenyrd laro emoselbuort yb detsefinam si emordnys acciS .esaesid citamuehr gniynapmocca na dna ,accis sitivitcnujnocotarek ,aim -otsorex htiw emordnys nergöjS a evah stneitap ynaM .dnalg eht fo yhporta htiw stneserp egats dne ehT .ssen -rednet ro niap elttil yrev htiw ,yhguod dna nellows ylesuffid era sdnalg ditorap htoB .ega fo sraey 06±05 nemow stceffa yltnanimoderp esaesid ehT :smotpmyS .sllec lailehtipeoym fo sdnalsi dna ,noitartlifni citycohpmyl laititsretni ,yhporta lamyhc -nerap stibihxe dnalg eht ,yllacigolotsiH .muilehtipe tcud yravilas eht fo snegitna tsniaga detcerid seidob -itna fo noitamrof eht yb deziretcarahc esaesid enum -miotua na si sitinedalais lailehtipeoyM :sisenegohtaP .)amredorelcs ,sitisoymylop ,susotamehtyre supul ,sitirhtra diotam -uehr( redrosid epyt-diotamuehr a dna )noitamircal desaerced( accis sitivitcnujnocotarek yb deinapmoc -ca sitinedalais lailehtipeoym fo stsisnoc emordnys nergöjS .)51.6 .giF( poleved yam emordnys accis A .noit -cudorp avilas ni enilced laudarg a yb dekram sitineda -lais cinorhc fo mrof enummiotua na si sihT :noitinifeD noisel lailehtipeohpmyl ngineb :mynonyS emordnyS nergöjS dna sitinedalaiS lailehtipeoyM .noitaplap yb msalpoen a morf hsiugnitsid ot tluciffid si taht dnalg eht fo tnemegralne rednetnon yllaitnes -se ,tnatsnoc ,mrif a si ,romut renttüK a dellac ,egats dne ehT .gnitae ot detaler si taht tnemegralne lufniap yletuca na seogrednu hcihw ,dnalg ralubidnambus eht fo gnillews mrif a htiw tneserp stneitaP :smotpmyS .noitammalf -ni eht rof msinahcem cinegohtap niam eht si ,stcud yrotercxe eht fo noitcurtsbo htiw denibmoc yllausu ,avilas eht fo noitisopmoc deretla nA :sisenegohtaP .dnalg de -tceffa eht fo gnillews ekil-romut ,tnenamrep a ni etan -imluc yam tI .sisaihtilolais dna noitcurtsbo htiw noita -icossa ni gnirrucco yllausu ,sitinedalais yrotammalfni cinorhc fo mrof nommoc tsom eht si sihT :noitinifeD romut renttüK ,dnalg ralubidnam -bus eht fo sitinedalais tnerrucer cinorhc :smynonyS sitinedalaiS gnisorelcS cinorhC .aimotsorex dekram htiw emord -nys ekil-nergöjS a tibihxe yam )SDIA( emordnys ycneicifed enummi deriuqca htiw stneitap dna ,sdnalg ditorap eht fo stsyc lailehtipeohpmyl laretalib dnif ot nommoc ylralucit rap si tI .)esaesid dnalg y ravilas VIH( suriv ycneicifedonummi namuh htiw detcefni stneitap ni nommoc ylevitaler si sdnalg y ravilas eht fo tnemegralne lacirtemmyS :noitcefni VIH .tneserp si noitammalfni suotamolunarg a nehw dedulc -xe eb dluohs tub erar y rev si dnalg y ravilas eht fo silihpyS .erar yllareneg si tI .yliradnoces dnalg eht evlov -ni yam dna dnalg ralubidnambus ro ditorap eht ot ytimixorp ni poleved yam tI .sisongaid laitneref fid eht ni dedulcni eb dluohs noitarolocsid niks suoecaloiv lacipyt a dna gnillews .)41.6 .giF( yrassecen netfo si dnalg eht fo noisicxE .stnega yrotammalfni-itna dna ,sciseglana ,scitoibitna htiw detaert si kcatta etuca nA :tnemtaerT .sesongaid laitnereffid erar era sisolucrebut dna sisoc -ymonitcA .tluciffid eb nac ssecsba cinegotned a morf noitaitnereffiD .ytivac laro eht fo amonicrac llec suom -auqs morf yllaicepse ,sisatsatem edon-hpmyl edulc -ni osla dluohs sisongaid laitnereffid ehT .gulp suocsiv ro enots a yb noitcurtsbo latcudartni morf dna snoisel laroartni rehto ro ,stsyc ,sromut ot eud erusserp cisnirt -xe sa hcus noitcurtsbo tcud yrotercxe fo sesuac rehto morf deriuqer si noitaitnereffiD :sisongaid laitnereffiD sselniap ,drah a htiw sisocymonitcA :smrof cinorhc rehtO .sgurd citatsolucrebut no seiler tnemtaerT .noitan -imaxe cigolotsih ro/dna gnitset cigoloiretcab yb dehsilbatse si sisongaid ehT .amyhcnerap raludnalg eht ylnommoc ssel dna ,detcef fa yltnanimoderp era sedon hpmyl raludnalgartni ehT .erar si sdnalg y ravilas eht fo sisolucrebuT :sisolucrebuT .yslap ev ren laicaf yllaicepse ,sticifed ev ren lainarc htiw detaicossa net fo si tI .)revef ditorapoevu cinorhcbus( emordnys tdrofreeH sa nwonk si sdnalg y ravilas dna )aevu eht ylniam( seye eht fo tnemevlovni suoenatlumiS .sdioretsocit roc htiw detaert si esaesid ehT .deriuqer si sisolucrebut morf noit -aitnereffiD .yspoib yb dehsilbatse si sisongaid ehT .tneserp si ainepolais on ro elttil dna ,dlim ylevitaler si niaP .rucco yam sdnalg y ravilas ronim eht fo tnemevlovnI .amyhcnerap raludnalg eht ot noitidda ni detcef fa eb yam sedon hpmyl º.yspoib lanoisicxeª na sa detapritxe eb nac dnalg ehT .segnahc yrotammalfni slaever yspo -ib noitaripsa eldeen-eniF .sesac detacilpmoc ni ylno yrassecen si IRM .dnuosartlu htiw noitcurtsbo tcud eht gnitartsnomed yb edam si sisongaid ehT :sisongaiD raludnalgartnI .gnillews tnatsnoc ,mrif yletaredom a swohs hcihw ,dnalg ditorap eht fo tnemevlovni laretalib ro laretal sisodioc -raS :emordnys tdrofreeH dna sitinedalais llec dioilehtipE -inu yb deziretcarahc yllausu si sdnalg y ravilas eht fo sitinedalais cinorhc fo smrof rehtO 4.6 xny rahP dna ytivaC larO II 641
  • 156. .sdnalg yravilas eht fo noitcnuf eht tcetorp ot pleh yam noitaidarri lanretxe dna nitalpsic htiw tnemtaert denib -moc gnirud enitsofima fo noitacilppa nA :sixalyhporP .)aet egas htiw ,.g.e( noitardyh tneuqerf ro ,etutits -bus avilas a gniretsinimda ,)enipracolip yad/gm 5 ” 3 ,.g.e( avilas fo noitcudorp eht gnitalumits sa hcus deirt eb dluohs serusaem citamotpmyS :tnemtaerT .stnialpmoc lufssert -sid htiw tfel era stneitap ynam tub ,sraey fo doirep a revo rucco yam yrevocer fo eerged emoS .poleved yam emordnys accis nwolb-lluf A .aisuega ro aisuegop -yh htiw denibmoc yltneuqerf ,eugnot eht fo gninrub dna aimotsorex era smotpmys niam ehT :smotpmyS .noitammalfni lasocum dna seirac latned ni stluser emordnys acciS .avilas eht ni egnahc evitatilauq dna esaerced evitatitnauq a gnisuac ,inica raludnalg suores eht ot si egamad ereves tsom ehT .yrevocer laitrap fo eerged elbairav a htiw yrujni elbisreverri esuac sesod noitaidar rehgiH .elbisrever si yrujni eht ,yG 51 naht ssel sesod tA .ssenyrd laro tnenamrep ro tneisnart dna yhporta htiw sdnalg yravilas eht fo noitammalfni na seticni )sdnalg yravilas eht ni detercxe si enidoi( ypa -reht enidoioidar ro noitaidarri lanretxE :sisenegohtaP sitinedalaiS noitaidaR .emordnys accis ni sitissolG b .emord htiw tneitap fo gnillews lare ditorap thgir a .noitavilas etalumits ot deirt eb nac enipracolip yad/gm 5 ” 3 fo nemiger A .diulf lamircal eht ecalper ot spord eye dna setutitsbus avilas laro fo esu eht sedulcni dna evitroppus si tnemtaert esiwrehtO .esaesid citamuehr a fo gnittes eht ni ylno detacidni si ypareht tnasserppusonummI :tnemtaerT .dnalg eht edistuo dna nihtiw htob samohpmyl nikgdoH-non fo ecnedicni desaercni na si erehT .)noitcefni ,noitarec -lu( noitamircal desaerced dna )seirac latned ,sitisoc -um( ainepolais fo ealeuqes eht dna sititorap tnerruc -er cinorhc era snoitacilpmoc tneuqerF :snoitacilpmoC -nys nergöjS a ni sdnalg ral -ubidnambus eht -talib dna dnalg eht fo gnillewS emordnys nergöjS .giF .flesti dnalg di -torap eht morf eussit elpmas ot yrassecen eb osla yam tI .segnahc cigolotsih lacipyt tibihxe dna sesac fo % 07 ±06 yletamixorppa ni devlovni era hcihw ,pil eht fo sdnalg yravilas ronim eht fo eno morf yspoib lanoisic Facial artery Facial vein 741 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. b a Hypoglossal nerve Stylohyoid muscle Submandibular gland Digastric muscle .noitarepo eht gnirud elbarenluv era ev ren lassolgopyh eht dna ,ev ren laicaf eht fo hcnarb ralubidnam lanigram eht ,ev ren laugnil ehT .dnalg ralubidnam Ligated excretory duct Marginal mandibular branch of the facial nerve Lingual nerve -bus tfel eht fo lavomer lacigruS dnalg ralubidnambus eht fo noitapritxE 41.6 .giF sdnalG y ravilaS ehT 6
  • 157. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .selam ni rucco % 09 dna ,laretalib yllanoisacco era sromut esehT .dnalg ditorap eht fo romut nommoc tsom dnoces eht dna amoneda cihpromonom nom -moc tsom eht si amohpmylonedatsyc ,dnalg ditorap eht fo elop roirefni eht ta detacol yllacipyT :noitinifeD musotamohpmyl amonedatsyc yrallipap ,romut snihtraW :smynonyS amohpmylonedatsyC .erar si tub amoneda cihpromoelp ni rucco ot nwonk si amonicraC .sromut regral htiw hsilpmocca ot tluciffid eb nac htoB .evren laicaf eht evreserp osla dna romut eht evomer ot reisae ti ekam lliw siht sa ,sromut rellams rof neve dednem -mocer si yregrus tpmorP .noitceser romut dnuos yl -lacinhcet a gniwollof doog si sisongorp ehT :sisongorP .evoba eeS :tnemtaerT .nemiceps lacigrus eht fo noitanimaxe no seiler sisongaid evitinifeD .noitacol dna tnetxe rom -ut no noitamrofni esicerp hsinruf lliw IRM ylbareferp ro TC ,sromut regral htiW .sesac fo egatnecrep egral ylriaf a ni amoneda cihpromoelp a sa romut eht yf -itnedi nac )831 .p( BANF .sromut laicifrepus dna llams fo sisongaid eht rof tneiciffus era noitanimaxe dnuos -artlu dna ,noitaplap ,noitcepsni ,yrotsih ehT :sisongaiD .ycnangilam fo ecnedive on swohs dna ,edis eno ot denifnoc yllausu ,elbavom yleerf si taht romut dnalg yravilas raludon ro mrif ,ssel -niap a fo taht si noitatneserp lacinilc ehT :smotpmyS .tniop -dnats tnemtaert a morf ytilacofitlum etaicerppa ot tnatropmi si ti tub ,erar era sromut lacofitluM .eluspac -oduesp a yb dednuorrus si romut eht yllareneG .nem naht yltneuqerf erom detceffa era nemoW .dnalg di -torap eht ni yltnanimoderp gnirrucco ,sdnalg yravilas eht fo amoneda nommoc tsom eht si tI .)61.6 .giF( de -hsilbatse llew neeb sah amoneda cihpromoelp fo erut -an lailehtipe eht ,msihpromoelp cigolotsih sti etipseD romut dexim ngineb :eman ciahcrA )5.6 ( amonedA cihpromoelP .noitarepo eht ot roirp siht fo demrofni eb tsum tneitap eht dna ,yreg -rus dnalg ditorap fo epyt yna ni stsixe yrujni evren laicaf tnenamrep ro yraropmet fo ytilibissop ehT .evren laicaf eht gnivreserp yl -efas elihw yaw siht ni devomer eb nac sromut ngineb tsoM .desicxe era evren eht fo suniresna sep eht ot lare -tal seussit raludnalg eht dna ,deifitnedi si knurt evren laicaf eht tsriF .sromut dnalg yravilas ngineb rof enod erudecorp nommoc tsom eht si ymotceditorap laretal a ,dnalg ditorap eht ni detacol era sromut tsom ecniS .sisongaid cigolohtap evitinifed a rof dna yg -olotsih eussit-nezorf evitarepoartni rof lairetam sediv -orp nemiceps ehT .desaercni yldekram si ecnerruc -er lacol fo ksir eht esiwrehto ;eussit yhtlaeh fo nigram a htiw lavomer etelpmoc fo stsisnoc sromut dnalg yravilas ngineb fo tnemtaert ehT .pets eno ni dehsilp -mocca yllareneg era tnemtaert dna yspoiB :tnemtaerT .yrujni evren laicaf dna noitanimessid llec romut fo ksir eht ot eud yspoib lanoisicni yb detagitsevni eb ton dluohs sromut dnalg yravilas ngineb yllacinilC .rom -ut dnalg yravilas ngineb a seifingis ,smotpmys rehto yb deinapmoccanu ,dnalg yravilas eht ni eludon elib -om ,esnet ro tfos ,sselniap a fo ecneserp ehT :sisongaiD tnemtaerT dna sisongaiD fo stcepsA lareneG amoneda cihpromoelP .giF .5.6 elbaT ni deweiver era sepyt nommoc ssel ;sromut nommoc tsom eht sebircsed tinu tneserp ehT .041 .p ,4.6 ni derevoc saw sihT .noitaplap dna ,noit sromuT ngineB -cepsni ,yrotsih eht yb dehsilpmocca eb yllareneg nac romut a fo noitaitnereffid tnangilam/ngineb ehT .ngin -eb era sromut dnalg yravilas fo % 07 yletamixorppA sdnalG yravilaS eht fo sromuT 7.6 xny rahP dna ytivaC larO II 841
  • 158. 941 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. esac ehT .deredisnoc eb syawla tsum evren laicaf eht fo noitceser elbissop ,dnalg ditorap eht fo esac eht nI .snosaer fo yteirav a rof ,revewoh ,elbarised ro elbissop syawla ton si lavomer romut etelpmoC .noiger romut eht gnitaidarri neht dna elbissop sa yletelpmoc sa romut eht gnivomer no desab si sromut dnalg yrav -ilas tnangilam rof tpecnoc tnemtaert ehT :tnemtaerT .sisongaid cigolotsih evitinifed a dedleiy sah yspoib romut lacig -rus eht retfa ylno dediced si tnemtaert fo nalp evitinif -ed eht esac siht nI .detceser eb tsum evren laicaf eht fi yllaicepse ,yrassecen eb yam erudecorp lacigrus egats -owt a ,lacoviuqe semitemos si ygolotsih eussit nezorf esuaceB .noitarepo eht gnirud snoitces nezorf etaulave nac tsigolohtap ehT .tnemeganam ecneulfni yllacitirc nac dna gninnalp tnemtaert ot detaler ylesolc si sis -ongaid cigolotsih evitinifed a rof nemiceps a gniniatbO .serutcurts tnecajda fo noisavni rof kcehc dna romut eht fo tnetxe eht enifed ot demrofrep eb dluohs TC ro IRM ,romut dnalg yravilas tnangilam a fo noicipsus lacinilc si ereht fI .BANF yb demrifnoc eb net -fo nac romut tnangilam a fo noicipsus ehT :sisongaiD .sromut dnalg yrav -ilas tnangilam fo daerps lacinilc eht ebircsed ot desu si noitacifissalc MNT ehT .041 .p no dessucsid erew romut dnalg yravilas tnangilam a fo sngis lacinilc ehT tnemtaerT dna sisongaiD fo stcepsA lareneG sromuT tnangilaM .tsyc detcefni na yb detacilpmoc eb yam esaesid ehT .erar era stnialpmoc dna ,rucco ton seod noitamrofsnart tnangilaM .dooG :sisongorP .noitatneserp lacinilc lacipyt a htiw sesac ni nekat eb yam hcaorppa tnatcepxe nA .elop ditorap roirefni eht ni romut eht fo noisicxe raluspacirep fo stsisnoc tnemtaerT :tnemtaerT .amohpmylonedatsyc htiw desufnoc eb osla yam stsyc cinegoihcnarb dna stsyc tcud yrav -ilaS .)VIH ni( stsyc lailehtipeohpmyl morf dna dnalg ditorap eht ni samohpmyl morf etaitnereffid ot tlucif -fid eb nac amohpmylonedatsyC :sisongaid laitnereffiD .nemiceps lacigrus eht morf edam si sisongaid cigolotsih evitinifed ehT .stsyc lacipyt erom ro eno etartsnomed yam dnuosartlU .amohp -mylonedatsyc fo sisongaid eht ot etubirtnoc ton seod yllareneg yspoib noitaripsa eldeen-eniF :sisongaiD .sesac fo % 01 yletamixorppa ni tneserp era sromut laretaliB .sticifed lanoitcnuf on era ereht dna ,lufniap ton si gnillews ehT .sesac emos ni raludon eb yam hcihw ,dnalg ditorap eht fo elop roirefni eht fo gnillews tnelodni ,tfos ylevitaler a htiw stneserp ohw 06 ega revo elam a si tneitap lacipyt ehT :smotpmyS .elor a yalp osla yam sesuriv deziretcarahcnu yltneserP .sedon hpmyl ni amyhcnerap raludnalg fo snoisulcni morf smrof romut eht taht deveileb si tI :sisenegohtaP .yad evitarepotsop ht ruof -tal eht htiw gnola devomer yllacigrus noisel eht evah ot desiv ehT .yad evitarepotsop dnoces eht no devomer si niard ehT .dnalg ditorap eht fo snoit rop lare eht no degrahcsid si tneitap eht dna ,llew gnilaeh si dnuow .noitarepo eht ret fa noitcnuf ev ren laicaf fo seitilamronba on swohs tneitap ehT .desolc si dnuow eht dna ,etis noitces -da si tneitap ehT :tnesnoc demrofni dna noitadnemmoceR .amoneda cihpromoelp a ylekil tsom ,amoneda ngin -ne ro seitilamronba rehto fo ecnedive on htiw dnalg ditor yletelpmoc si romut raludnalgartni eht dna ,demrof rep si ym enod si hcihw ,BANF si yduts txen ehT .sedon hpmyl degral .eussit gnidnuorrus eht dna eluspac sti htiw gnola devomer suoenatucbus yltcerid si eludon eht ecnis ylsselniap dna ylisae sisongaid evitpmuserp eht smrifnoc ygolotsih noitces-nezorF -eb a morf sllec sebircsed tsigolohtap ehT .elbaplap ylisae dna amoneda cihpromoelp fo -er eht ta decalp si niard noitcus A . -otceditorap laretal A .romut eht ot laidem nur taht sehcnarb -ap eht ni ssam dilos a setartsnomed dnuosartlU :stset rehtruF -artni nO .lamron era sgnidnif cipocsotO .yhtaponedahpmyl derotinom ylsuounitnoc si noitcnuf ev ren laicaF .aisehtsena lamron sticile dnalg ditorap eht fo egassam ,noitanimaxe laro -sae ti sekam sihT .yhpargoymortcele yb noitarepo eht gnirud si noitcnuf ev ren laicaF .tcud nesnetS eht morf wolf y ravilas -tacol si romut eht hcihw revo ,knurt ev ren eht yfitnedi ot rei .lacirtemmys ev ren laicaf eht seifitnedi noegrus eht ,knurt eht gniwolloF .de lareneg rednu demrof rep si noitarepo eht dna ,dezilatipsoh si ehS .y regrus desoporp eht ot stnesnoc tneitap ehT :tnemtaerT fo ecnedive on si ereht dna ,deton era seitilamronba elbaplap rehto oN .elbidnam eht fo sumar lacit rev eht fo t rap roiretsop .llew sleef tneitap eht esiw rehtO .emit revo degralne ylla ralucirua taerg( sev ren :sgnidniF yletamixorppa rucco yam gnitaews ,oslA .elcirua dna keehc eht ni ssenbmun -nu dna niks eht ot evitaler elbavom yleerf ,retemaid ni mc 5.2 eht retfa shtnom lareves gnitae gnirud dnalg ditorap eht revo -don ehT .ebolrae thgir eht woleb elbaplap si ,seussit gniylred ,gnitaews y rotatsug( egamad ev ren fo tluser a sa noitarepo eht revo detacol si dna dniheb morf elbisiv ylraelc tsom si elu .)emordnys laropmetolucirua ro ,emordnys yerF fo eerged emos esuac yam )ev ren eludon esnet a ,noitanimaxe tA eludon sselniap a htiw stneserp namow dlo-raey-25 A eht ,y rujni ev ren laicaf fo ksir eht tuoba demrofni si tneitap ehT -la sah eludon eht taht setats tneitap ehT .rae thgir eht woleb -issop erar eht dna ,htworg romut reht ruf htiw ksir fo esaercni -udarg evah yam ti taht tub ºezis emas eht tuobaª neeb syaw suoenatuc fo noisivid ehT .tnempoleved amonicrac fo ytilib troper esac a :romut ditorap ngineB sdnalG y ravilaS ehT :yrotsiH 5.6 6
  • 159. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .)93±63 .pp ,4.3 ees ,spalf tnemecnavda( niks dna ,)tfarg tnemecalper ro ssapyb( yretra ditorac lanretni eht ,)gnitfarg evren( evren laic ± -af eht rof deredisnoc eb yam serusaem evitcurtsnoceR .romut eht fo tnetxe eht no gnidneped ,sedon hpmyl lacivrec ro/dna ,slessev ,niks ,elbidnam ,enob laropmet eht fo lavomer )latotbus( eht ro noitavreserp evren laic -af tuohtiw ro htiw ymotceditorap latot a eriuqer yam %1 < srehtO samohpmyl nikgdoH-non yltsoM samohpmyl rehto ekiL sisongorp rooP % 2±1 %1 < ± rucer ot dnet samoignahpmyL amohpmyL amocraS %1 < ditorap eht ni yllausU nigiro lailehtipenon fo sromut tnangilaM srehtO amoignahpmyl nmuloc ºserutaeFª eeS %2 ,amoignameH evomer ot ysae ,dnalg sisongorp dooG % 2±1 amopiL nigiro lailehtipenon fo sromut ngineB amonicrac sisongorp rooP %3 detaitnereffidnU sesatsatem edon -hpmyl raludnalgartni morf noitaitneref fid seriuqeR amonicrac sisongorp rooP %2 llec suomauqS samoneda cihpromoelp detaertnu fo % 5±3 ni spoleveD amoneda cihprom sisongorp rooP sisongorp rooP laviv rus raey-5 ,nemow ni nommoc eroM laviv rus raey-5 y ravilas ronim morf sesirA -oelp ni amonicraC % 03 etar noitartlifni amonicraconedA laviv rus raey-01 laruenirep dna ralucsavirep %5 % 57 etar ;sesac fo % 07 ni sdnalg %3 % 57 etar dnalg ditorap eht ni yllausu amonicrac %3 % 3±2 citsyc dionedA amonicrac llec ranicA % 09 si sromut edarg romut no sdnepeD -ap eht ni nommoc tsoM raey-5 ;noitaitneref fid -ilas ronim ro dnalg ditor - wol rof etar laviv rus etalap eht fo sdnalg y rav amonicrac %5 diomredipeocuM nigiro lailehtipe fo sromut tnangilaM )amoneda tcud y rav -ilas ,.g.e( samoneda sisongorp dooG %5 cihpromonom rehtO nem ni % 09 ,laretalib eb nac ,dnalg ditor amoneda dnalg ditorap amohpmylonedatsyC tnangilam oN ,amoneda cihpromonoM noitamrofsnart -ap eht ni nommoc tsom sisongorp dna esruoC serutaef rehtO sisongorp dooG eht ni nommoc tsoM % 51 % 05±04 sromut dnalg yravilas lla fo egatnecreP cihpromoelP nigiro lailehtipe fo sromut ngineB romut fo emaN sdnalg yravilas eht fo sromut tnangilam dna ngineb fo weivrevO 5.6 elbaT xny rahP dna ytivaC larO II 051
  • 160. 151 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .5.6 elbaT ni dezirammus era sromut esehT .elbarovafnu eb ot sdnet sisongorp ehT .dnalg ditorap eht ni yltnanimoderp rucco ,sromut tsom ekil ,dna erar yllareneg era sromut tnangilam rehtO sromuT tnangilaM dna samonicraC rehtO .% 03 ylno si etar lavivrus raey -01 eht tub ,% 57 si etar lavivrus raey-5 ehT .tneuqerfni era seruc tub ,ylwols sworg yllareneg amonicrac citsyc dioneda ,sesac gnitanimluf wef a morf edisA :sisongorP .sesatsatem eht fo htworg wols yltneuqerf eht no gnidneped ,tneserp era sesatsatem yranomlup nehw neve etairporppa eb yam yregruS .sisab esac-yb-esac a no dediced eb dluohs dna sisatsatem tneuqerf dna etar htworg wols eht ot eud detupsid si )yretra ditorac ,enob laropmet ,evren laicaf( serutcurts rojam secifircas taht erudecorp lacidarartlu na fo eulav ehT .romut eht fo ytivitisnes -oidar roop eht ot eud lacigrus si tnemtaerT :tnemtaerT .sisat -satem suonegotameh fo setis lanoitidda rof deneercs eb dluohs noteleks dna sgnul ehT .941 .p eeS :sisongaiD .romut eht yb noitartlifni laruenirep ylrae ,lacipyt yb desuac sticifed evren ro niap ot sdael noitartlifni lacoL .noitac -ol romut no tnedneped era smotpmys ehT :smotpmyS .sisongorp eht ot pihsnoitaler emos raeb yam seirogetac cigolotsih eseht dna ,dehsiugnitsid era sepyt ralubut dna ,mrofirbirc ,diloS .ecnaraeppa cigol -otsih detaitnereffid-llew dna ngineb ylevitaler a sah romut siht ,ycnangilam lacinilc sti etipseD :ygolotsiH .sesatsatem suonegotameh daerps -ediw dna ecnerrucer dipar htiw esruoc gnitanim -luf a ekat sesac rehtO .nommoc era sesatsatem edon -hpmyl tub ,esruoc wols ,ngineb ylevitaler a ekat yam romut ehT .noitartlifni laruenirep dna ralucsavirep yb dna esruoc elbairav ylhgih a yb dekram si amon -icrac citsyc dioneda fo erutcip lacinilc ehT :noitinifeD amordnilyc :eman ciahcrA amonicraC citsyC dionedA .)% 07 etar lavivrus raey-5( noitceser etelpmoc a gniwollof doog si sisongorp ehT :sisongorP .romut diomredipeocum eeS :tnemtaerT .amonicrac citsyc dioneda dna amonicraconeda morf noitaitnereffid cigolotsih eriuqer ylniam sromut esehT :sisongaid laitnereffiD sdnalG y ravilaS ehT .941 .p ees :sisongaiD .noitartlifni dna htworg romut lacol no dneped smotpmys ehT :smotpmyS .detceted eb nac esalyma dna gniniats )SAP( ffihcS ±dica cidoirep no evitisop selunarG .stnenopmoc lat -cud dna ranica sedulcni eussit romut ehT .revewoh ,de -taitnereffid llew ylevitaler era samonicrac llec ranica tsoM .dehsiugnitsid era sedarg romut suoirav ,amon -icrac diomredipeocum fo esac eht ni sA :sisenegohtaP .nem naht erom detceffa era nemow dna ,ega fo sraey 06 dna 04 neewteb si ecned -icni kaep ehT .ezisatsatem ot ycnednet elttil sah dna dnalg ditorap eht ni yltnanimoderp sworg taht romut evisavni yllacol a si amonicrac llec ranicA :noitinifeD amonicraC lleC ranicA .% 09 si sromut edarg-wol ,detaitnereffid-llew htiw stneitap rof etar lavivrus raey-5 ehT .edarg rom -ut eht no ylgnorts sdneped sisongorp ehT :sisongorP .yparehtoidar evitarepotsop ogrednu stneitap tsoM .dedda si )433 .p ees( noitcessid kcen a ,tneserp era sesatsatem edon-hpmyl fI .enob lar -opmet eht fo snoitrop dna evren laicaf eht fo noitcurts -nocer dna noitceser eht edulcni yam yregrus ehT .nois -icxe lacidar yramirp fo stsisnoc tnemtaerT :tnemtaerT .5.6 elbaT ees :sisongaid laitnereffiD .941 .p ees :sisongaiD .edarg romut eht no gnidneped ,sesatsatem edon-hpmyl dna ,yslap evren laicaf ,niap sesuac ti retal ro renooS .)141 .p ,21.6 .giF( gnillews lufniapnon a sa snigeb romut ehT :smotpmyS .nommoc ssel si sisatsatem )yran -omlup( suonegotameh ;etuor suonegohpmyl eht yb srucco yllausu sisatsateM .snoisel edarg-rewol naht sisongorp reroop ylbaredisnoc a gnivah sromut edarg -rehgih htiw ,sisongorp eht senimreted noitaitnereffid romut fo edarg ehT .)sesac fo % 52 yletamixorppa( srom -ut edarg-hgih detaitnereffid ylroop erom dna )sesac fo % 57 yletamixorppa( sromut edarg-wol detaitneref -fid-llew neewteb edam si noitcnitsid A :sisenegohtaP .stneitap gnuoy ni neve rucco nac dna sdnalg yravilas eht fo romut tnangilam nommoc tsom eht si tI .etalap eht fo sdnalg yravilas ronim dna dnalg ditorap eht ni yltnanimod -erp srucco amonicrac diomredipeocuM :noitinifeD amonicraC diomredipeocuM 6
  • 161. 7 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 162. III 7 8 9 10 11 12 13 14 15 Ear Audiology (Auditory Testing) Hearing Disorders in Children— Pediatric Audiology The External Ear The Middle Ear Inner Ear and Retrocochlear Disorders Vestibular Disorders Facial Nerve Lateral Skull Base Anatomy and Physiology of the Ear 7.1 Basic Anatomy and Physiology of the Ear 154 Peripheral Auditory System 154 Central Auditory System 158 7.2 Anatomy and Function of the Cochlea 160 Structure of the Cochlea 160 Function of the Cochlea 161 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 163. Nerves Bone Levator veli palatini muscle Eustachian tube Internal carotid artery Cochlea Semicircular canals Auditory ossicles Vestibular labyrinth Mastoid air cells Facial nerve Tympanic cavity Vestibulocochlear nerve .wolley ni nwohs si evren raelhcocolubitsev ehT .)der( rae renni dna ,)neerg( rae elddim ,)eulb( rae lanretxe eht :strap eerht otni dedivid eb nac metsys y rotidua larehpirep ehT Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. External ear Inner ear Middle ear Tensor veli palatini muscle Internal jugular vein Tympanic membrane External auditory canal Chorda tympani metsys yrotidua larehpireP -ro dne ralubitsev eht fo metsys lanac ralucricimes eht dna elubitsev eht otni dedividbus si tI .enob suortep eht ni deddebme si hcihw ,rae renni ehT · enob laropmet eht fo sllec ria eht dna ,selcsum lar -ua-artni ,selcisso yrotidua ,ytivac cinapmyt ,enarb -mem cinapmyt eht fo gnitsisnoc ,rae elddim ehT · lanac yrotidua lan -retxe dna elcirua eht fo gnitsisnoc ,rae lanretxe ehT · :)1.7 .giF( strap eerht otni dedivid si metsys yrotidua larehpirep ehT .giF ,aelhcoc eht fo erutcurts detacilpmoc eht neviG .nag -ro yrosnes siht tceffa nac taht sredrosid xelpmoc eht gnidnatsrednu rof sisab a edivorp suht dna sutarappa ralubitsev dna yrotidua eht fo selpicnirp cigoloisyhp dna cimotana cisab eht ebircsed ot si siht fo laog ehT .41±01 sretpahC ni detneserp era ,sutarappa ralubitsev eht ot gniniat -rep yllaicepse ,sliated rehtruF .)361±061 .pp ,2.7 ( tinu etarapes a ni debircsed era noitcnuf dna ymotana sti .gniraeh nam -uh rof nrettap dnuos tnatropmi tsom eht si hceepS .noitingo -cer nrettap dnuos dna gniraeh lanoitcerid ni latnem -urtsni ylralucitrap si dna noitamrofni citsuoca eht sessecorp rehtruf hcihw ,metsys yrotidua lartnec ehT · .)472±272 .pp ,metsyS ralubitseV eht fo noitcnuF dna ymotanA tnaveleR yllacinilC 1.31 ni debircsed si rae eht fo noitcnuf ralubitsev ehT .slangis laruen otni meht ssecorp dna snoitairav erusserp-ria cidoirep eviecrep ot si met -sys yrotidua larehpirep eht fo noitcnuf ehT .)ºraeª eht( metsys ralubitsev dna yrotidua larehpirep ehT · :snoitcnuf eseht tuo gniyrrac rof elbisnopser era smetsys gniwollof ehT .noitatneiro laitaps rof dna ytilibats dna ecnalab gniniatniam rof tnatropmi si metsys ralubitsev ehT .snoitcerid laitaps lla ni snoitcnuf taht metsys noitat -neiro dna gninraw a sa gnivres osla elihw ,noitacinum -moc laicos ni elor lartnec a syalp snamuh ni gniraeH .)472±272 .pp ,1.31 ees( ecnalab dna noitatneiro laitaps rof srotceffe eht dna sutarappa ralubitsev eht neewteb snoitcennoc eht sehsilbatse hcihw ,metsys ralubitsev lartnec ehT · metsyS yrotiduA larehpireP .noruen larehpirep eht fo espanys lart -nec eht yb demrof si yradnuob lanoitcnuf ehT .mets -niarb eht sretne evren raelhcocolubitsev eht erehw etis eht ta detacol si smetsys lartnec dna larehpirep eht neewteb yradnuob cimotana dna cigolohprom ehT raE eht fo ygoloisyhP dna ymotanA cisaB 1.7 raE III 451
  • 164. 551 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. eht sezilauqe yllacidoirep hcihw ,ebut naihcatsue eht yb detalugerretnuoc era segnahc erusserp tneibmA .ylno noitcerid eno ni stca ,erusserp citsuoca gnitanret -la eht ekilnu ,erusserp citats eht taht dnim ni gniraeb ,Bd 021 ta edutilpma erusserp dnuos eht ot tnelaviuqe ylhguor si m 2 fo egnahc edutitla nA .egnar citsuoca eht ni rucco taht segnahc erusserp ria cimanyd eht naht retaerg semit ynam era yehT .racelbac a ni gnidir ro gniylf ni sa ,segnahc edutitla tnacifingis ot esnopser ni rucco snoitairav erusserp cirehpsomta tsetaerg ehT .segnahc edutitla dna rehtaew ot eud xulf fo etats tnatsnoc a ni si hcihw ,erusserp ria citats eht ezilauqe tsum ti :mrofrep ot noitcnuf tnatropmi dnoces a sah ti ,segnahc erusserp cirehpsomta fo ecaf eht ni neve ,semit lla ta gnihctam ecnadepmi evitceffe niatniam ot rae elddim eht rof tuB .zHk 1 yletamixorppa si ycneuqerf tahT .yltneicif -fe tsom dettimsnart si ygrene dnuos hcihw ta ycneuq -erf tnanoser a sah rae elddim eht ,rae lanretxe eht ekiL .etalptoof sepats eht dna enarbmem cinapmyt eht fo secafrus gnittimsnart eht neewteb ytirapsid ezis 1 : 02 yletamixorppa eht yb elb -issop edam si sihT .diulf rae-renni eht ot ria gnitarbiv eht fo ygrene eht fo lla yllautriv timsnart ,seicneuqerf niatrec ta ,dna elbissop sa llams sa ssol noissimsnart siht peek ot si rae elddim eht fo ksat ehT .)2.7 .giF( ecafrus diulf eht morf detcelfer eb ot dnuos tnedicni eht fo %99 naht erom esuac dluow rae renni dellif-diulf eht ot snoitarbiv ria fo noissimsnart tcerid ehtÐdnuos fo noitagaporp eht ot sreffo muidem hcae taht ecnatsiser tnereffid eht ,.e.iÐdiulf dna ria fo secnad -epmi citsuoca tnereffid eht ot euD .gnihctam ecnadep -mi si rae elddim eht fo noitcnuf niam ehT :ygoloisyhP .inapmyt rosnet dna suidepats eht ,selcsum lar -ua-artni owt eht ot detcennoc osla era selcisso yrotid -ua ehT .ytivac cinapmyt eht fo stnetnoc lautca eht pu ekam ,inapmyt adrohc eht htiw rehtegot ,dna rae eld -dim eht fo sutarappa noitcudnoc dnuos eht mrof selc -isso ehT .selcisso yrotidua eerht fo niahc a yb rae renni eht ot deknil yllacinahcem si nrut ni hcihw ,enarbmem cinapmyt eht yb lanac yrotidua lanretxe eht morf detar -apes si tI .ytivac cinapmyt eht si ecaps rae elddim lap -icnirp ehT .rae renni eht dna ,arud eht ,lluks eht edisni morf sesunis suonev ,yretra ditorac lanretni eht ,evren laicaf eht sa hcus serutcurts tnatropmi yllanoitcnuf sesolcne ro no sredrob rae elddim eht ,yllacihpargopoT .sllec telbog sniatnoc taht muilehtipe detailic yrotaripser a yb denil si ti ,sesunis eht ekiL .sunis lasanarap dezi -laiceps ylhgih a sa deweiv eb yam ,neht ,rae elddim ehT .)1.7 .giF ees( ebut naihcatsue eht aiv xnyrahposan eht htiw etacinummoc seitivac esehT .sllec ria diotsam dna ytivac cinapmyt eht otni dedividbus era taht seiti -vac dellif-ria fo desirpmoc si rae elddim ehT :ymotanA raE elddiM .tnemriapmi lanoitcnuf suoires esuac ton seod elcirua na fo ssol eht dna ,ecnatropmi ronim ylevitaler fo era stceffe eseht ,revewoh ,elohw eht nO .ria gnivom fo stceffe citsuoca tnatsnoc eht gnihsinimid ybereht ,ecnelubrut ria gnitaerc yb kaerb -dniw a sa snoitcnuf osla elcirua ehT .enalp lacitrev eht ni ecruos dnuos a gnizilacol rof yllaicepse ,sisylana citsuoca ni elor tnatropmi na sah hcihw ,sm 2.0 yletam -ixorppa fo yaled dnuos feirb a setaerc yawhtap regnol ylthgils sihT .xilehitna dna xileh eht aiv etuor tceridni na dna ytivac lahcnoc eht hguorht etuor tcerid a :tsixe syawhtap citsuoca tnereffid owt ,elcirua eht fo epahs eht yb sevaw dnuos fo noitcarfer laitnereffid eht ot gniwO .sdia gniraeh fo sdlomrae eht yb ro ,senohprae tresni ,nemurec yb deretla eb yam ycneuqerf tnanoser ehT .nagro epip a ni ria fo snmuloc eht ot ralimis ,ret -teb etarbiv shtgnelevaw niatrec taht gninaem ,ecnan -oser no desab si tub sevaw dnuos fo edutilpma eht ni esaercni na evlovni ton seod noitacifilpma ehT .gniraeh egamad nac egnar ycneuqerf ralucitrap siht ni esion yhw snialpxe sihT .zHk 4 ot 2 morf egnar eht ni ylfeihc ,sdnab ycneuqerf detceles seifilpma taht lennuf cit -suoca na mrof rehtegot lanac rae dna elcirua ehT .yaw gnitanimircsid a ni serutcurts rae elddim evitisnes eht ot sevaw dnuos stimsnart hcihw annetna citsuoca na fo taht si rae lanretxe eht fo noitcnuf ehT :ygoloisyhP .)802 .p ,raE lanretxE eht fo noitanimaxE dna ymotanA laicepS ,1.01 ees( muetsoirep dna muird -nohcirep rieht yb niks eht ot dehcatta era hcihw ,enob fo dna egalitrac elbixelf fo desopmoc era rae lanret -xe eht fo stnemele evitamrof ehT .)lanac rae ,sutaem citsuoca lanretxe( lanac yrotidua lanretxe eht dna )an -nip( elcirua eht fo stsisnoc rae lanretxe ehT :ymotanA raE lanretxE .)SNC( metsys suovren lartnec eht ot snag -ro dne larehpirep eht stcennoc dna lanac yrotidua lan -retni eht ni snur tI .metsys yrotidua larehpirep eht fo trap si )IIIV evren lainarc( evren raelhcocolubitsev ehT .ycneic -iffe ralucitrap htiw dettimsnart era hceeps fo seic -neuqerf lapicnirp eht taht yaw a hcus ni detanidro -oc era snoiger eerht eseht fo smetsys citsuoca ehT .)061 .p ,aelhcoC eht fo noitcnuF dna ymotanA ,2.7 ees( nagro dne yrotidua eht si hcihw ,aelhcoc eht dna )472±272 .pp ,metsyS ralubitseV eht fo noitcnuF dna ymotanA tnaveleR yllacinilC ,1.31 ees( nag raE eht fo ygoloisyhP dna ymotanA 7
  • 165. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .nwohs ton si evren ralubitsev eht ,ytiralc roF .wolley ni nwohs si evren raelhcoc eht ot noitcennoc laruen ehT .)eulb krad( sneinuer sutcud worran eht yb detcen -nocretni era )neerg( aelhcoc dna )eulb( htnirybal ralubitsev ehT Saccule Ductus reuniens Cochlear duct Utricle Semicircular canals Cochlear nerve suonarbmem rehtonA .tcud raluccasolucirtu eht ,htnir -ybal suonarbmem eht fo tcud rehtona yb detcennoc era eluccas dna elcirtu ehT .272 .p no debircsed era htnirybal ralubitsev eht ni sllec yrosnes eht fo noitcnuf dna erutan ehT .eluccas eht dna ,elcirtu eht ,slanac ralucricimes eerht fo desopmoc si htnirybal ralubitsev ehT .sneinuer sutcud worran eht yb detcennocretni era hcihw ,)htnirybal raelhcoc( aelhcoc eht dna htniry -bal ralubitsev eht otni dedivid si tI .sllec riah sa nwonk osla era taht sllec yrosnes gniraeb-ailic sniatnoc dna ,hpmylodne eht ,diulf hcir-muissatop a htiw dellif si htnirybal suonarbmem ehT :htnirybal suonarbmeM .htnirybal eht dellac ylevitcelloc era taht stcud detcennocretni elpitlum fo stsisnoc rae renni eht ,enob laropmet eht fo trap suortep eht ni detacoL raE rennI rae renni eht fo htnirybal suonarbmeM .giF eht stneserper dna etalptoof sepats eht yb derevoc si rae elddim eht ot rae renni eht sknil taht wodniw lavo ehT .htnirybal suonarbmem eht fo stcud gnitcen -noc eht dna ,tcud raelhcoc eht fo esab eht ,elcirtu eht ,eluccas eht sniatnoc taht ytivac egral a smrof elubit -sev eht ,aelhcoc dna slanac ralucricimes eht neewteB .amertoc -ileh eht yb xepa raelhcoc eht ta detcennoc era hcihw ,inapmyt alacs dna ilubitsev alacs eht dellac stcud etar -apes owt setaerc tnemegnarra sihT .aelhcoc ynob eht fo sllaw retuo dna renni eht neewteb dehcatta si tcud raelhcoc ehT .epahs rieht secudorper dna slanac raluc -ricimes suonarbmem eht sesolcne htnirybal ynob ehT .elubitsev eht dna ,aelhcoc eht ,metsys lanac ralucric -imes eht :strap eerht otni dedividbus eb nac htnirybal ynob ehT .tnemtrapmoc diulf ralullecartxe eht fo taht ot ralimis yrev si ,hpmylodne eht ekilnu ,hpmylirep eht fo noitisopmoc ehT .hpmylirep htiw dellif ecaps a yb detarapes era htnirybal ynob dna suonarbmem ehT .enob suortep eht nihtiw htnirybal ynob eht ni ded -debme si htnirybal suonarbmem ehT :htnirybal ynoB .472±272 .pp ,1.31 ni ylluf derevoc era htnirybal ralubitsev eht fo esoht dna ,)061 .p( txen eht ni debircsed era aelhcoc eht fo ygoloisyhp dna ymotana ehT .snrut larips flah -eno dna owt sekam hcihw ,)aidem alacs( tcud raelhc -oc eht si aelhcoc eht fo htnirybal suonarbmem ehT .rae renni eht fo sessecorp enum -mi eht ni dna noitaluger hpmylodne ni elor a yalp ot deveileb si dna noitcnuf yroterces a evah ot sraep -pa tI .dootsrednu ylluf ton si cas citahpmylodne eht fo noitcnuf ehT .)1.7 ees( enob suortep eht fo ecafrus roir -etsop eht no cas citahpmylodne eht ot sdnetxe hcihw ,)tcudeuqa ralubitsev( tcud citahpmylodne eht :tcud raluccasolucirtu eht morf sesira erutcurts enihtnirybal .etalptoof sepats eht fo tnemecalpsid emertxe gnitneverp yb rae renni eht tcetorp snoitcennoc esehT .serusserp citats eht ezilauqe ot pleh osla selcisso yrotidua eht neewt -eb snoitcennoc ralucitra ehT .rae elddim eht nihtiw segnahc erusserp tneverp yleritne tonnac tub ytivac cinapmyt eht dna tnemnorivne eht neewteb serusserp .rae renni eht tcetorp dna sutarappa noitcudnoc dnuos eht fo noitcnuf eht niatniam selcisso yrotid -ua eht fo stnioj eht ,)b ni enil kcalb( rae elddim eht ni erusserp evitagen a ecudorp taht segnahc erusserp citats htiW .neerg ni yllacitamehcs nwohs era stnioj sti dna niahc ralucisso ehT .etalp -toof sepats eht dna enarbmem cinapmyt eht neewteb aera ni ecnereffid eht yb deifidom si ecnadepmi ehT b .rae renni eht fo ecafrus diulf eht ta detcelfer eb dluow ygrene dnuos eht fo %99 naht erom ,rae elddim eht fo niahc ralucisso desopretni eht tuohtiW a .)erusserp ria( secnereffid erusserp citats rof setas -nepmoc osla taht remrofsnart ecnadepmi na si rae elddim ehT Static negative pressure Sound waves b Sound waves Reflection > 99 % a rae elddim eht fo noitcnuF .giF raE III 651
  • 166. .lanac yrotidua lanretni eht ni ylesolc yrev ti sehcaorppa tub esruoc sti tuohguorht evren raelhcocolubitsev eht morf etar -apes yllacimotana si )092 .p osla ees( evren laicaf ehT .laicurc si noissimsnart eht fo gnimit esicerp ehT .noissimsnart atad latigid ot dene -kil eb nac taht ssecorp a ni sespanys eht fo level eht ta )slaitnetop noitca( slangis cigoloiboruen xelpmoc otni demrofsnart ydaerla si noitamrofni ehT .refsnart noitamrofni evissap sa debircsed eb nac evren raelhc -ocolubitsev tnereffa eht fo noitcnuf ehT .srebif tne -reffa eht naht detanileym llew ssel era yeht yllareneg tub ,tneserp osla era srebif tnereffE .metsniarb eht ni ielcun raelhcoc dna ralubitsev eht ot dael hcihw ,srebif tnereffa sniatnoc ylniam evren raelhcocolubitsev ehT .)061 .p ,6.7 .giF ees( aelhcoc eht fo suloidom ynob eht ni tub lanac yrotidua lanret -ni eht ni detacol ton si )noilgnag raelhcoc larips( noilg -nag raelhcoc ehT .)evren yrallupma roiretsop ,evren raluccas ,evren rallupmaolucirtu( nagro dne ralubitsev eht fo serutcurts eht ot detubirtsid era srebif evren suoirav hcihw morf noilgnag ralubitsev eht smrof evren ralubitsev eht ,lanac lanretni eht fo sudnuf eht nI .serutcurts etarapes sa raeppa sevren raelhcoc dna ral -ubitsev eht erehw ,lanac yrotidua lanretni eht ni tner -appa yllacimotana semoceb noisividbus sihT .evren raelhcoc roirefni roiretsop eht morf tcnitsid si hcihw ,evren ralubitsev eht ,trap roirepus roiretna na fo stsis -noc ti ,revewoh ,yllanoitcnuF .ecnaraeppa suoenegom -oh ylssorg a sah taht knurt evren a sa metsniarb eht sevael )IIIV evren lainarc( evren raelhcocolubitsev ehT .sun -is lasortep roirefni eht ot dna niev raluguj eht fo blub roirepus eht ot rae renni eht morf doolb niard sniev lareveS .slessev rae elddim eht htiw esomotsana yam slessev esehT .yretra raelhcoc dna yretra ralubitsev eht otni sedivid ti erehw ,lanac yrotidua lanretni eht hguorht evren raelhcocolubitsev eht htiw snur tI .yret -ra ralisab eht ro yretra ralleberec roirefni roiretna eht morf sesira yllausu hcihw ,yretra enihtnirybal eht morf ylppus doolb sti sevired rae renni ehT :ylppus doolB ralucricimes roiretsop denoitces ylesrevsnart eht dna ,elubitsev eht ,aelhcoc eht fo snrut ehT .htnirybal ynob eht fo serutcurts eht setartsnomed ylraelc yhpargomot detupmoc ecils-nihT .enob laropmet tfel eht hguorht nacs laixa siht ni deyalpsid ylraelc era lanac .stluda ni eussit suorbif yb delaes netfo si dna nerdlihc ni ylno nepo yltnetsisnoc si ti ,ylekil tsoM .sucitsuca surop lanretni eht woleb dimaryp eht fo ecafrus roiret -sop eht ta sdne dna wodniw dnuor eht woleb inapmyt alacs eht ta snigeb tcud sihT .tcudeuqa raelhcoc eht sa osla nwonk ,tcud citahpmylirep eht aiv ecaps )FSC( diulf lanipsorberec dionhcarabus eht htiw setacinum -moc htnirybal ynob eht fo ecaps citahpmylirep ehT .ytivac cinapmyt eht dna htnirybal ynob eht neewteb gninepo dnoces a sedivorp wodniw dnuor eht ,enarbmem elibom a yb delaes dna inapmyt alacs eht fo dne eht ta wodniw lavo eht ot ro -irefni detacoL .wodniw dnuor eht yb devres si noitcnuf sihT .dettimsnart ylevitceffe eb nac snoitarbiv eht taht os dedeen si ºevlav erusserpª a ,hpmylirep elbisserp -mocni htiw dellif si htnirybal ynob eritne eht esuaceB .hpmylirep eht ot rae elddim eht morf det -timsnart era snoitarbiv citsuoca dehctam-ecnadepmi erehw etis eht si tI .htnirybal eht ot ºecnartne citsuocaª evreN raelhcocolubitseV Bone Air in middle ear Vestibule Auditory ossicles Facial nerve Mastoid air cells Auditory ossicles (malleus andincus) Middle cranial fossa 751 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. Bony labyrinth Posterior semicircular canal Cochlea Internal auditory canal Posterior cranial fossa Tympanic cavity Sphenoid sinus htnirybal ynoB .giF raE eht fo ygoloisyhP dna ymotanA 7
  • 167. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. Cochlear aqueduct Cochlea d Eighth week of development Endolymphatic sac Vestibule Semicircular canals c Sixth week of development Pars sacculocochlearis Endolymphatic duct Pars utriculovestibularis b Fifth week of development Otic vesicle (labyrinthine vesicle, otocyst) .tsycoto eht yb dellortnoc si hcihw ,evren raelhcocolubitsev eht fo tnempolev -ed aiv lanac yrotidua lanretni eht fo ygoloyrbme tnednepedni yllaitnesse eht yb delellarap si htnirybal eht fo tnempoleveD .)d( delioc semoceb dna siraelhcocoluccas srap eht fo noisnetxe ralu -but a sa smrof tcud raelhcoc eht ,skeew htnin ot htneves eht nI .)c( siralubitsevolucirtu srap eht morf mrof slanac ralucricimes eerht eht ,keew htxis eht nI .)b( siraelhc -ocoluccas srap rewol eht dna siralubitsevolucirtu srap reppu eht gnimrof ,dedlofni semoceb tsycoto eht ,keew htfif eht nI .)a( elcisev etarapes a mrof ot ffo sesolc dna setanigavni gninekciht sihT .tnempoleved cinoyrbme fo skeew htruof dna driht eht ni evoorg laruen dna mredotce suoenatuc eht neewteb gninekciht lailehtipe na morf smrof tsycoto ehT tnempoleved rae renni fo elbatemiT .lamredosem si elus -pac cito eht ;nigiro lamredotce fo si rae renni suonarbmem ehT .hcuop laegnyrahp tsrif eht morf poleved ebut naihc -atsue dna ytivac cinapmyt eht elihw ,nigiro lamyhcnesem fo era selcisso yrotidua ehT .asocum lamredodne dna ,re -yal suorbif lamyhcnesem ,reyal lamredipe lamredotce sti htiw sreyal mreg eerht lla senibmoc enarbmem cinapmyt eht dna ,simredipe eht ni noisserped a sa strats lanac yrotidua ehT .noitisop tes-wol a ypucco ot dnet selcirua demroflam yhw gninialpxe ,tnempoleved rehtruf htiw dalahpec setarg -im dna selcrebut lamyhcnesem xis morf demrof si elcirua ehT .mredosem dna mredotce eht morf spoleved rae lanretxe ehT sreyal mreG a Fourth week of development .noitacifisrevid dellac si yawhtap yrotidua gnidnecsa eht fo ytreporp siht ;sretnec rehgih eht ta suoremun erom emoceb yllareneg snoruen ehT .slevel lla ta tneserp era snoitcennoc laretalloc suorem -un ,yawhtap yrotidua gnidnecsa eht fo smetsys tcnit -sid yllacigoloisyhp dna yllacimotana eseht sediseB .sulumits citsuoca duol yltneic -iffus a ot esnopser ni )evren laicaf eht fo hcnarb a( evren suidepats eht yb elcsum suidepats eht fo noit -cartnoc secudni hcihw ,xelfer laidepats eht si elp -maxe nA .SNC eht ni slevel suoirav ta sretnec yros -nesnon dna yrosnes rehto htiw snoitcennoc sehsil -batse metsys sihT :metsys yrosnesylop ro ladomyloP · noitamrofni laropmet sa hcus sretemarap rehto no yler dna sisylana ycneuqerf fo tnednepedni ylegral era taht gnissecorp lartnec fo sedom rehto era met -sys cipotonot eht ot lellaraP :metsys cipotonotnoN · .xetroc larberec eht sa raf sa syawhtap yrotidua lart -nec eht fo emos ni deniatniam si ºelpicnirp cipoton -otª sihT .evren citsuoca eht ni srebif cificeps ot seic -neuqerf niatrec sngissa ydaerla aelhcoc eht ni sruc -co taht gnissecorp ycneuqerf ehT :metsys cipotonoT · :esnes lanoitcnuf a ni elbahsiugnitsid era ,yllacimot -ana etarapes yltcirts ton elihw ,smetsys gniwollof ehT raE eht fo ygoloyrbmE 1.7 .ebol laropmet eht ni ylniam detacol era hcihw ,xetroc yrotidua eht fo saera laretalartnoc eht ot sumalaht eht dna ,niarbdim eht fo sulucilloc roirefni eht ,sexelpmoc yravilo roirefni owt eht aiv ylevisulcxe ton tub ylniam snur syawhtap yrotidua eht ,suelcun raelhcoc eht tsaP .edis eno morf yleritne stnereffa sti seviecer ,ielcun re -hto ynam ekilnu ,suelcun raelhcoc ehT .)5.7 .giF( setan -imret evren raelhcoc eht erehw ,suelcun raelhcoc eht ta metsniarb eht ni snigeb metsys yrotidua lartnec ehT metsyS yrotiduA lartneC .1.7 ni nwohs era tnempoleved rae renni fo elbatemit eht dna serutcurts yrotidua suoirav eht ot esir evig taht sreyal mreg ehT .rae elddim eht fo seilamona htiw detaicossa yltneuqerf era lanac yrotidua lanretxe eht fo snoitam -roflam ,dnah rehto eht nO .strap rehto fo snoitamrof -lam htiw denibmoc ylirassecen ton si rae eht fo trap eno gnitceffa noitamroflam a ,tluser a sA .tnempolev -ed cinoyrbme etarapes ssel ro erom a ogrednu lanac yrotidua lanretni dna ,rae renni ,rae elddim ,elcirua ehT metsyS yrotiduA larehpireP eht fo tnempoleveD dna ygoloyrbmE raE III 851
  • 168. .senalp laitaps rehto lla ni noitat -neiro rof gniraeh no yler tsum dna enalp latnorf eht ni ylno noitamrofni lausiv seviecer gnieb namuh a esuac -eb ,snamuh ni devlove ylhgih yrev era yehT .rehto hcae morf detarapes ylraelc eb syawla tonnac dna yr -atnemelpmoc era snoitcnuf owt esehT .)?ohw ?tahw( noitingocer nrettap dnuos dna )?erehw( noitazilac -ol dnuos :ssecorp siht ni dehsiugnitsid era snoitcnuf cisab owT .slangis yrotidua eht ezingocer dna etarapes ot si SNC eht fo ksat ehT .slangis fo xim xelpmoc a sa ytiledif mumixam htiw SNC eht ot deyaler dna detcel -loc si noitamrofni yrotidua ,metsys larehpirep eht nI metsyS yrotiduA lartneC eht fo noitcnuF .noitam -rofni fo wolf eht gnillortnoc ni tsissa yehT .SNC eht ni sretnec rewol ot rehgih morf snoitcennoc eht fo ynam ni stnereffa eht rebmuntuo srebif tnereffe eht ,srebif tnereffe wef a ylno sniatnoc evren raelhcoc eht elihW .nwohs ton si metsys tnereffe xelpmoc ehT .evren raelhcoc laretalispi eht ot ylno detcennoc si hcihw fo hcae ,ielcun raelhcoc eht ta tpecxe slevel lla ta tsixe snoitcennoc-ssorc suoremuN .edis eno no yawhtap yrotidua tnereffa lartnec eht fo margaid deifilpmiS Trapezoidal body Superior olivary nucleus .deviecrep si ºesionª ylno ;noitingocer nrettap evlovni ton seod tub etal -erroc lacisyhp lanretxe na skcal osla sutinniT .dlrow edistuo eht ni etalerroc lacisyhp a tuohtiw noitingocer nrettap dnuos era snoisulli ro snoitanicullah yrotiduA .noitingocer nrettap dnuos fo mrof dezilaiceps a dere -disnoc eb yam cisuM .snrettap dnuos gnignahc yldi -par gnizingocer fo elpmaxe tnatropmi tsom eht si noit -acinummoc namuh ni secnetnes dna ,sesarhp ,sdrow ,selballys otni noitanibmoc rieht dna sdnuos hceeps fo noitingocer ehT .yrotisnart dna cimanyd yllaitnesse si ºnoitingocer erutcipª yrotidua ,metsys lausiv eht ni dezingocer si rehtona retfa erutcip eno elihW .esion ro ,secruos ºsuoenartxeª morf secruos dnuos ro noit -amrofni yrotidua ºderisedª fo noitarapes eht sedulc -ni noitingocer nrettap ro noitacifitnedi dnuoS .noitin -gocer nrettap dnuos rof noitadnuof laitnesse na mrof ,neht ,snoitcnuf detaicossa sti dna gniraeh lanoitceriD .metsniarb dna aelhcoc eht ni noitamrofni dnuos eht fo gnissecorp laruen yranimilerp eht no seiler tI .gni -nrael dna ecneirepxe no desab si taht noitcnuf larber -ec evitingoc a si ,ecruos dnuos a fo noitacifitnedi dna gniman eht sevlovni hcihw ,noitingocer nrettap dnuoS .emit emas eht ta dezilacol eb ot secruos citsuoca erom ro eno stimrep metsys siht ,noitingocer fo smret ni ecruos dnuos eht yfitnedi ot gnivah tuohtiW .ecruos eht morf rehtraf rae eht naht ytisnetni retaerg htiw dna reilrae ecruos dnuos eht ot resolc rae eht sehcaer dnuos :metsniarb eht ni syawhtap noitamrofni yrotid -ua laruanib eht no ylegral desab si noitazilacol dnuoS Vestibulocochlear nerve 951 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. Cochlea Ventral cochlear nucleus Lateral lemniscal nucleus Dorsal cochlear nucleus Lateral lemniscus Inferior colliculus Auditory radiation Medial geniculate body Auditory cortex in the transverse temporal gyrus yawhtap yrotidua lartneC .giF raE eht fo ygoloisyhP dna ymotanA 7
  • 169. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .xepa raelhcoc eht ta seicneuqerf wol rof dna esab raelhcoc eht ta seicneuqerf hgih rof enarbmem ralisab eht fo snoitarbiv lamixam ecudorp sevaw esehT .decudorp eb nac sevaw gnilevart hcihw ni )eulb( secaps citahpmylirep dna ,)neerg( itroC fo nagro ,)der( enarb -mem ralisab eht setartsnomed aelhcoc deliocnu na fo ledoM .egnaro ni nwohs si tcud raelhcoc dellif-hpmylodne ehT .eulb ni nwohs era ,hpmylirep niatnoc hcihw ,inapmyt alacs dna ilubitsev alacs ehT .animal larips ynob eht raen noilgnag larips eht mrof dna slanac ynob llams ni nur taht srebif evren etarapes otni sedivid dna ereht sdne evren raelhcoc ehT .suloid -om eht fo retnec eht hguorht denoitces neeb sah aelhcoc ehT Cochlear nerve Spiral ganglion Basilar membrane Organ of Corti Spiral lamina Basal Apical Scala tympani Modiolus Scala vestibuli enarbmem ralisab eht fo ledoM .giF Scala tympani Scala vestibuli Nerve fibers Organ of Corti Cochlear duct Helicotrema Reissner membrane Basilar membrane Spiral ligament aelhcoc eht hguorht noitces laixA .giF daorb eht sedivid aelhcoc eht ,gnidoc laruen siht mrof -rep oT .sulumits dnuos eht fo gnimit dna erutan eht stcelfer ylesicerp taht seslupmi laruen fo nrettap a otni stneve yrotidua etalsnart ot si aelhcoc eht fo noitcnuf niam ehT .ecnatropmi lacinilc dna cigoloisyhp yek fo si aelhcoc eht ,gniraeh rof nagro yrosnes lautca eht sA .dessucsid osla era snoitacilpmi lacinilC .elpicnirp cipotonot eht dna reif -ilpma raelhcoc eht fo pleh eht htiw ksat siht smrofrep aelhcoc eht woh swohs sihT .nagro eht fo yticapac gni -ssecorp laruen eht ot dehctam era taht sdnab ycneuq -erf worran otni dnuos eht fo murtceps ycneuqerf aelhcoC eht fo erutcurtS -imal larips eht morf gnitrats nagro itroC eht fo noiger llec yrosnes eht srevoc ,slirbif dna lairetam suohproma fo desopmoc erutcurts ralulleca na ,enarbmem lairot -cet ehT .sllec gnitroppus dna yrosnes eht sniatnoc dna suloidom eht gnicaf enarbmem ralisab eht fo trap ren -ni eht no seil )8.7 .giF ,nagro larips( itroC fo nagro ehT .aelhc -oc eht gnola setis tnereffid ta gnirrucco edutilp -ma mumixam tnedneped-ycneuqerf a htiw ,enarb -mem ralisab eht fo seitreporp lacinahcem eseht no desab si evaw gnilevart evissap eht fo noitamrof ehT .aera lacipa eht ni seicneuqerf rewol ot dna aelhcoc eht fo aera lasab eht ni seicneuqerf rehgih ot denut si ecnanoser stI .xepa eht ta naht aelhcoc eht fo esab eht ta tnailpmoc ssel dna reffits yldekram si enarbmem ehT .aelhcoc eht fo esruoc eht gnola egnahc enarbmem ralisab eht fo seitreporp lacinahcem ehT .wodniw dnuor eht ot amertocileh eht morf drawnwod snur dna hpmylirep htiw dellif osla si tI .enarbmem ralisab eht woleb seil inapmyt alacs ehT .amertocileh eht yb inapmyt alacs eht ot detcennoc si ti aelhcoc eht fo xepa eht tA .wodniw lavo eht fo aera eht ni aelhcoc eht fo esab eht ta snigeb ilubitsev alacs ehT .)8.7 .giF osla ees( enarbmem eht ta detaerc si ecnereffid laitnetop a ,ecaps ralullecartxe eht ni sa emas eht si hpmylirep eht fo noitisopmoc eht esuaceB .enarbmem renssieR niht eht yb aidem alacs eht fo ecaps citahp -mylodne eht morf detarapes si dna ,hpmylirep sniat -noc ,tcud raelhcoc eht evoba seil ilubitsev alacs ehT .)8.7 .giF osla ees( ecaps ralullecartni eht fo taht ot ralimis si hpmylodne eht fo noitisopmoc cinoi ehT .hpmylodne htiw dellif si hcihw ,)tcud raelhcoc( aidem alacs eht fo roolf eht smrof enarbmem ralisab eht ,nagro itroC eht htiw rehtegoT .llaw raelhcoc retuo eht fo tnemagil larips eht dna ,suloidom eht morf gnitcejorp flehs ynob a ,animal larips eht neewteb sehcterts ,xepa raelhcoc eht ta renniht dna )mm 5.0( rediw ylbaredisnoc dna aelhcoc eht fo esab eht ta kciht ylevitaler dna )mm 1.0( worran si hcihw ,)7.7 ,6.7 .sgiF( enarbmem ralisab ehT .inapmyt alacs dna ,ilubitsev alacs ,aidem alacs eht :seitivac etarapes eerht sniatnoc tI .xepa raelhcoc eht ot mc 5.3±3 fo htgnel a rof )suloidom( aelhcoc eht fo sixa eht dnuora slarips lanac raelhcoc ynob ehT aelhcoC eht fo noitcnuF dna ymotanA 2.7 raE III 061
  • 170. :snoitcnuf lacinahcem tnereffid owt fo dia eht htiw smelborp xelpmoc eseht sevlos aelhcoc ehT .slevel erusserp ni secnereffid egral yrev yb dna esion yb derepmah osla si noitcudsnarT .slangis laruen otni noitamrof -ni citsuoca fo noitcudsnart laropmet 1 : 1 a sedulcerp stnetnoc ralullec dna ,noitavrenni ,epahs rieht ni yldekram reffid hcihw ,llec riah retuo dna renni na fo margaid citamehcS Outer hair cell sllec riah raelhcoC .giF .nwohs ton si noitcennoc siht ytiralc rof tub ,sllec riah retuo eht fo ailic eht ot detcennoc yllautca si enarbmem lairotcet ehT .)egnaro( hpmylodne eht morf )eulb( ecaps citahpmylirep eht setarapes hcihw ,enarb -mem raluciter eht mrof sllec gnitroppus eht neewteb snoit -cnuj thgiT .enarbmem ralisab eht no stser itroC fo nagro ehT [Na+] [K+] Perilymph + 85 mV + 155 mV Tectorial membrane 161 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. Efferent neurons Afferent neurons Subsynaptic cistern Nucleus Mitochondria Submembranous cistern Cuticular plate Hensen body Stereocilia Inner hair cell Basilar membrane Efferent nerve fibers Afferent nerve fibers Scala tympani Spiral lamina Inner hair cells Outer hair cells [Na+] [K+] Cochlear duct Endolymph Reticular membrane itroC fo nagrO .giF sihT .dnoces hcae dessecorp eb ot seslupmi derdnuh lareves naht erom on swolla hcihw ,doirep yrotcarfer citsiretcarahc a htiw serutcurts laruen ot dettimsnart era ztreh dnasuoht lareves fo egnar lacipyt eht ni snoitarbiV .erutcurts laropmet rieht ni seil snoitarbiv citsuoca ni deniatnoc noitamrofni eht fo hcum ecnis ,noituloser laropmet fo melborp a yllacisab si slan -gis laruen otni noitamrofni citsuoca fo noitalsnart ehT aelhcoC eht fo noitcnuF .reifilpma raelhcoc eht fo ºrotomª ro rotceffe eht sa deweiv era sllec riah retuo eht ,tnemegnarra dna ymotana rieht sa llew sa sgnidnif eseht no desaB .zH 000,03 fo ycneuq -erf a ot pu snoitcartnoc cimhtyhr ogrednu nac yeht taht sllec riah retuo detalosi no stnemirepxe morf wonk eW .srebif evren raelhcoc tnereffe yb ylniam deilppus era dna snoitcennoc tnereffa wef evah sllec riah retuo ehT .enarbmem lairotcet eht ot dehcatta ylmrif era ailicoerets riehT .)8.7 .giF ees( hpmylirep yb dednuorrus era yeht ,ecaps citahpmylodne eht otni stcejorp hcihw ,dne detailic rieht morf tpecxE .sllec gnitroppus fo krowten xelpmoc a yb xepa dna esab rieht ta ylno derohcna era dna ,aelhcoc eht gnola swor eerht ni degnarra yllareneg era ,lacird -nilyc era sllec riah retuo ehT .aelhcoc eht ni )000,21 yletamixorppa( sllec riah renni naht sllec riah retuo erom semit ruof ot eerht era erehT :sllec riah retuO · .seslupmi evren otni noitamrofni citsuoca mrofsnart hcihw º,sllec gniraehª lautca eht era sllec riah renni ehT .evren raelhcoc eht fo srebif tnereffa lareves ot detcen -noc si llec riah renni hcaE .edasilap suounitnoc a mrof ailicoerets riehT .)8.7 .giF ees( sllec gnitroppus yb dednuorrus era dna aelhcoc eht gnola wor elgnis a ni degnarra era hcihw ,sllec riah renni 0003 naht erom sniatnoc aelhcoc eht yllamroN :sllec riah rennI · :)9.7 .giF( dehsiugnitsid era sllec riah fo sepyt owT .llec yros -nes eht rof sulumits yrotaticxe etauqeda na setareneg ailicoerets tsegnol eht drawot esab sti ta eldnub ailicoe -rets eht fo noitcelfed ynA .slirbif esrevsnart yb detcen -nocretni era taht sdor ffits ,ynit era sevlesmeht ailic -oerets ehT .syarra lanogaxeh ni rehtegot dekcap dna swor lanidutignol ni degnarra era ailicoerets ehT .ecaf -rus dezilaiceps a no htgnel gniyrav fo ailicoerets fo eld -nub a yb detnuomrus srotpeceronahcem era sllec riaH .yradnuob egatlov a smrof enarbmem raluciter eht ,tnemegnarra siht fo esuaceB .enarbmem ralucit -er eht woleb ecaps citahpmylirep eht dna ,enarbmem lairotcet dna ailic eht sniatnoc hcihw ,enarbmem eht evoba ecaps citahpmylodne eht neewteb noititrap a setaerc dna rehtona eno htiw sllec yrosnes eht fo secaf -rus detailic eht stcennoc enarbmem raluciter ehT .an raE eht fo ygoloisyhP dna ymotanA 7
  • 171. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .wodniw dnuor eht ta dezilauqe era etalptoof sepats eht fo stnemevom yb decudni segnahc erusserp ehT .nrettap dnuos eht fo noitatneserper edurc a gnitaerc ,tnedneped-ycneuqerf era evaw gnilevart eht yb enarbmem ralisab eht fo snoitcelfed mumixam ehT .evaw gnilevart evissap eht fo ledom elacs-noN Helicotrema Envelope curve of basilar membrane vibration at 500 Hz Envelope curve of basilar membrane vibration at 5000 Hz .txet eht ni srebmun ot refer srebmun delcric ehT .sllec riah retuo dna enarbmem ralisab eht neewt -eb snoitarbiv edutilpma-wol rof kcabdeef evitisop a no desab si hcihw ,reifilpma raelhcoc eht fo noitatneserper citamehcS Round window membrane Middle ear Impedance matching (middle ear) passive traveling wave Basilar membrane Cochlear amplifier 1 Transduction Afferent cochlear nerve fibers Basilar membrane seicneuqerf owt ta noitarbiv enarbmem ralisaB 3 2 4 Outer hair cells Inner hair cell Tectorial membrane reifilpma raelhcoC .giF .ydob namuh eht ni ecnereffid laitnetop ral -ullecartxe tsegral eht si laitnetop raelhcocodne ehT .)161 .p ,8.7 .giF ees( hpmylirep dna hpmylodne eht fo snoitisopmoc cinoi tnereffid eht no desab Vm 58 yletamixorppa fo egatlov a setareneg tI .yrettab a ekil skrow hcihw ,laitnetop raelhcocodne eht yb derewop si sllec riah retuo eht fo yticapac elitom ehT .noitarb -iv eht seifilpma taht kcabdeef evitisop a ni gnitluser ,)Â( sllec riah retuo eht fo noitarbiv cisnirtni na secud -orp sihT .sulumits yrotaticxe na gnitaerc ,aelhcoc eht ot laidar detcelfed era yeht ,enarbmem lairotcet eht ot detcennoc era ailic rieht esuaceB .)Á( enarbmem ralisab eht ot dehcatta sllec riah retuo eht secalpsid evaw gnilevart sihT .)À :11.7 .giF( enarbmem ralisab eht ni evaw gnilevart tnedneped-ycneuqerf a ecud -ni hpmylirep eht ni sevaw erusserp ehT :gniwollof sa era stnevE .enarbmem ralisab eht ta nrettap dnuos deliated ,prahs a ni tluser )11.7 .giF( reifilpma raelhcoc eht yb noitacifilpma dna gninut enif sihT .snoitarb -iv edutilpma-wol yfilpma hcihw ,itroC fo nagro eht ni sllec riah retuo eht fo ytivitca eht yb elbissop edam ylfeihc si sihT .noitcnuf raelhcoc lacinahcemorcam evissap eht yb decudorp snoitarbiv enarbmem ralisab eht enut-enif ot sevres noitcnuf lacinahcemorcim ehT reifilpmA raelhcoC :noitcnuF lacinahcemorciM .revewoh ,sis -ylana citsuoca gnitanimircsid a rof edurc oot hcum si .giF sevaw gnilevart evissap eseht fo noituloser ehT .xepa eht raen snoitarbiv mumixam ecudni seicneuqerf wol elihw ,aelhcoc eht fo esab eht raen enarbmem rali -sab eht fo noitarbiv mumixam esuac seicneuqerf hgiH .srebif evren cificeps ot seicneuqerf eht gningissa ybereht ,enarb -mem ralisab eht fo saera gnidnopserroc ni seicneuq -erf niatrec fo noitatneserper eht ,.e.iÐyticipotonoT · dna sisylana ycneuqerf evissaP · :rof swolla msinahcem siht ,8291 ni ysekeB yb debircseD .)01.7 .giF ees( enarbmem eht gnola etis tnereffid a ta noitcelfed mumixam a sesuac ycneuqerf hcaE .enarb -mem ralisab eht ni sevaw gnilevart etareneg hpmyl -irep eht ot etalptoof sepats eht morf dettimsnart era taht sevaw dnuoS .)7.7 .giF ees( enarbmem ralisab eht fo dna inapmyt dna ilubitsev alacs eht fo tnemegnar -ra laiceps eht no desab si aelhcoc eht fo noitcnuf sihT evaW gnilevarT :noitcnuF lacinahcemorcaM .dootsrednu ylluf tey ton era ssecorp siht fo sliated cigoloisyhp eht ,revewoH .elbissop yllacisyhp si tahw fo timil eht ta snoitarbiv ssecorp ot elba si aelhcoc eht ,snoitcnuf reifilpma dna sisylana ycneuqerf sti htiW .revewoh ,detalerretni ylesolc era snoitcnuf owt ehT .noitacifilpma htiw erom slaed noitcnuf lacinahc -emorcim eht elihw ,sisylana ycneuqerf htiw denrec -noc ylniam si noitcnuf lacinahcemorcam ehT .level ral -ullec eht ta noitcnuf lacinahcemorcim a dna tnemtrap -moc diulf eht nihtiw noitcnuf lacinahcemorcam a otni dedividbus rehtruf eb nac aelhcoc eht fo snoitcnuf ehT .reifilpma raelhcoc eht fo dia eht htiw deifingam era edutilp -ma wol ta snoitarbiV :noitacifilpma lacinahcemoiB · .elpicnirp cipotonot eht si sihT .snoitacol cificeps ta srebif evren ot dengis -sa era seicneuqerf niatreC :sisylana ycneuqerF · raE III 261
  • 172. .meht eviecrep ot dedeen ton si reifilp -ma na esuaceb ssenduol dehsinimidnu fo era stneve dnuos duol saerehw deviecrep ton era sdnuos tfos ,re -ifilpma raelhcoc eht fo ssol htiW .gnissecorp dnuos fo scimanyd lamronba yb desuac ssol gniraeh raelhcoc fo ngis lacinilc a si tnemtiurceR .ssenduol fo htworg lam -ronba eht ro ,tnemtiurcer fo nonemonehp eht rof elbis -nopser yltrap tsael ta si reifilpma raelhcoc eht fo ssoL .laitnet -op raelhcocodne eht gnitceffa ybereht ,siralucsav airts eht fo msilobatem eht retla nac edimesoruf sa hcus sciteruid pool dna ,sllec riah eht fo msilobatem eht egamad nac scitoibitna edisocylgonima ,elpmaxe roF .yaw siht ni ssol gniraeh raelhcoc ot dael nac sgurD .noitcnufsyd ot elbitpecsus osla si siralucsav airts dna sllec riah eht fo msilobatem dezilaiceps ylhgih ehT .)662 .p ees( sisucybserp ro ,ssol gniraeh detaler-ega ni rotcaf a eb osla yam dna )562±062 .pp ees( ssol gniraeh decudni-esion fo esuac eht si reifilpma raelhcoc eht fo gnidaolrevo lacinahceM .sedaced ynam rof elbats sniamer dna ylsselwalf snoitcnuf yllare -neg metsys eht taht elbakramer erom eht lla ti sekam sihT .snamuh ni etareneger yeht taht ylekilnu si ti dna ,llams ylevitaler si aelhcoc eht ni sllec yrosnes fo rebmun ehT .etats evitca yllacinahcem a ni ti gnipeek ,ilumits citsuoca ot desopxe yltnatsnoc si aelhcoc ehT snoitacilpmI lacinilC .noissime citsuocaoto suoenatnops aÐrae renni eht morf dettime enot tniaf a si zH 2591 ta kaep ehT .enohporcim eborp a gnisu lanac rae lamron a ni ylsuoenatnops dedrocer murtceps ycneuqerf a tneserper )stnemerusaem owt( sevruc desopmirepus owt ehT 1 600 1 800 2 000 2 200 2 400 Level (dB SPL) 361 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. Frequency (Hz) – 20 1 400 – 10 0 10 20 snoissime citsuocaoto suoenatnopS .giF .)191±981 .pp ,snoissimE citsuocaotO ees( detceted eb osla nac reifilpma raelhcoc eht morf stcu -dorp noitrotsiD .lanac rae eht ni dedrocer eb osla nac taht snoissime dekove secudni )kcilc a ,.g.e( edistuo eht morf aelhcoc eht no gnitca sulumits citsuoca nA .snoitacol niatrec ta sllec riah eht fo tnemegnarra lacirtemmysa ylthgils a morf tluser yeht taht si yroeht enO .reifilpma raelhcoc gninoitcnuf a fo ecnedive sa snosrep gniraeh-lamron ynam ni seicneuqerf niatrec ta rucco ,)21.7 .giF ,sEAOS( snoissime citsuocaoto suo -enatnops dellac ,aelhcoc eht yb dettime sdnuos esehT .lanac rae eht ni decalp enohporcim evitisnes ,llams a yb sdnuos tniaf sa detceted eb nac reifilpma raelhcoc eht fo snoitarbiv larutan eseht ,rekaepsduol a fo enarb -mem eht ekil lanac rae eht otni snoitarbiv eht stime hcihw ,enarbmem cinapmyt eht ot rae elddim eht hguorht aelhcoc eht morf noihsaf edargorter ni osla tub )edargetna( edisni ot edistuo morf ylno ton snoit -arbiv stimsnart rae eht esuaceB .noitrotsid ot tcejbus si dna noitarbiv fo sedom larutan evah ot sdnet reifilp -ma raelhcoc eht ni taht ekil noitacifilpma raenilnoN .metsys la -noitcnufnon dna elbatsnu na ni tluser dluow snoitarb -iv gnorts dna kaew fo noitacifilpma lanoitroporp ehT .rotcaf noitacifilpma eht retaerg eht ,ygrene lanoitarbiv eht rewol ehT .LPS Bd 06 yletamixorp -pa ta detarutas semoceb dna yaw raenil a ni noitcnuf ton seod reifilpma raelhcoc eht ,level dnuos eht ot noitroporp ni sworg evaw gnilevart evissap eht elihW snoissimE citsuocaotO±noitcnuF raenilnoN .hpmylodne eht fo gnimaerts laidar yb dekove ylbaborp si sulumits eht dna ,yltcerid sllec eht etalumits ton seod enarbmem ralisab eht fo noitarbiv ehT .sllec riah renni eht rof sulumits siht otni demrof -snart si enarbmem ralisab eht fo noitcelfed eht woh nwonk tey ton si tI .)Ã( sllec riah renni eht rof sulumits etauqeda na secudorp aelhcoc eht ot laidar ailic eht fo noitcelfed a ,sllec riah retuo eht fo esac eht ni sA .slait -netop evren otni noitarbiv citsuoca eht fo sulumits lac -isyhp eht mrofsnart sllec riah renni ehT :noitcudsnarT .ssecorp noitacifilpma evitca eht fo noitassec ro noitcuder a ot sdael egatlov eht ni noitcuder yna dna ,dleif egatlov siht ni dednepsus era sllec riah retuo ehT .tcud citahpmyl -odne eht sredrob taht tnemagil larips eht fo noiger dezilaiceps a ,siralucsav airts eht ni sessecorp egnahc -xe-noi evitca yb deniatniam si tneidarg laitnetop ehT .hpmylodne eht dna sllec riah retuo eht fo msalpotyc eht neewteb stsixe Vm 551 yletamixorppa fo ecnereffid laitnetop retaerg neve nA raE eht fo ygoloisyhP dna ymotanA 7
  • 173. 8 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 174. III Ear 7 8 9 Anatomy and Physiology of the Ear 10 11 12 13 14 15 Hearing Disorders in Children— Pediatric Audiology The External Ear The Middle Ear Inner Ear and Retrocochlear Disorders Vestibular Disorders Facial Nerve Lateral Skull Base Audiology (Auditory Testing) Examination of the Ear and Clinical Auditory Testing 166 History 166 Inspection and Otoscopy 166 Clinical Hearing Tests 167 8.2 Basic Principles of Audiometry 171 Basic Concepts in Acoustics 171 Audiologic Examination 175 8.3 8.4 Objective Hearing Tests 184 Immittance Measurements 184 Auditory Evoked Potentials (AEPs) 186 Otoacoustic Emissions (OAEs) 188 8.5 8.1 Rehabilitation and Hearing Aids 192 Indications and Possibilities of Auditory Rehabilitation 192 Hearing Aid Fitting in Adults 192 Cochlear Implant in Adults 194 Behavioral Audiometric Testing 178 Pure-Tone Audiometry 178 Speech Audiometry 178 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 175. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. rae elddim yfitnedi ot elbissop si ti ,enarbmem cinap -myt niht a htiW .ycnerapsnart elbairav dna roloc hsi -yarg a sah enarbmem cinapmyt lamron ehT .tnioj ral -ubidnamoropmet eht fo ecnenimorp eht yb derucsbo si ti esuaceb ,epocsoto eht htiw nees eb tonnac enarb -mem cinapmyt eht fo elgna roiretna eht ,yltneuqerf -ni toN :enarbmem cinapmyt eht fo noitaulave lacinilC .)822±012 .pp( 11 dna 01 sretpahC ni debircsed era lanac rae eht fo gnisnaelc dna seitilamronbA .enarb -mem cinapmyt dna lanac rae eht fo weiv raelc a drof -fa dluohs sihT .lanac rae eht fo noitrop laidem evitis -nes-niap dna ynob eht gnihcuot tuohtiw tub eassirbiv eht tsap ti gnitresni ,ecnadiug lausiv rednu lanac rae eht otni decudortni ylwols si muluceps ehT .noitan lanac rae eht fo noitanimulli etauq -eda dna erusopxe doog edivorp ot desu eb dluohs muluceps elbissop tsegral ehT .epocs eht ecudortni ot drawpu dna draw -kcab elcirua eht sllup yltneg renimaxe ehT .reifingam detnuom -leviws dna eldnah yrettab a sah epocsoto dleh-dnah ehT -imulli dna erusopxe retteb sedivorp muluceps daorb a taht dnim ni gnipeek ,stniartsnoc cimotana ot mrof -noc dluohs muluceps rae eht fo retemaid ehT .trap ynob laidem eht htiw enil ni lanac eht fo trap suon -igalitrac laretal eht gnirb dna lanac rae lanretxe eht snethgiarts revuenam sihT .noitcart evissecxe gnidiova ,noitanimaxe eht rof drawpu dna drawkcab yltneg de -tator si elcirua ehT .epocsorcimoto na gnisu tsigoloto na yb ro )1.8 .giF( epocsoto dleh-dnah a htiw demrof -rep si ypocsotO :)902 .p ,1.01 osla ees( euqinhceT .euqinhcet cipocsoto luferac ylralucit -rap a tnarraw yeht ,tneserp nehW .)322±812 .pp ,4.01 dna 612 .p ,3.01 ees( anretxe sitito etacidni sngis esehT .niap rof kcehc ot elcirua eht no llup dna ssenrednet lagart rof kcehc dluohs renimaxe eht ,ypocsoto gnimrofrep erofeB ypocsotO saera gnidnuorrus ro elcirua eht fo gnillews dna ssendeR · )FSC( diulf lanipsorberec ,doolb ,sup ,sucum ,nemurec :egrahcsid dna lanac rae lanretxe eht ni gnitsurC · sracs lacigruS · lanac rae ro elcirua eht fo epahs eht ni segnahC · :ot nevig eb dluohs noitnettA .sgnidnuorrus sti dna elcirua eht fo noitcepsni hguoroht a htiw trats syawla dluohs gniraeh dna rae eht fo noitanimaxE Swivel magnifier ypocsotO dna noitcepsnI .tnatropmi osla era seirujni rae rehto ro ,noitarofrep enarbmem cinapmyt ,yregrus rae suoiverp yna fo snoit -pircseD .egrahcsid larua ro niap sa hcus smotpmys lanoitidda tuoba ksa dluohs renimaxe eht ,gniraeh ro rae eht gnivlovni stnialpmoc cificeps sah tneitap eht fI ogitreV · sutinniT · )sisucaopyh( gniraeh dehsinimiD · :redrosid rae renni na fo smotpmys tnatropmi tsom eerht eht tuoba denoitseuq eb dluohs tneitap yrevE ypocsotO .giF .stset noitcnuf dna ,)ypocsoto( noitceps -ni ,gnikat yrotsih fo stsisnoc gnitset yrotidua ,noitan -imaxe lacinilc yna ekiL .gniraeh fo noitagitsevni reht yrotsiH -ruf eht rof stset cificeps erom tceles ot desu eb neht nac stset eseht fo stluser ehT .stset elpmis fo snaem yb gniraeh fo ssendedis dna ytirgetni eht no noitam -rofni eriuqca ot si gnitset yrotidua lacinilc fo laog ehT gnitseT yrotiduA lacinilC dna raE eht fo noitanimaxE 1.8 raE III 661
  • 176. 761 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .enob lainarc eht fo noitarbiv secudni osla muh duol a ecnis ,muh tneitap eht gnivah yb detceted eb osla nac noitazilaretaL :tset gnimmuH .)c 3.8 .giF( reduol sa deviecrep si dnuos eht dna ,aelhcoc gninoitcnuf yllamron eht ni tneserp si ygrene lanoitarbiv erom ,tluser a sA .)gniksam ssel( aelhcoc eht hcaer ot sdnuos tneibma rof tluciffid erom si ti dna rae elddim eht hguorht aelhcoc eht morf dettimsnart ylroop erom si ygrene lanoitarbiv eht esuaceb rae detceffa eht ot dezilaretal si krof gni -nut eht ,ssol gniraeh evitcudnoc a sah tneitap eht fI · .)b 3.8 .giF( rae gniraeh-retteb eht ot dezilaretal si krof gninut eht ,ssol gniraeh laruenirosnes sah tneitap eht fI · .rehto eht ro edis eno ot dezilaretal eb lliw dnuos eht ,tset lam -ronba na nI .srae eht neewteb yawdim draeh si dnuos eht os dna ,sedis htob no duol yllauqe sa deviecrep era snoitarbiv eht ,lamron si gniraeh nehW :noitaterpretnI .aelhcoc eht ot noitcudnoc enob yb dettimsnart era snoitarbiv ehT .)a 3.8 .giF( daeherof eht ro xetrev eht no yllausu ,lluks eht fo enildim eht ni decalp si krof gninut ehT :euqinhceT :tset rebeW .niks eht yb gninepmad emocrevo dna enob eht ot snoitarbiv eht timsnart ot redro ni enob lainarc eht tsniaga ylmrif desserp eb tsum krof gninut gnitarbiv eht fo esab eht ,noitcudnoc enob tset oT .aera ecafrus egral a htiw esab daorb a evah dluohs krof gninut ehT .lacoviuqe netfo era egnar rehgih siht ni stluser tset dna ,zH 0001 yletamixorppa si rae elddim eht fo ycneuqerf tnan -oser ehT .snoitarbiv ycneuqerf-wol fo noitpecrep eht morf ecnerefretni ot eud gnitset yrotidua rof elbatius ton era seicneuqerf rewoL .desu si zH 0 08 dna 052 tuoba neewteb setarbiv taht krof gninut A :euqinhceT .stset krof gninut htiw yltcerid detceted ton si ssol gniraeH .metsys yrotidua eht fo serutcurts laruen eht ro aelhcoc eht ni esuac sti sah ssol gniraeh laruen -irosnes saerehw ,rae elddim ro lanac yrotidua lanret -xe eht fo esaesid yb desuac si ssol gniraeh evitcudnoC .)4.8 .giF( tset enniR eht dna )3.8 .giF( tset rebeW eht :esoprup siht rof etauqeda era stset owT .ssol gniraeh laruenirosnes dna evitcudnoc neewteb etaitnereffid ot si stset krof gninut fo laog ehT stseT kroF gninuT stseT gniraeH lacinilC .tnardauq roirepus roiretsop eht ni detaicerppa ylraelc tsom si enarbmem cinapmyt eht fo ytilibom eht ,elur a sA .)132 .p ,raE elddiM eht fo noitanimaxE ,1.11 ees( epocsoto citamuenp elgeiS a gnisu yb ro revuenam avlaslaV a mrofrep tneitap eht gnivah yb detset eb nac ytilibom stI .enarbmem eht ni stcefed ro sracs yb ro rae elddim eht ni nois -uffe yb detcirtser eb yam enarbmem cinapmyt eht fo ytilibom ehT .etarbiv ot elba eb tsum enarbmem cinapmyt eht ,noitcnuf sti mrofrep oT :elibom si tI · .ecnaraeppa detaitnereffidnu na sah enarbmem cinapmyt eht dna deifitnedi eb regnol on nac serutcurts eseht ,tneserp si noitammalfni etuca na nehW .)2.8 .giF( dehsiugnitsid eb nac eld -nah suellam dna gnir suonigalitracorbif eht sa hcus serutcurts cimotana lamroN :detaitnereffid si tI · .raeppasid sexelfer thgil lamron eht ,noitammalfni ot eud nel -lows semoceb muilehtipe htooms eht nehW .enarb -mem eht fo noitisop eht no gnidneped ,enarbmem cinapmyt lamron eht no setis rehto ta nees eb yam snoitcelfer rehto tub ,tnardauq roirefni roiretna eht ni nees netfo si ºthgil fo enocª A .yaw lacipyt a ni thgil stcelfer taht muilehtipe suomauqs htooms yb derevoc si enarbmem cinapmyt ehT :thgil stcelfer tI · :seitreporp eerht gniwollof eht stibihxe enarbmem cinapmyt lamron ehT .)352 ±822 .pp ,11 retpahC osla ees ,2.8 .giF( inapmyt adrohc eht ro sucni eht fo ssecorp gnol eht sa hcus serutcurts Umbo TMJ prominence Light reflex .enarbmem cinapmyt thgir a setartsulli erugif ehT .elbairav era roloc dna ycnerap -snart stI .skramdnal cimotana suo -irav syalpsid dna ecafrus htooms a gnitacidni xelfer thgil a sah enarbmem cinapmyt lamron ehT Long process of incus (visible through membrane) Short process of malleus Fibrocartilaginous ring enarbmem cinapmyt eht fo ecnaraeppa lamroN .giF )gnitseT y rotiduA( ygoloiduA 8
  • 177. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .gnitset cirtemoidua yb ylno denimreted eb dluohs ssol gniraeh fo eerged evitatitnauq eht yadot dna ,srot -caf dellortnocnu ynam no dneped dna esicerpmi era stnemerusaem esehT .srebmun derepsihw ro nekops raeh dluoc tneitap eht hcihw ta egnar eht gninimret -ed yb detset saw ssol gniraeh fo eerged eht ,ylremroF .serudecorp tset cirtemoidua etairp -orppa gnitceles rof yrassecen si taht noitamrofni lac -inilc eht ylppus stset krof gninut dna tset hceeps ehT .ssol gniraeh fo noitaulave etarucca na ekam naht rehtar srae tfel dna thgir eht neewteb ecne -reffid dlohserht a tceted ot desu tset gnineercs elpmis a si sihT .srebmun nekops taeper dna ot netsil tneit -ap eht gnivah yb sdohtem tset detnemurtsni tuohtiw dessessa yllacinilc eb nac ssol gniraeh fo ytireves ehT -rep yam rae etisoppo eht ,gniksam tuohtiW .)071 .p ,a 6.8 .giF ees( tset enniR eht gnimrofrep erofeb rae etisoppo eht ksam ot yrassecen si ti ,rehto eht naht edis eno no retteb si gniraeh laruenirosnes nehW · .evitagen si tset enniR ehT .)b 4.8 .giF( lanac rae eht edistuo naht diotsam eht no reduol sa deviecrep si dnuos eht ,tneserp si ssol gniraeh evitcudnoc nehW · .)a 4.8 .giF( regnol sdnoces 51 tsael ta stsal dna dnuos detcudnoc-enob naht reduol sa deviec -rep si dnuos detcudnoc-ria ,tset enniR evitisop a nI · .noitcudnoc enob yb naht noitcudnoc ria yb retteb aelhcoc eht ot dettimsnart si noitarbiv krof gninut eht tset )evitisop( lamron a nI :noitaterpretnI .srae htob neewteb ro ni ssenduol lauqe htiw deviecrep si dnuos eht ,lacirtemmys si gniraeh nehW a .lluks eht fo enildim eht no krof gninut gnitarbiv a gnicalp yb demrofrep si tset rebeW ehT .edis detceffa eht ot dezi -laretal si dnuos eht ,ssol gniraeh evitcudnoc laretalinu htiW c .rae retteb eht ot dezila -retal si dnuos eht ,ssol gniraeh laruenirosnes laretalinu htiW b .)evoba ees( lanac rae eht edistuo tsuj noitisop a ot detfihs si )niaga kcurts gnieb tuohtiw( krof gninut eht nehT .elbiduani semoceb dnuos eht nehw renimaxe eht sllet tneitap eht dna ,diotsam eht ot desserp dna kcurts si krof gninut ehT :dlo -hserht rof gnitset yb derapmoc eb nac noitcudnoc enob dna ria ,reduol si hcihw erusnu si tneitap eht fI · .)noitcudnoc enob( noitisop dno -ces eht ni taht htiw )noitcudnoc ria( noitisop tsrif eht ni ssenduol eht erapmoc ot dlot si tneitap ehT · .diotsam eht tsniaga ylmrif krof gninut eht gnisserp yb detset si noitcudnoc enob dna ,ti gnihcuot tuohtiw lanac rae eht edistuo tsuj krof gninut eht gnidloh yb detset si noit -cudnoc ria ,snoitidnoc dradnats etaerc oT :euqinhceT .)srae tfel dna thgir eht serapmoc hcihw ,tset rebeW eht ekilnu( rae emas eht ni noitcudnoc enob dna ria fo slevel eht serapmoc tset enniR ehT :elpicnirP :tset enniR .)381±871 .pp ees( yrtemoidua enot-erup yb dessessa yllausu si noitautis siht ni dlohserht gniraeh eht dna ,revewoh ,stset enituor ni deksam ylerar si rae etisoppo ehT .tset enniR evitagen -oduesp a ot gnidael ,noitcudnoc ria aiv rae tset eht naht noitcudnoc enob aiv reduol sa dnuos eht eviec Affected tseT hceepS Healthy .deterpretni ylevitinifed eb tonnac taht sgnidnif ºlacigolliª dleiy yam stset eseht ,revewoh ,yllanoisaccO .stset enniR dna rebeW eht fo noitanibmoc a morf deniatbo eb nac taht noitamrof -ni eht swohs 5.8 .giF :stset krof gninut eht gniterpretnI Healthy a Normal hearing Healthy b Sensorineural hearing loss Affected Healthy c Conductive hearing loss tset rebeW ehT .giF raE III 861
  • 178. .sretem 4 yletam -ixorppa ta draeh eb yllamron nac tneitap eht morf yawa denrut daeh eht htiw derepsihw srebmuN .yawa sretem 6 yletamixorppa morf derepsihw srebmun tigid-owt dnatsrednu nac tcejbus eht ,tset lamron a nI .elbigilletni llits era srebmun eht hcihw ta ecnatsid eht fo smret ni detats eb nac ssol gniraeH :noitaterpretnI .deniatniam eb snoitidnoc tset tnatsnoc taht laitnesse si tI .level lanoitasrevnoc lamron a ta nekops eb yam srebmun eht ,yrassecen fI .elbigilletni emoceb sdrow eht hcihw ta egnar eht senimreted dna resolc sevom renimaxe eht ,srebmun eht dnatsrednu ton seod tneit -ap eht fI .sretem 6 fo ecnatsid a morf tneitap eht draw -ot srebmun srepsihw ohw ,renimaxe eht drawot rae tset eht snrut tneitap ehT .renimaxe eht fo weiv stneit -ap eht skcolb dna rae tsetnon eht sksam tnatsissa ehT .)7.8 .giF( elbaliava era tnatsissa na dna etius gnitset egral a fi sretem ni detset eb nac gniraeh fo egnar ehT .tnemnorivne tset dezidradnats a edivorp dna tset eht gnirud level ssenduol tnatsnoc a niatniam dluohs renimaxe ehT .level ssenduol lamron a ta nekops srebmun eht htiw detaeper si tset eht ,lanac rae eht edistuo tsuj derepsihw nehw doots -rednu ton llits era srebmun eht fI .rae tset eht morf secnatsid rellams ylevissergorp ta niaga meht stnes -erp renimaxe eht ,srebmun eht dnatsrednu ton seod tneitap eht fI .duola sdrow eht taeper ot tneitap eht stcurtsni dna tneitap eht morf yawa denrut daeh sih htiw srebmun tigid-owt srepsihw renimaxe eht woN .)6.8 .giF( regnif eht htiw nottoc eht gnilggiw yltneg yb esion gniksam a gnita -erc dna lanac rae tsetnon eht otni daw nottoc tsiom a gnitresni yb enod si sihT .gniraeh revossorc edulcerp ot deksam eb dluohs rae tsetnon ehT .rae hcae rof yletar -apes detset si level lanoitasrevnoc lamron a ta hceeps dna hceeps derepsihw gniraeh rof egnar ehT :euqinhceT Bilateral symmetrical conductive hearing loss Bilateral symmetrical sensorineural hearing loss Rinne test on the lateralized side Rinne test on both sides .)thgir rewol ta nwohs( ssol gniraeh laruenirosnes laretalib htiw stneitap ni tluser eht morf tnereffid yllaitnatsbus ton si )enniR evitisop dna rebeW lacirtemmys( tluser lamron A .stset krof gninut eht htiw ssol gniraeh evitcudnoc dna laruenirosnes fo noitacifissalC Conductive hearing loss on the lateralized side Midline stset krof gninuT .noit -cudnoc ria naht degnolorp erom ro/dna reduol gnieb sa deviecrep si noitcudnoc enob ,tneserp si ssol gniraeh evitcudnoc nehW b .noitcudnoc enob naht noitarud regnol fo ro/dna reduol gnieb sa deviecrep si noitcudnoc ria ,ssol gniraeh evitcudnoc fo ecnesba eht nI a .ssenduol sti ro/dna krof gninut eht rof dlohserht yrotidua eht enimreted ot rae emas eht ni derap -moc era noitcudnoc enob dna riA b Negative Rinne test 961 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. Sensorineural hearing loss on the nonlateralized side Lateralized Weber test .giF a Positive Rinne test tset enniR ehT .giF )gnitseT y rotiduA( ygoloiduA 8
  • 179. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .sedis tfel dna thgir eht neewteb secneref -fid ezingocer nac dna tset elpmis siht htiw gniraeh ssessa ylbailer nac renimaxe na ,ecitcarp emos htiW .rae taht ni hceeps rof ssenfaed lanoit -cnuf evah ot deredisnoc si tneitap eht ,level duol neve ro lamron a ta rae eht ot esolc nekops nehw elbigillet -ninu era srebmun eht fI .seicneuqerf hceeps hgih rof tsael ta ,ssol gniraeh ereves evah ot deredisnoc si tneit -ap eht ,lanac rae eht edistuo tsuj derepsihw nehw yl -no dootsrednu era ro elbigilletninu era srebmun eht fI .weiv stneitap eht gni -dleihs elihw rae tsetnon eht sksam tnatsissa na ,egnar gniraeh tset oT tset egnar gniraeH .tneserp si ssol gniraeh nehw rae tset eht ot resolc meht srepsihw ro ,tneitap eht morf yawa denrut elihw srebmun srepsihw renimaxe ehT b .giF .dnah rehto eht htiw weiv stneitap eht sdleihs dna dnah eno htiw rae tsetnon eht sksam renimaxe ehT a .tset gnineercs elpmis a sa edis hcae no yletarapes detset si srebmun nekops rof gniraeH tset hceepS .giF raE III 071
  • 180. 171 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .ria ni dnuos fo noitpec -rep eht rof dezilaiceps si gniraeh namuH .muidem a ni ylmrofinu setaga -porp tI .krof gninut a esac siht ni ,ecruos gnitarbiv a yb decudorp si dnuoS sevaw dnuos fo noitagaporp dna noitcudorP .giF .enob sa hcus aidem dilos ni s/m 0005 yletamixorp -pa ot ria ni s/m 043 morf segnar dnuos fo yticolev ehT -ni na ro ,nottub a gnihsup sa hcus ,noitcaer yratnulov a fo mrof eht ni dedrocer eb yam ilumits citsuoca na ot esnopser ehT .scitsuoca fo selpicnirp lacisyhp cisab eht fo emos gniweiver yb tinu siht nigeb ew ,denifed yllacisyhp era taht ilumits citsuoca syolpme ti ecniS .snoitcnuf yrotidua fo tnemerusaem eht si yrtemoiduA .)191±481 .pp( 4.8 ni dessucsid era ,yrtemoidua evitcejbo ni derusaem era hcihw ,sesnopser yratnulovnI .)381±871 .pp( 3.8 ni ylluf erom debircsed si dna sesnopser yratnulov no desab si yrtemoidua laroivaheB .elcsum suidepats eht fo noitcartnoc sa hcus esnopser cigoloisyhp yratnulov .redrosid gniraeh a fo noitacifitnauq · dna ,noitazilacol · ,noitceted · :eht era yrtemoidua lacinilc fo slaog ehT .ycneuqerf sti no gnidneped ,detcelfer yltrap dna debrosba yltrap si dnuos ,elur a sA .debrosba ro detcelfer rehtie si ti ,retaw ot ria morf sa ,rehtona ot muidem eno morf slevart dnuos nehW scitsuocA ni stpecnoC cisaB murtcepS ycneuqerF dnuoS dnuoS fo noitagaporP dna noitcudorP .)dlohserht enot-erup( gniraeh fo ytivit -isnes tnedneped-ycneuqerf eht enimreted ot ygo -loidua ni desu era yehT .stnemerusaem citsuoca rof detius llew era ,erutan ni rucco ylerar hcihw ,senot eruP .noitarbiv eht fo esahp dna ,edutilpma ,ycneuq -erf eht yb debircsed ylesicerp eb nac tI .)a 9.8 .giF( noitarbiv ladiosunis elgnis a fo stsisnoc enot erup A · :)9.8 .giF( murtceps ycneuqerf eht dellac era dna tneve dnuos a etutitsnoc rehtegot nekat seicneuqerf eseht fo llA .seicneuqerf suoirav fo pu edam yllausu si dnuos A .snamuh yb sulumits yrotidua na sa deviecrep eb nac zH 000,02 ±02 yletamixorppa fo egnar eht ni seicneuqerF yticolev noitagaporP · erusserp dnuoS · ycneuqerF · :seitre -porp gniwollof eht fo smret ni debircsed eb nac sevaw dnuos ehT .)enob sa hcus muidem dilos a ro ,diuqil ,ria( muidem citsale na ni sevaw dnuos sa etagaporp hcihw )8.8 .giF( snoitarbiv lacinahcem yb decudorp si dnuoS yrtemoiduA fo selpicnirP cisaB 2.8 )gnitseT y rotiduA( ygoloiduA 8
  • 181. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .ygoloidua dna scitsuoca ni serusserp dnuos rof desu si elacs cimhtiragol a yhw si sihT .seitiladom yrosnes lla rof eurt sdloh ,wal renhceF ±rebeW eht dellac ,noitpecrep dna sulumits neewteb pihsnoitaler cimhtiragol sihT .elacs raenil a no naht rehtar ,noihsaf cimhtiragol a ni serusserp dnuos tne -reffid fo slevel ssenduol eht seviecrep rae namuh ehT .egnar cimanyd eht dellac si trofmocsid tuohtiw sulumits cit -suoca na eviecrep nac nosrep a hcihw revo egnar ehT .01.8 .giF ni nwohs era stneve nommoc htiw detaicossa seulav erusserp dnuos fo selpmaxE .gniraeh fo dlohserht lamron eht naht retaerg semit noillim 1 yletamixorppa si hcihw ,aP 02 yletamixorppa fo erusserp dnuos a ta dehcaer si dlohserht niap ehT .erusserp cirehpsomta eht naht rewol edutingam fo sredro 01 si hcihw ,)dlohserht gniraeh eht ,aP 5±01 ” 2( aP 02 sa llams sa snoitairav erusserp dnuos eviec -rep tsuj nac gniraeh namuH .aP 501 fo redro eht no si erusserp cirehpsomta eht ,nosirapmoc yB .euqehtocsid a ni erusserp dnuos eht ot lauqe yletamixorppa si aP 1 -isyhp eb nac edutilpma erusserp fo snoitairav esehT .selucelom dna smota fo noitcaferar dna noitasned -noc gnitanretla eht yb desuac erusserp ria cirehpsom -ta fo snoitautculf llams ylemertxe era sevaw dnuoS erusserP dnuoS .noitacifitnedi fo snaem a sa evres ot eciov eht gnilbane ,syawria reppu eht fo ecnanoser eht yb de -taludom yllaudividni si seicneuqerf cisab fo murtceps ehT .)983±683 .pp ,1.81 ees( sdroc lacov eht fo snoitarb -iv yb decudorp si nemow ni zH 002 dna nem ni zH 001 yletamixorppa fo ycneuqerf latnemadnuf esohw ,eciov eht si snamuh rof ecruos dnuos tnatropmi tsom ehT .)onaip ,niloiv ,.g.e( ycneuqerf latnemadnuf eht fo selpitlum largetni era seicneuqerf esohw ,scinomrah erom ro eno sulp ycneuqerf latnemadnuf a sniatnoc dnuos lacisuM b .)enot krof gninut a ,.g.e( mrof -evaw ladiosunis a secudorp ycneuqerf elgnis A :enot eruP a .)remmahkcaj a morf esion eht ,.g.e( denim -reted eb tonnac hctip A .rehtona eno fo selpitlum largetni ton era taht seicneuqerf cidoirepnon suoremun fo stsisnoc esioN c .sulumits citsuoca nommoc tsom eht raf yb si esioN .rehtona eno fo selpitlum largetni ton era yeht ,.e.iÐ)c 9.8 .giF( detalernu yllacinomrah era taht seicneuqerf elpitlum gniniatnoc stneve dnuos fo stsisnoc esioN · .onaip a no deyalp eton emas eht morf niloiv a no deyalp eton a hsiugnit -sid ylisae nac renetsil eht ,senotrevo eht fo artceps tnereffid eht no desaB .)b 9.8 .giF( senotrevo cinom -rah sti ,yb dezingocer eb nac dna ,yb deziretcarahc si dnuos ehT .ycneuqerf latnemadnuf eht fo selpit -lum largetni era hcihw ,senotrevo cinomrah sulp yc -neuqerf latnemadnuf a fo stsisnoc dnuos lacisum A · :)aP( lacsap eht si tnemerusaem fo tinu ehT .derusaem yllac rab 01 = 2m/N 1 = aP 1 Frequency Frequency Frequency Amplitude Amplitude Amplitude Frequency analysis Time Time Time Sound pressure (Pa) Sound pressure (Pa) Sound pressure (Pa) Oscillogram a Pure tone c Noise b Musical sound esion dna ,dnuos lacisum ,enot :ilumits yrotidua tnereffid fo artceps ycneuqerf ehT .giF raE III 271
  • 182. 1 : 0.001 1 : 0.01 1 : 0.4 1 : 2.3 1 : 0.2 1 : 0.1 )1I : 2I( ygrene dnuos ot ytisnetni dnuos fo oitaR 1 : 0.01 1 : 2.3 1 : 0.2 1 : 8.1 1 : 4.1 1 : 0.1 Bd 02 Bd 01 Bd 6 Bd 5 Bd 3 Bd 0 )1p : 2p( oitar )1L±2L( ecnereffid erusserp dnuoS level erusserp dnuoS ytisnetni dnuos dna ,erusserp dnuos ,level erusserp dnuos neewteb pihsnoitaleR 1.8 elbaT .Bd 6 yb desaercni si level erusserp dnuos eht dna ,1.8 elbaT ot gnidrocca Bd 3 yb sesaerc -ni level ygrene dnuos ehT .delbuod si ygrene dnuos eht ,aera na ni detarepo si ssenduol lauqe fo remmahkcaj dnoces a nehW Sound pressure 111 dB SPL -raeh eht nehw deniatbo si enil devruc a ,siht fo esuac -eB .dlohserht lamron a eveihca ot dedeen era slevel erusserp dnuos retaerg ylbaredisnoc dna ,seicneuqerf rewol dna rehgih ta evitisnes ssel semoceb gniraeH .slaudividni gniraeh-lamron ,gnuoy ni LPS Bd 0 tuoba fo level erusserp dnuos a ot sdnopserroc dna zHk 4 ±1 yletamixorppa fo egnar eht ni tsehgih si tI .tnednep -ed-ycneuqerf si gniraeh fo ytivitisnes ehT :noitanalpxE .yrt -emoidua enot-erup ni ton tub yrtemoidua hceeps ni desu si ti ,ygoloidua nI .ygolonhcet dia gniraeh gnidulc -ni ,ygolonhcet ni desu ylediw si taht elacs lacisyhp a si )LPS Bd( level erusserp dnuos ehT :snoitacilppA .11.8 .giF dna 1.8 elbaT ni nwohs era re -wop dnuos dna erusserp dnuos neewteb pihsnoitaler eht dna selpmaxe lanoitiddA !Bd 6 yb sesir level erus -serp dnuos eht ,delbuod si erusserp dnuos eht nehW .detcartbus ro dedda eb tonnac seulav lebiceD Sound energy 108 dB secruos dnuos fo noitammuS .giF .smret lacisyhp ni retaerg semit 000,001 si hcihw ,esaercni aP 4.4 a ot sdnopserroc LPS Bd 011 ot 001 morf esaerc -ni na tub ;aP 44 yb sesaercni erusserp dnuos eht ,LPS Bd 01 ot 0 morf ,Bd 01 yb desaercni si level erusserp dnuos eht nehw ,elpmaxe roF .slebiced wol ta naht slevel lebiced hgih ta retaerg yletanoitroporpsid si seu -lav lacisyhp ni esaercni eht ,elacs cimhtiragol a htiw gnilaed era ew ecniS :snoitaluclac dna noitaterpretnI :9791±131 OSI ot gnidrocca ,ro ]LPS Bd[ aP 02/p 01gol ” 02 = pL 20 μPa 0 10 20 30 40 50 60 70 80 90 100 110 120 140 150 Sound level in dB(A) Auditory threshold Recording studio Bedroom Reading room Living room Office Conversation Street traffic Assembly line Discotheque Jackhammer Jumbo drilling rig Pain threshold Jet engine test stand Stud driver Pistol Assault rifle Sound source or situation 371 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 105 dB SPL 105 dB 100 μPa ]LPS Bd[ 0p/p 01gol ” 02 = pL 1 mPa 10 mPa 100 mPa 1 Pa 10 Pa 130 100 Pa 1 000 Pa 160 170 Sound pressure serusserp dnuos suoirav fo selpmaxE .giF :swol -lof sa si pL level erusserp dnuos eht rof alumrof ehT .)woleb ,snoitacilppA ees( level erusserp dnuos rof sdnats LPS xiffus ehT .)lleB maharG rednaxelA ,enohpelet eht fo rotnevni eht rof deman ,Bd( slebiced ni detats si level erusserp dnuos ehT .seulav lacisyhp fo egnar egral eht ylraelc erom eta -icerppa ot dna rehtegot resolc selacs cigoloisyhp dna lacisyhp eht gnirb ot su selbane smhtiragol fo esu ehT .zHk 3 dna 2 neewteb enot suounitnoc a eviec -rep tsuj nac renetsil lamron a hcihw ta erusserp eht ,.e.iÐgniraeh fo dlohserht eht ta erusserp dnuos eht si sihT .aP 02 sa eulav ecnerefer eht denifed sah )OSI( noitazidradnatS rof noitazinagrO lanoitanretnI ehT .level eht dellac si oitar erusserp dnuos gnitluser ehT .0p eulav ecnerefer detangised a ot p erusserp dnuos derusaem eht gnitaler yb detaerc eb nac elacs erusserp-dnuos cimhtiragol A :snoitinifeD )LPS Bd( leveL erusserP dnuoS )gnitseT y rotiduA( ygoloiduA 8
  • 183. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .sulumits eht fo murtceps dna noitarud eht sa hcus sretemarap lacisyhp rehto no osla tub level erusserp dnuos eht no ylno ton sdneped noitpecrep siht esuaceb ,ssenduol fo noitpecrep evitcejbus eht gnibircsed rof noiretirc roop a si level erusserp dnuos eht tuB .level sti yb yllacisyhp debircsed si sulumits a fo ytisnetni ehT ssenduol dna level ssenduoL .level niatrec a sdeecxe sserts citsuoca eht nehw srucco yltnetsisnoc )STT( tfihs dlohserht yraropmet fo eerged emoS .sserts citsuoca na gniwollof ro gnirud dlohserht yrotidua eht fo gnisiar laudarg a setoned ti ;noitatpada morf tnereffid si eugitaf yrotiduA .)281 .p ,tset yaced trahraC ,3.8 ees( yrujni laruen fo sisongaid eht ni yllacinilc deilppa saw nonemonehp siht ,ylremroF .tneserp eb ot dias si noitatpada lamronba ,sulumits eht fo seitreporp lacisyhp eht no sdneped hcihw ,erusaem niatrec a sdeecxe noitatpada fI .noitpecrep ssenduol ni enilced dipar a yb dein -apmocca yllausu ,emit revo sesaerced noitaticxe larueN .noit -alumits tnatsnoc ot esnopser ni srucco taht sulumits citsuoca na fo noitpecrep eht ni egnahc cigoloisyhp a si noitatpadA eugitaf yrotidua dna noitatpadA .sulumits tset eht fo noitpecrep stneverp taht esion htiw deksam si rae tsetnon ehT .detset gni -eb si rae eno ylno nehw y rtemoidua ni tnatropmi si gniksaM .sretemarap laropmet dna lartceps elpmis gnisu debircsed yletarucca eb tonnac ,ssenduol ekil ,taht no -nemonehp citsuocaohcysp lareneg a si ,gniksam dellac ,ssec -orp sihT .stneve dnuos suoenatlumis-raen ro suoenatlumis rehto yb dehsinimid eb nac tneve dnuos a fo noitpecrep ehT gniksaM .ssenduol evitcejbus fo rotacidni doog a ylirassecen ton era stnemerusaem eht ,reve -woh ,niagA .)A( Bd ,.e.i ,)A( etubirtta eht yb detangised si level dnuos derusaem ehT .dlohserht y rotidua eht ot dehctam si hcihw ,retlif A eht yllausuÐsretlif dradnats dna srotcaf noitcer -roc gnisu derusaem si ,elpmaxe rof ,esion teertS .stnemerus -aem lacinhcet yranidro rof desu ton era ssenduol dna level ssenduol rof erusaem fo stinu citsuocaohcysp evitcejbus ehT .cte ,senos 4 ot snohp 06 ,senos 2 ot tnelaviuqe era snohp 05 os dna ,eulav enos eht selbuod snohp 01 gniddA .zH 0001 fo ycneuqerf a ta snohp 04 ot tnelaviuqe si enos enO .enos eht no desab ssenduol evitcejbus rof elacs etarapes a fo tnempoleved eht detpmorp sihT .sesaercni ytis -netni dnuos eht sa ssenduol ni niag a fo noitpecrep evitcejbus eht gnibircsed rof roop netfo era elacs nohp eht no seulav ehT .snohp 06 fo level ssenduol a hcaer ot LPS Bd 08 yletamixorp -pa fo erusserp dnuos a evah tsum ,elpmaxe rof ,enot zH-05 a tuB .snohp 06 fo ssenduol evitcejbus a sah LPS Bd 06 ta enot zH-0001 a ,suhT .nohp eht si ssenduol evitcejbus fo tinu ehT .level ssenduol eht sebircsed LPS Bd ni enot eht fo level erus -serp dnuos eht neht ,dnuos eht sa ssenduol emas eht gnivah sa deviecrep si enot zH-0001 eht nehW .zH 0001 ta enot a fo ssenduol eht htiw dnuos a fo ssenduol evitcejbus eht erapmoc ot desu si taht ytitnauq citsuocaohcysp a si level ssenduol ehT .Bd 5 ylno fo ycarucca na ot denimreted si yrtemoidua enot-erup ni dlohserht eht ecnis ylralucitrap ,ecnacifingis citsongaid on evah dna llams era sdohtem tnereffid htiw detaicossa era taht secnereffid eht ,tneitap evitarepooc a ni deilppa ylluferac era sdohtem lacinilc yranidro nehW .ygoloidua lacinilc rof lacitcarp ton era dna gnimusnoc-emit yrev era sdohtem esehT .yllacitamehtam denimret -ed eb neht nac dlohserht lautca ehT .semertxe eseht neewt -eb slevel suoirav ta sdoirep tnelis dna ilumits detcetednu dna detceted fo oitar eht enimreted ot yrassecen si ti ,noitanimret -ed dlohserht a ekam oT .ycneuqerf lauqe htiw detcetednu ro detceted eb lliw doirep tnelis eht dna sulumits eht ,dlohserht y rotidua eht woleb llew si level sulumits eht fi tuB .edam ylisae si noitaitnereffid eht ,dlohserht yrotidua eht evoba llew si sulumits eht fo level eht fI .langis citsuoca na draeh sah eh ton ro rehtehw gnitacidni ,doirep hcae retfa sdnops -er tcejbus ehT .ecnelis fo sdoirep gnol yllauqe htiw gnola redro modnar ni ilumits citsuoca eht gnitneserp evlovni yllac -isab sdohtem esehT .deniatrecsa eb nac gniraeh fo dlohserht lautca eht taht os dlohserht eht htiw gnola airetirc eseht erusaem ot desu era sdohtem laiceps ,scitsuocaohcysp nI .detset snosrep eht fo ,saib ro ,airetirc lanretni eht ot naht ytiliba gniraeh lautca ot ssel etaler taht sdlohserht tnereffid owt dleiy lliw sihT .langis retniaf hcum a ot dnops -er yam rehtona elihw ,draeh si ti taht gnilangis erofeb yllac -oviuqenu dna ylgnicnivnoc enot a tceted ot evah yam tcejbus enO .tniopdnats citsuocaohcysp a morf gniraeh lacitnedi evah stcejbus eht hguoht neve stcejbus tset tnereffid rof denim -reted eb yam seulav dlohserht tnereffid ,y rtemoidua lacinilc ni desu noitanimreted dlohserht fo dohtem eht fo sseldrageR .enot eht sraeh llits eh ton ro rehtehw setacidni tcejbus eht dna deirav si enot eht fo level erusserp dnuos eht tset siht nI .seic -neuqerf tnereffid ta detneserp senot evaw-enis rof denimret -ed si dlohserht siht ,y rtemoidua enot-erup lacinilc nI .deviec -rep eb llits nac taht sulumits citsuoca na fo level erusserp dnuos muminim eht ro ,dlohserht ytisnetni etulosba eht snaem syawla tsomla ºdlohserhtª mret eht ,revewoh ,ygoloidua nI .dlohserht ecnereffid eht dellac si sihT .ytreporp lacisyhp emos ot drager htiw reffid taht ilumits y rotidua owt neewteb deviec -rep eb nac taht ecnereffid tsellams eht ot refer yam dlohserhT dlohserhT .woleb debircsed ylfeirb era stpecnoc eseht fo lareveS .scitsuocaohcysp morf devired era ºssenduolª dna ºdlohserhtª sa hcus stpecnoC .ygoloidua fo hcum rof sis -ab cifitneics eht smrof suht dna gniraeh dna sulumits citsuoca eht fo seitreporp lacisyhp eht neewteb spihsnoitaler eht sei -duts ,neht ,scitsuocaohcysP º.gniraehª ti llac ew ,sulumits cit -suoca na ot sdnopser nosrep a nehW .esnopser laroivaheb eht dna sulumits a fo seitreporp lacisyhp eht neewteb pihsnoitaler eht seiduts taht scisyhpohcysp fo hcnarb a si scitsuocaohcysP scitsuocaohcysP 1.8 raE III 471
  • 184. .snosrep desopxe yllanoitapucco ni ssol gniraeh decudni-esion fo noit -ceted ylrae eht rof ro ,elpmaxe rof ,snrobwen ni smel -borp gniraeh tceted ot desu si gnineercs cigoloiduA .redrosid gniraeh dezingocernu na tceted ot dengised si gnineercs saerehw ,snoitanimaxe citsongaid ni red -rosid gniraeh demuserp ro nwonk a sah ydaerla tneit -ap eht ,elur a sA .)31.8 .giF( tnemriapmi gniraeh rof neercs ro esongaid ot desu eb yam stset cirtemoiduA noitanimaxE cigoloiduA fo sdohteM .sdohtem tset etairporppa tsom eht gnisu elbissop sa yltneiciffe sa melborp lacinilc eht sserdda ot edam eb tsum trof -fe nA .slaog eseht gniveihca ni ssenlufesu gniyrav fo era yrtemoidua ni desu era taht sdohtem suoirav ehT redrosid gniraeh a yfitnauQ · )yrtemoidua citsongaid( redrosid gniraeh a yfissalC · redrosid gniraeh a tceteD · :slaog niam gniwollof eht sah tI .gniraeh fo snoit -cnuf eht tset ot dengised si noitanimaxe cigoloiduA noitanimaxE cigoloiduA fo slaoG .sulumits citsuoca eht fo erusserp lacisyhp eht no desab si taht ,reve -woh ,elacs erusserp-dnuos a htiw gnilaed llits era eW .margoidua eht daer ot reisae ti gnikam ,level gniraeh Bd 0 eht ta enil latnoziroh a sa detneserper si dlohserht gniraeh lamron eht ,hparg fo epyt siht nI .elacs )ºlevel gniraehª( LH Bd eht dellac si elacs lebiced evitaler sihT .LPS Bd 52 yletami -xorppa si ,elpmaxe rof ,zH 052 ta dlohserht ehT .)6657 dna 983 OSI( seicneuqerf tnereffid rof sdlo-raey-81 gniraeh-lamron fo sdlohserht yrotidua eht no desab OSI eht yb denimreted seulav ot detcerroc era LPS Bd ni derusaem seulav eht ,nosaer siht roF .dlohserht lamron a htiw dlohserht derusaem eht gnirapmoc naht tseretni ssel fo si erusserp dnuos lacisyhp eht ,yg -oloidua ni derusaem si dlohserht enot-erup eht nehW )LH Bd( sleveL gniraeH rof elacS lebiceD .)woleb ees ;yrtemoidua ni ,.g.e( yllacitsongaid desu si taht elacs LH Bd eht htiw noisufnoc diova ot dedda si ºLPSª noisnetxe ehT .)21.8 .giF ni evruc der( )LPS Bd( level erusserp dnuos lacisyhp eht tsniaga dettolp si dlohserht gni 500 noitanimaxE cigoloiduA 250 Frequency [kHz] 1 2 3 4 6 8 12 60 60 70 70 80 90 90 100 100 110 110 120 120 10 20 20 Physical sound pressure level (dB SPL) 50 80 Hearing loss (dB HL) 50 30 10 – 10 .)LH Bd 0( noitalupop lamron a ot evitaler ssol gniraeh setac -idni yltcerid elacs LH Bd ehT .enil latnoziroh a sa dettolp si )neerg( dlohserht y rotidua lam -ron eht dna ,)tfel eht no elacs neerg ,LH Bd( yllacinilc desu si srotcaf noitcerroc gnidnops -erroc htiw elacs A .)thgir eht no elacs der dna evruc der ,LPS Bd( elacs level erusserp dnuos lacisyhp a tsniaga det -tolp nehw enil devruc a smrof dlohserht y rotidua lamron ehT 40 Normal threshold in physical unit dB SPL 0 Normal threshold in dB HL 571 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. Frequency (Hz) 125 40 30 0 – 10 selacs LH Bd dna LPS Bd eht fo nosirapmoC .giF )gnitseT y rotiduA( ygoloiduA 8
  • 185. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .srotcaf laicos dna lanosrep ynam no sdneped hcihw ,pacidnah gniraeh fo eerg -ed lautca eht tuoba gnihton syas dna sesoprup noit -atneiro rof ylno lufesu si noitacifissalc fo epyt sihT .)2.8 elbaT( sgnidnif cirtemoidua no desab ytireves fo sedarg suoirav otni deifissalc eb nac sredrosid gniraeH tnemriapmI gniraeH fo noitacifissalC evitatitnauQ .desu si ssol gniraeh laruenirosnes mret etisopmoc eht dna ,gnitset cigoloidua yb dehsiugnitsid ylisae ton era stnenopmoc eht ,yllareneG .)662 .p osla ees ;ssol gniraeh laruen( serutcurts laruen fo seitilamron -ba yb dna )ssol gniraeh yrosnes( noitcnufsyd raelhcoc yb desuac ylekil tsom era sisucybserp fo sesac lac -ipyt ,elpmaxe roF .serutcurts suoirav gnivlovni noisel denibmoc a yb desuac eb osla yam sredrosid gniraeH .)redrosid gniraeh lart -nec =( metsys suovren lartnec eht fo noisel a morf de -hsiugnitsid si dna )ssol gniraeh laruen =( noisel evren yrotidua na ot yltcirts deilppa si mret eht netfo tuB .aelhcoc eht ot lartnec seil esuac esohw redrosid gni -raeh yna ot srefer yllacisab tnemriapmi raelhcocorteR .noitanimreted noisel-fo-etis rof lufesu yrev eb osla nac seiduts gnigamI .sredrosid gniraeh ni noitan -imreted noisel-fo-etis fo ssecorp eht sweiver 41.8 .giF .metsys yrotidua eht fo serutcurts laruen eht ro aelhcoc eht sevlovni noisel eht erehw ,ssol gniraeh laruenirosneS · dna ;rae elddim ro lanac rae eht ni si noisel eht erehw ,ssol gniraeh evitcudnoC · :neewteb hsiugnitsid ot elba eb dluohs noitanimaxe lacinilc ehT .sisongaid eht gniworran rof tnatropmi era )071±661 .pp ,1.8 ees( noitanimaxe lacisyhp dna yrotsih lacinilc esicerp A .serut -curts ro erutcurts ralucitrap a ot ygolohtap lasuac eht gnizilacol ,.e.iÐnoitanimreted noisel-fo-etis si gnitset cigoloidua dna lacinilc fo tcepsa tnatropmi nA .xetroc yrotidua eht ni secnabrutsid yrotalucric ot lanac rae lanretxe eht ni nemurec eht morf ,metsys yrotidua eht fo level yna ta eil yam redrosid gniraeh a fo esuac ehT noitanimreteD noiseL-fo-etiS .)191±481 .pp ,4.8 ees( esnopser cigoloisyhp yratnulovni na tnes -erper taht sretemarap derusaem ºylevitcejboª no desab snoitcnuf gniraeh stset yrtemoidua evitcejbO · .tcejbus tset eht morf esnopser yratnulov yllausu dna evitca na no desab si )381±871 .pp ,3.8 ees( yrtemoidua laroivaheB · :esnopser detset eht fo erutan eht ot gnidroc -ca deifissalc era yrtemoidua citsongaid ni sdohteM .gnineercs cigoloidua ni dna ygoloidua citsongaid ni derusaem era sesnopser tneitap yratnulovni dna yratnulov htoB Auditory evoked brain-stem potentials Otoacoustic emissions Objective methods Otoacoustic emissions Speech audiometry Electrophysiologic methods Response audiometry Pure-tone audiometry Immittance measurements Pure-tone audiometry Behavioral audiometric methods Noise audiometry Objective methods Audiologic screening Behavioral audiometric methods Diagnostic audiology Audiologic methods sdohtem tset cigoloiduA .giF raE III 671
  • 186. .nois -neherpmoc hceeps fo ssol etelpmoc a sa yllanoitcnuf denifed netfo si ssenfaed os dna ,seicneuqerf wol fo noitpecrep lanoitarbiv eht tuo elur ot tluciffid si tI .gni -raeh fo esnes eht fo ssol a ot srefer ssenfaed deriuqcA .noitatilibaher ni dna srettam ecnarusni rof tnatropmi era sdohtem esehT .yrtemoidua hceeps ro margoidua enot-erup eht no desab ssol gniraeh egatnecrep eht enimreted ot desu eb nac sdohtem lanoitatupmoc suoirav ,noitidda nI %001 .gniraeh rieht tsol evah ohw slaudividni htiw derapmoc stpec -noc egaugnal dna hceeps tnereffid yllatnemadnuf evah slaudividni gniraehnon ,tluser a sA .dehsilbat -se ton era noitanohp fo snrettap lartnec eht dna ,ruc -co ot sliaf tnempoleved siht ssenfaed latinegnoc htiW .tnempoleved egaugnal dna hceeps ot detaler ylesolc si dna efil fo sraey tsrif eht gnirud spoleved gniraeH .gniraeh fo ecnesba eht ot srefer ssenfaed latinegnoC Higher centers (auditory evoked potentials) Bd 011 > Bd 04±02 %04±02 Bd 06±04 %06±04 Bd 09±06 %08±06 Bd 011±09 %59±08 %02±0 % ni ssol gniraeH ssenfaeD ssol gniraeh dnuoforP ssol gniraeh ereveS ssol gniraeh etaredoM ssol gniraeh dliM noitangiseD Bd ni ssol gniraeH gniraeh lamroN Bd 02 < ytireves yb ssol gniraeh fo noitacifissalC 2.8 elbaT Cochlear (otoacoustic emissions) Middle ear (immittance measurements) Neural (retrocochlear) (auditory evoked brainstem potentials) Sensorineural hearing loss (Rinne test positive, pure-tone audiometry) 771 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. Brainstem (auditory evoked brainstem potentials) Central External auditory canal (otoscopy) .sisongaid noisel-fo-etis a gnikam ni desu era taht stset cigoloidua tnatropmi tsom eht swohs trahcwolf sihT Conductive hearing loss (Rinne test negative, pure-tone audiometry) Hearing disorder sredrosid gniraeh ni noitanimreted noisel-fo-etiS .giF )gnitseT y rotiduA( ygoloiduA 8
  • 187. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. segnahc dipar dna murtceps ycneuqerf daorb a morf tluser taht snrettap lacipyt yalpsid slangis hceepS .sdia gniraeh htiw stneitap gnittif dna noitatilibaher gniraeh ni tnat -ropmi ylralucitrap si yrtemoidua hceepS .gnitset cir -temoidua ni elor rojam a sah slangis hceeps fo esu eht ,yltneuqesnoC .hceeps fo noitingocer dna noitpecrep eht edulcni gniraeh namuh fo snoitcnuf laitnesse ehT yrtemoiduA hceepS .regnol yna decitcarp ylerar era stset dlohserhtarpus cissalc ehT .stnem -erusaem eseht gniniatbo rof elbaliava won era )evitcejbo yllausu( stset elbailer erom dna relpmiS .tset )ISIS( xedni ytivitisnes tnemercni trohs dna ,tset rehcsüL ,tset relwoF eht era stset dlohserhtarpus fo selp -maxE .)471 .p ,1.8 ees( noitatpada lamronba ro )281 .p ,3.8 ees( tnemtiurcer tceted nac stnemerusaem esehT .slevel dlohserhtarpus ta demrofrep osla era stnemerusaem ,dlohserht enot-erup eht ot noitidda nI stseT dlohserhtarpuS .)352±152 .pp ees( noitaxif sepats citorelcsoto ni )hcton trahraC( seic -neuqerf etaidemretni ta hcton noitcudnoc enob a yb deinapmocca ssol evitcudnoc ro ,)582 .p ,a 41.31 .giF( esaesid er›inØM fo tesno eht ta ssol gniraeh ycneuqerf-wol ,)262 .p ,5.21 .giF( ssol gniraeh decudni -esion gniyfingis zHk 6±4 ta hcton a sa hcus ,redrosid gniraeh eht fo erutan eht tcelfer taht snrettap lacipyt wohs yam margoidua enot-erup eht ni dlohserht ehT .)b 51.8 .giF( ssol gniraeh evitcudnoc a sah tcejbus eht ,)level ssenduol rehgih a seriuqer noit -cudnoc ria yb noitpecrep fi ,.e.i( dlohserht noitcudnoc enob eht naht rehgih si dlohserht noitcudnoc ria eht fI .)a 51.8 .giF( lauqe eb dluohs noitcudnoc enob dna noitcudnoc ria rof sdlohserht eht ,noitcudnoc dnuos lamron dna noitarbilac reporp htiW :noitaterpretnI .rae renni eht ot dnuos tset eht gnittimsnart ,noitarbiv otni stnetnoc lainarc dna senob lainarc eht stes ecived sihT .daeherof ro diotsam eht tsniaga desserp rotarbiv a htiw derusaem si noitcudnoc enob rof dlohserht ehT .)961 .p ees( esion htiw rae tsetnon eht gniksam yb detneverp si gniraeh-ssorC .senohp tresni laiceps ro senohpdaeh gnisu noitcudnoc ria yb ylno rae eno ot detneserp tsrif era senot ehT :euqinhceT .elbailer ssel emoceb stnemerusaem eht dna ,)zHk 4 >( seicneuqerf rehgih ta srucco noitrotsid eroM .noitcudnoc ria rof esoht naht rewol Bd 05±04 era taht seulav mumixam ot ylno derusaem eb nac noitcudnoc enob rof dlohserht eht yhw si hcihw ,senohpdaeh naht dnuos ecudorp ot ygrene erom ylbaredisnoc seriuqer rotarbiv enob A .yrtemoidua enituor naht noitairav laudividniretni retaerg wohs stset eseht tub ,)yrtemoidua enot-hgih( zHk 61 ot 8 morf sdlohserht gnirusaem rof elbaliava era sretemoidua laicepS .senohpdaeh yranidro htiw de -tarbilac yletarucca eb tonnac level erusserp dnuos eht ,zHk 8 naht rehgih senot htiw dna ;snoitasnes yrotarb -iv morf hsiugnitsid ot tluciffid era zH 521 woleb seic -neuqerF .noitatneserp rieht lortnoc dna ssenduol dna ycneuqerf gniyrav fo senot erup etareneg ot desu si retemoidua na dellac ecived cinortcele nA :tnempiuqE evitingoc rehgih gnidulcni metsys yrotidua eritne eht tset nac sdohtem eseht ,elpicnirp nI .tcejbus tset eht morf esnopser yratnulov yllausu ,evitca na no desab era yehT .ygoloidua citsongaid ni sdohtem tset desu ylnommoc tsom eht era stset cirtemoidua laroivaheB .yrtemoidua hceepS · dna ;dohtem tset cirtemoidua nommoc tsom eht si hcihw ,yrtemoidua enot-eruP · :slangis hceeps dna senot ot esnopser yrotidua evitcej -bus eht no ylegral desab si gnitset lacinilC .snoitcnuf yrtemoiduA enoT-eruP )d 51.8 .giF( noitcudnoc enob rof dlohserht desaercni nA · noitcudnoc dnuos deriapmi gnitacidni ,noitcudnoc enob htiw derapmoc ssol noitcudnoc ria retaerG · :ssol gniraeh dexim a etacidni sngis cihpargoidua gniwollof ehT .)852 .p ,a 1.21 .giF dna c 51.8 .giF( seicneuqerf wol ta naht seicneuqerf hgih ta erom net -fo ,desiar si dlohserht gniraeh ehT .noitcudnoc enob dna ria rof sdlohserht eht neewteb dnuof si ecnereffid tnacifingis on ,tneserp si ssol gniraeh laruenirosnes fI .noitcudnoc enob dna noitcudnoc ria htob rof detset era sdlohserht eht dna ,srae thgir dna tfel eht rof yletar -apes enod si sihT .sevatco-flah ro sevatco yb gnisaerc -ni ,zHk 8 ot zH 521 morf seicneuqerf ta derusaem yllausu si dlohserht ehT .)471 .p ,1.8 ees( dlohserht gniraeh eht gninimreted yb derusaem si senot evaw -enis erup ot ytivitisnes eht ,yrtemoidua enot-erup nI noitanimreteD dlohserhT gnitseT cirtemoiduA laroivaheB 3.8 raE III 871
  • 188. -duol gnisu ylsuoenatlumis srae htob ot ro senohp -daeh gnisu rae eno ot detneserp eb nac lairetam ehT .retemoidua na gnisu slevel detangised ta detneserp ylbicudorper si dna sksid tcapmoc no mrof dezidrad -nats ni elbaliava si lairetam hceeps ehT :elpicnirP .rae tfel eht ni ssol gniraeh evitcudnoC b .neerg ni nwohs si hceeps lanoitasrevnoc ni rucco yllacipyt taht slevel dna seicneuqerf fo egnar ehT .rae thgir eht rof margoidua enot-erup lamroN a .edis tfel eht no ssol gniraeh laruenirosnes dna evitcudnoc dexiM d .edis thgir eht no ssol enot-hgih htiw tnemriapmi laruenirosneS c .noitingocer hceeps dna noitceted hceeps rof sisab eht mrof snrettap esehT .sdnocesillim fo sdoirep ni slevel dna seicneuqerf fo tolp ot desu era sesnopser eseht dna ,slevel dnuos tne -reffid ta dootsrednu si tahw staeper tcejbus tset ehT .slevel dnuos hceeps eht enimreted ot )sepols noit -atnemercni dna sretlif( niamod emit dna ycneuqerf eht ni snoitcnuf gnirusaem level cificeps sesu yrtem -oidua hceepS .egareva lacitsitats a sa ylno tub ylesic -erp detats eb tonnac slangis hceeps fo level eht ,esion ro senot deniatsus ekilnU .secnetnes ro ,)seednops dellac selballys desserts yllauqe ro gnol owt htiw sdrow ro sdrow ciballysonom ,.g.e( selballys fo sreb -mun tes a htiw sdrow ,selballys fo tsisnoc yam lairet -am tset ehT .tnemnorivne dleif-dnuos eht ni srekaeps .slangis hceeps fo noitceted eht rof dlohserht eht naht rehtar hceeps fo )gnidnatsrednu( noitin -gocer eht serusaem yllareneg yrtemoidua hceepS 1 2 3 4 6 8 12 Frequency [kHz] – 10 0 10 20 30 40 50 60 70 80 90 100 110 120 125 250 500 Frequency [Hz] Hearing loss [dB HL] Hearing loss [dB HL] Air conduction right ear Bone conduction right ear 1 – 10 0 10 20 30 40 50 60 70 80 90 100 110 120 1 2 3 4 6 8 12 Frequency [kHz] Air conduction left ear Bone conduction left ear – 10 0 10 20 30 40 50 60 70 80 90 100 110 120 d Mixed hearing loss 2 3 4 6 8 12 Frequency [kHz] 125 250 500 Frequency [Hz] Hearing loss [dB HL] Hearing loss (dB HL) Air conduction right ear Bone conduction right ear Main frequencies and levels for speech – 10 0 10 20 30 40 50 60 70 80 90 100 110 120 – 10 0 10 20 30 40 50 60 70 80 90 100 110 120 1 2 3 4 6 8 12 Frequency [kHz] Air conduction left ear Bone conduction left ear – 10 0 10 20 30 40 50 60 70 80 90 100 110 120 b Conductive hearing loss 971 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 125 250 500 Frequency [Hz] – 10 0 10 20 30 40 50 60 70 80 90 100 110 120 c Sensorineural hearing loss 125 250 500 Frequency [Hz] – 10 0 10 20 30 40 50 60 70 80 90 100 110 120 a Normal pure-tone audiogramm yrtemoidua dlohserht enot-eruP .giF )gnitseT y rotiduA( ygoloiduA 8
  • 189. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. -sed a ta detneserp era sdrow ehT .sdrow ciballysonom 05 fo stsil fo hcae gnitsisnoc stset tes-nepo desu ylnommoc fo selpmaxe era 6-UN ro ,22-W ,05-BP ehT .lareneg ni egaugnal eht fo taht ot sdnopserroc sdrow eseht ni sdnuos suoirav eht fo noitubirtsid eht taht gninaem ,decnalab yllacitenohp yllausu era stsil eht dna ,sdrow 05 ot 01 neewteb evah yam tsil hcaE .selballys fo rebmun dexif a htiw sdrow fo stsil lareves fo yllacipyt tsisnoc yehT .stset tes-nepo yliramirp sesu yrtemoidua hceeps lacinilc enituoR .gniraeh saw eh hcihw noitceles eht morf drow eht sesoohc tneit -ap ehT .detneserp si sdrow eseht fo eno dna ,sdrow fo noitceles a tneitap eht evig stset tes-desolC .gniraeh si ehs ro eh tahw staeper tneitap eht dna ,sesarhp ro sdrow elgnis esu stset tes-nepO .lairetam hceeps rieht ot gnidrocca detaitnereffid eb nac stset hceepS epyt eht fo )x( sdrow rebmun elballys-ruof dna )o( sdrow tset ciballysonom rof sevruc noitingocer hceeps lamroN .assicsba eht no level dnuos htiw dettolP .tseT hceepS grubierF eht ni desu .)61.8 .giF( evruc noitingocer hceeps ro noitcnuf noitanimircsid a .)71.8 .giF( serutcurts laruen ro aelhcoc eht ot egamad yb desuac taht ekil gnissecorp hceeps lam -ronba fo sngis era slevel dnuos rehgih ta noitingocer hceeps ni enilced a dna ytilibigilletni fo ssoL .sdrow ciballysonom rof noitcnuf ytisnetni-ecnamrofrep eht fo gninettalf a ot sdael ssol gniraeh laruenirosneS .slevel hgih yltneiciffus ta deveihca llits si nois -neherpmoc %001 ,os nevE .slevel dnuos rehgih draw -ot tfihs lellarap a swohs noitcnuf ytisnetni-ecnam -rofrep eht ,ssol gniraeh evitcudnoc htiw stneitap nI .)61.8 .giF ni elacs wolley ,LPS Bd 5.81 ta si srebmun rof enilesab orez eht( level noisneherpmoc %05 eht ta decalp yllausu si ,erofereht ,ssol gniraeh hceeps rof elacs ehT .)TRS( sdlohserht noitingocer-hceeps dellac si tniop sihT .elgna thgir a )tsomla( ta evruc eht stces -retni assicsba eht ot lellarap enil a erehw tniop eht ta daer yletarucca tsom si ssol gniraeh hceeps ehT .slevel rehgih dna rewol ta tuo snettalf dna noisneherpmoc %05 ta tsepeets si noitcnuf ytisnetni-ecnamrofrep ehT .)dnuorg -yalp ,erawdrah ,ekacnap( elballys hcae no sisahp -me lauqe htiw nekops sdrow elballys-owt era hcihw ,seednops fo desopmoc era stsil desu yllacipyT .detset gnieb era elballys eno naht erom htiw sdrow nehw repeets emoceb dna tfel eht ot tfihs lliw noitcnuf sihT .)61.8 .giF( noitcnuf ytisnetni-ecnamrofrep eht sa osla nwonk ,evruc noit -ingocer hceeps a sdleiy sihT .)LPS Bd ni level ssenduol hceeps( slevel dnuos eht tsniaga dettolp si sesnops -er tcerroc fo egatnecrep eht dna ,level dnuos detangi stseT hceepS .noit -ingocer hceeps cirtemoidua ecneulfni osla yralubacov dna egaugnal evitan sa hcus srotcaf laudividnI .hceeps rotom dna ,yromem ,noisneherpmoc egaugnal sa hcus snoitcnuf evitingoc rehgih no osla tub gniraeh no ylno ton sdneped margoidua hceeps lacipyt a fo tluser eht ,suhT .seires tset hcae ni yltcerroc draeh sah tcejbus eht taht secnetnes ro ,sdrow ,selballys fo egatnecrep eht setacidni margoidua hceeps ehT :noitaterpretnI 0 10 20 30 40 50 60 70 0 100 80 90 100 110 120 Speech sound level (dB SPL impulse, linear) 80 10 90 Speech hearing loss (dB) 20 30 40 50 60 70 80 90 Number test left ear 60 50 40 30 20 Percent intelligibility loss 70 20 Percent correct 30 40 50 10 60 70 Monosyllabic word test left ear 80 10 90 0 100 Normal 50% recognition for number test 18.5 dB SPL (SRT) yrtemoidua hceepS .giF raE III 081
  • 190. .)oitar NS( oitar esion-ot-langis eht sa nwonk ,level hceeps eht dna level esion eht neewteb ecnereffid eht naht stset eseht ni tseretni ssel fo si ,level esion detceles eht no sdneped hcihw ,secnetnes eht fo level erusserp dnuos etulos -ba ehT .deveihca si noitingocer hceeps fo eerged debircserp a litnu deirav era slevel dnuos hceeps eht ,level tnatsnoc a ta detneserp yllausu si esion eht elihW .secnetnes nekops ksam erofereht nac dna hceeps sa tnetnoc ycneuqerf emas eht sah stset eseht ni detneserp esion ehT .esion ni noitpecrep hceeps gnitset rof lufesu ylralucitrap era stset ecnet -neS .serusaem evitatilibaher rehto dna sdia gniraeh gnit -tif rof y rtemoidua hceeps ni desu erofereht era stset ecnet -neS .sdrow elgnis naht rehtar secnetnes ni deyevnoc si noit -acinummoc yrotidua ni gninaem ,elur a sA :stset ecnetneS .sseug ot tluciffid erom eb ot thguoht era secnet -nes hcuS .)ºder si roloc rac ruoy egnahc oGª( ton si ecnetnes eritne eht tub ,lufgninaem era ecnetnes a ni sdrow eerht fo puorg evisseccus hcae taht os detcurtsnoc era secnet -nes citehtnys neT :tset )ISS( noitacifitnedI ecnetneS citeht -nyS desu ylnommoc eht si elpmaxe nA .secnetnes rof deilp -pa eb osla nac stes desolC .deirav era ,ºbac ± bat ± bad ± bagª ro ºkcab ± tab ± gab ± dabª sa hcus ,sdrow tnanosnoc ±lewov±tnanosnoc ni tnanosnoc lanif ro laitini eht hcihw ni ,tset )FAAF( erutaeF y rotiduA evitanretlA ruoF eht ro ,ºnik ± nit ± niht ± nipª sa hcus ,sdrow ruof fo eno fo stsisnoc sulumits eht hcihw ni ,)TCC( tseT tnanosnoC ainrofilaC eht era selpmaxE .sulumits a sa gniraeh saw eh taht drow eht stceles tneitap eht ,sdrow eseht morF .detneserp si sdnuos ralimis htiw sdrow fo noitceles a hcihw ni ,sdrow ciballys -onom rof tsixe stset tnereffid ynaM .tset desolc a sa detnes -erp eb nac secnetnes ro sdroW :stset hceeps tes desolC stset hceeps lanoitiddA 10 20 30 40 50 60 70 80 90 Speech sound level (dB SPL impulse, linear) 100 110 120 100 2.8 10 Percent correct 30 40 50 60 90 80 70 80 90 Speech hearing loss (dB) 60 50 40 30 Percent intelligibility loss 20 70 20 Monosyllabic word test Number test 20 90 Normal monosyllabic word recognition curve 10 Intelligibility loss 20 % Roll-over 0 181 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 0 0 Gradual increase in intelligibility 30 40 10 50 60 70 80 Normal number recognition curve 100 noitcnuF ytisnetnI-ecnamrofreP hceepS lamronbA .giF )gnitseT y rotiduA( ygoloiduA 8
  • 191. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .)tset eeL( duola daer ot tcejbus gniraeh a rof elbissopmi ti sekam kcabdeef sihT .yaled thgils a htiw mih ot kcab ti gniyalp dna eciov stcejbus eht gnidrocer yb deveihca si tceffe ralimis A .ssol gniraeh cinagro htiw tneitap eht tcef -fa ton lliw tub ylduol erom kaeps dna retlaf ot reregnilam eht sesuac gniksam siht ,ssol gniraeh cinagronon a htiW .eciov nwo sih fo gnirotinom dna noitpecrep stneitap eht tpursid ot senohpdaeh hguorht detneserp si esion laretal -ib ,duola sdaer tneitap eht elihW .tset gnidaer drabmoL eht yb detceted eb nac ssol gniraeh cinagronon laretaliB .deviecrep ton si ti esuaceb tset eht tceffa ton seod edis detceffa eht no enot lanoitidda eht ,ssol gniraeh cinagro na htiW .edis ºdoogª eht no draeh regnol on si dna edis ºroopª eht no ylno deviecrep si enot eht esuaceb enot reduol ylthgils a htiw edis ºroopª eht fo noitalumits yb deinapmocca si enot elbid -ua ylraelc siht nehw dnopser ton lliw reregnilam ehT .edis ºdoogª eht rof dlohserht eht evoba llew si taht detneserp si enot A .rae rehto eht ni langis eht eviecrep ton od dna re -duol sa deviecrep si langis eht hcihw ni rae eht ot langis cit -suoca laruanib a ezilaretal stcejbus taht noitavresbo eht no desab si tset rettal ehT .tset regnetS eht dna ,Bd 05±04 yletamixorppa ta dlohserht gniraeh revossorc lamron a fo ecnesba eht slaever hcihw ,)tset kcebnegnaL( tset gniraeh revossorc eht era ssol gniraeh cinagronon laretalinu htiw stneitap ni desu sdohtem cirtemoidua laroivaheb laicepS · .tneserp si tnemriapmi raelhcocorter ,erom ro Bd 03 si yaced eht fI .noitatpada lamronba etacidni seulav yaced dlohserht rehgiH .Bd 01 naht erom on yb desaercni eb tsum level eht ,noitatpada lamron htiw stcejbus nI :noitaterpretnI .)yrassecen fi semit lare -ves enod eb yam siht( Bd 5 yb desaercni si level eht ,deviecrep regnol on si enot eht nehW .s 06 rof detneserp si dlohserht eht evoba Bd 5 enot suounitnoc a ,denimreted neeb sah dlohserht gniraeh eht retfA .noitanimreted dlohserht yranidro rof desu era noitarud s 5.0 yletamixorppa fo senoT :euqinhceT .tset yaced trahraC eht htiw detceted eb nac )471 .p ,1.8 ees( noitatpada lamronbA tset yaced trahraC · :sdohteM .y rtemoidua enot-erup ni naht y rtemoidua hceeps ni tnem -riapmi gniraeh ssel wohs yam ssol gniraeh cinagronon htiw stcejbus ,tluser a sA .senot erup fo ssenduol eht naht ylevit -cejbus ssessa ot tluciffid erom hcum si slangis hceeps fo ssen -duol ehT .dlohserht noitingocer hceeps dna dlohserht enot -erup eht neewteb ycnapercsid a yb detseggus osla si gningieF .)sesnops -er gnignahc ,emit noitcaer( seuc laroivaheb niatrec no desab dlohserht gniraeh ºeslafª a tcepsus yam renimaxe decneir -epxe nA .yadot decitcarp ylediw ton era yeht tub ,gniregnilam ro ssol gniraeh cinegohcysp mrifnoc ro tseggus nac taht stset cirtemoidua laroivaheb laiceps fo rebmun a osla era erehT .ssol gniraeh fo gningief eht esolcsid ylkciuq nac taht elbaliava era )191±481 .pp ,4.8 ees( stset evitcejbO .ssol gni -raeh cinegohcysp sah ohw tneitap a yb noitpeced-fles si ,reve -woh ,nonemonehp nommoc erom raf A .melborp gniraeh gni -tsixe na fo ytireves eht etareggaxe yam sreregnilam rehtO .la -udividni gniraeh-lamron a yb tnemriapmi gniraeh fo gningief etarebiled eht ot srefer gniregnilaM .dlohserht gniraeh desaerc -ni na gnitacidni esnopser eslaf yllanoitnetninu ro yllanoit -netni na ticile yam stset cirtemoidua laroivaheB :snoitacidnI ssol gniraeh cinagronon rof stseT º.duol ootª ro º,duol y revª º,duolª º,muidemª º,tfosª º,tfos yrevª sa )zH 0004 ,0002 ,0001 ,005( seicneuqerf suoirav ta dna slevel ssenduol suoirav ta detneserp slangis fo ssenduol evitcejbus eht setar tcejbus ehT .egnar cimanyd rieht nihtiw ssenduol gnisaercni eviecrep stcejbus woh seta -ulave )gnilacs egnar cimanyd( tnemerusaem egnar cimanyD · .duol ylbatrofmocnu sa langis eht seviecrep tcejbus tset eht hcihw ta ,murtceps ycneuqerf worran a htiw esion ylbareferp ro ,enot erup a fo level eht gninimreted yb enod si sihT .)LLU( level ssenduol elbatrofmocnu eht enimreted ot si dohtem tselpmis ehT · :euqinhceT .dia gniraeh a rof dettif stneitap ni demrof -rep eb dluohs egnar cimanyd eht fo noitaulave cirtemoidua na ,yltneuqesnoC .ton dluohs slangis duol saerehw elbissop sa hcum sa deifilpma eb dluohs slangis tfos esuaceb ,stnalp -mi raelhcoc dna sdia gniraeh htiw stneitap gnittif ni elor roj -am a yalp egnar cimanyd eht fo noitrotsid dna noitcuder ehT .tnemriapmi gniraeh laruenirosnes htiw stneitap ni decuder yltnacifingis si ,egnar cimanyd eht dellac ,slevel ssenduol lufesu fo egnar eht ,tluser a sA .elbatrofmocnu ro reduol sa deviecrep era slaudividni gniraeh-lamron yb detarelot llew era taht senot ,.e.iÐsdnuos dlohserhtarpus fo noitpecrep eht ni rucco yam etisoppo eht ,deviecrep yltniaf ro draeh ton rehtie era level dnuos hgih ylevitaler a ta senot taht tluser eht htiw ,desaerc -ni si dlohserht gniraeh eht hguohtlA .tnemtiurcer dellac ,noitpecrep ssenduol ni esaercni lamronba na si tceffe noitrot -sid lacipyt A .slevel dlohserhtarpus ta stceffe noitrotsid ecud -orp ot tpa si ssol gniraeh laruenirosnes ,361 .p ,2.7 ni deton sA gnilacs egnar cimanyD .sesoprup cificeps rof desu era taht serudecorp cirtemoidua laroivaheb rehto fo rebmun a era ereht ,)y rtemoidua hceeps dna enot-erup( y rtemoidua lac -inilc enituor ni desu stset cirtemoidua laroivaheb eht sediseB stset cirtemoidua laroivaheb rehtO 3.8 raE III 281
  • 192. .detset ylevitceles eb nac dna noitibihni laudiser dellac si nonemonehp sihT .doirep regnol a rof ,ylerar yrev ,ro emit trohs a rof raeppa -sid ot sutinnit eht esuac lliw gniksam eht yllanoisacco dna ,re -vewoh ,esion yb deksam eb tonnac sutinnit fo esac yrevE .sut -innit eht sraeh regnol on tneitap eht hcihw ta esion gniksam eht fo ssenduol eht senimreted renimaxe ehT .esion htiw sut -innit eht pu revoc ot edam si tpmetta na ,gniksam sutinnit nI .lausunu era seulav rehgih ;dlohserht gniraeh eht evoba Bd 01±5 tuoba ylno serusaem yllausu sutinnit fo ssenduol ehT .ssenduol eht neht ,tsrif denimreted si )ycneuqerf( hctip ehT .sutinnit laretalinu htiw rae etisoppo eht ot ro yllaretalispi detneserp eb yam langis gnihctam ehT .sutinnit eht fo ssenduol dna ,ycneuq -erf ,retcarahc evitcejbus eht sehctam ylesolc tsom taht esion ro enot a dnif ot edam si tpmetta na ,gnihctam sutinnit nI .sdohtem cirtemoidua laroivaheb yb ylno detaulave eb nac dna ylevitcejbo detset eb tonnac taht noitasnes evitcejbus a si )652 .p ,1.21 ees( sutinniT :sdohteM .troppar a gnihsilbatse dna re -reffus sutinnit a fo stnialpmoc eht gnidnatsrednu retteb ni dia nac dna noitasnepmoc ytilibasid ni tnatropmi ylniam era yehT .pu-wollof rof lufesu yrev ton era yeht os dna ,roop si stnem -erusaem sutinnit fo ytilibicudorper ehT .noitanimreted noisel -fo-etis rof yllaicepse ,stnemerusaem sutinnit fo eulav citson -gaid eht gnissessa ni suoituac yrev eb tsum eW :snoitacidnI tnemerusaem sutinniT c .gnitset y rotidua lartnec ni ecnat -ropmi ronim ylno fo si noitanimaxe siht erofereht dna ,gni -raeh lanoitcerid fo tnemriapmi tnacifingis esuac ton od sred -rosid gniraeh lartnec ynaM .yawhtap yrotidua lartnec eht fo snoruen metsniarb yb ylfeihc deganam si gniraeh lanoitceriD .)seerged ni elgna( yltcerid gniraeh lanoitcerid erusaem ot elb -issop ti ekam sputes dleif-dnuos xelpmoC .daeh eht fo retnec eht ta gnitanigiro sa deviecrep llits si dnuos eht hcihw ta srae owt eht neewteb sulumits citsuoca na ni ecnereffid level ro lar -opmet eht gninimreted yb detset eb nac gniraeh lanoitceriD b 381 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. a .)c .gif srae tfel dna thgir eht ot detneserp era slangis hceeps evititepmoc ,tnereffid ,.e.iÐdohtem citohciD ± .)b .gif ,hceeps laruanib gnitanretla( srae tfel dna thgir eht ot yletanretla detneserp era hceeps eht fo stnemgeS ± .)a .gif ,noitammus laruanib( srae tfel dna thgir eht ot detnes -erp era langis hceeps emas eht morf artceps tnereffiD ± :elbaliava era snoitpo suoiraV .snoitidnoc tluciffid rednu noitingocer hceeps laruanib no desab era snoitcnuf y rotidua lartnec fo stset cirtemoidua laroivaheb suoremuN · :sdohteM .)191±581 .pp ,4.8 ees( slaitnetop dekove y rotidua dna xelfer suidepats eht era stset evitcejbo niam ehT .sredrosid gniraeh lartnec tceted ot desu era stset cirtemoid -ua laroivaheb dna evitcejbo fo noitanibmoc a netfO .sredrosid gniraeh lartnec dna larehpirep neewteb ylesicerp hsiugnitsid ot elbissop ylerar si ti ecnis ,revewoh ,eerged a ot ylno dehsilp -mocca eb nac sihT .gniraeh larehpirep morf etarapes redrosid gnissecorp y rotidua lartnec a tceted ot dengised era sredrosid gniraeh lartnec rof stseT .esion dnuorgkcab htiw enod si gni -tset nehw yllaicepse ,llew sa snoitcnuf y rotidua lartnec stset syawla y rtemoidua hceeps ,tluser a sA .noitingocer hceeps lart -nec sedulcni hcihw ,noitingocer nrettap yrotidua dna gniraeh lanoitcerid era snoitcnuf y rotidua lartnec tnatropmi tsom ehT sredrosid gniraeh lartnec rof stseT )noitaunitnoc( stset cirtemoidua laroivaheb rehtO 3.8 )gnitseT y rotiduA( ygoloiduA 8
  • 193. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .margonap -myt a sa dettolp dna enohporcim detargetni na yb tnemurtsni gnirusaem a ot def si enot eborp eht fo noitrop detcelfer ehT .xelfer suidepats a ekove esion ro senot lanoitidda dna ,)marg -onapmyt( lanac rae eht ni erusserp evitagen ro evitisop a seta -reneg pmup ria nA .)zH 022 yllausu( enot eborp a htiw derus -aem si ecnadepmi citsuoca ehT .strop ssecca suoirav sah taht eborp a htiw delaes yllacitemreh si lanac yrotidua lanretxe ehT Tone and noise generator → Measurement of stapedius reflex Microphone and probe tone → Measurement of acoustic immittance Probe Air pump → Pressure change in the ear canal → Measurement of tympanogram stnemerusaem ecnattimmI .giF .)551 .p ,1.7 ees ,rae elddim eht yb gnihctam ecnadepmi( ecnatsis -er elttil htiw diulf raelhcoc eht ni sevaw ecudni nac yeht taht yaw a hcus ni ria ni sevaw dnuos eht smrof -snart rae elddim ehT .enarbmem cinapmyt eht fo ecnailpmoc eht sa ot derrefer osla si noitprosba dnuoS .snoitarbiv fo mrof eht ni ygrene dnuos fo tnuoma egral a sbrosba ecnadepmi wol htiw metsys a ,yl -esrevnoC .elttil yrev sbrosba dna ygrene dnuos eht fo tsom stcelfer ecnadepmi citsuoca hgih a htiw metsys A .sevaw dnuos fo noitprosba eht ot sreffo )rae elddim eht ,.g.e( metsys eht taht ecnatsiser eht fo erusaem a si metsys citsuoca na fo ecnadepmi ehT :noitinifeD stnemerusaeM ecnattimmI .tset eht fo noitaterp -retni eht ot ton ,esnopser sulumits eht fo noitcel -es eht ot setaler sdohtem eseht fo ytivitcejbo ehT .derrucco sah esnopser sulumits a rehtehw hsilbatse yllareneg lliw tnemerusaem fo sdohtem detsissa-re -tupmoc ,nredom tuB .yrtemoidua evitcejbo ni tneserp si esnopser a ton ro rehtehw ecnedifnoc etelpmoc htiw denimreted eb syawla tonnac tI :noitaterpretnI -oib eht ,)stnemerusaeM ecnattimmI ees( xelfer laid -epats eht fo tsisnoc yam sesnopser esehT .sretemar -ap ºevitcejboª dna sesnopser cigoloisyhp yratnulovni no desab snoitcnuf gniraeh erusaem taht stset syolp -me yrtemoidua evitcejbO .tneitap eht morf esnops -er evitca na gniticile tuohtiw gniraeh tset ot elbissop ti sekam yrtemoidua evitcejbo ,yrtemoidua laroivaheb ni desu sdohtem citsuocaohcysp evitcejbus eht ekilnU .tnem -riapmi evitingoc ro latnem htiw stneitap dna ,)202 .p ,2.9 ees( nerdlihc llams ,stnafni ni lufesu osla era stset cirtemoidua evitcejbO .stluser cirtemoidua laroivah -eb fo noitaterpretni eht ni dia sgnidnif tset evitcejbO .)snoissimE citsuocaotO ees( aelhcoc eht fo snoitarbiv citsuoca eht ro ,)slaitnetoP dekovE yrotiduA ees( serutcurts laruen fo slaitnetop cirtcele .)191±881 .pp osla ees( aelhc -oc eht ni snoitarbiv lacinahcemoib evitca dekove yllacitsuoca ro suoenatnops yb decudorp era taht lanac rae eht ni stneve dnuos erusaem ot desu si eborp enohporcim a :)sEAO( snoissime citsuocaotO · .)881±681 .pp osla ees( seuqinhcet gnigareva dna sedortcele ecafrus gnisu dezylana era xetroc larberec ro ,snoruen tcart yrotidua ,evren yr -otidua ,aelhcoc eht fo sesnopser cirtceleoib dekove yllacitsuoca :)sPEA( slaitnetop dekove yrotiduA · .eborp larua-artni na htiw derus -aem era enarbmem cinapmyt eht fo ecnadepmi citsuoca eht ni segnahc :stnemerusaem ecnattimmI · :seuqin -hcet suoirav gnisu yrtemoidua evitcejbo ni yllacinilc derusaem era esnopser fo sepyt niam eerhT :sdohteM :)81.8 .giF( yllacinilc demrofrep era gnitset ecnadepmi fo sepyt niam owT .snoitalupinam lanretxe cificeps yb desuac era taht segnahc ecnadepmi eht naht yrtemoidua ni tseretni ssel fo si ecnadepmi fo eulav etulosba ehT .rewol eb lliw eulav ecnadepmi ehT .enarbmem cinapmyt ffits a naht ygrene ssel tcelfer dna ygrene erom brosba lliw ,elpmaxe rof ,enarbmem cinapmyt gnitarbiv yleerf A .srotcaf laudividni dna enot eht fo ycneuqerf eht sa llew sa aelhcoc dna ,rae elddim ,enarbmem cinap -myt ,lanac rae eht gnisirpmoc metsys citsuoca llarevo eht no sdneped enot eborp siht fo eulav ecnadepmi ehT .lanac rae eht otni ,zH 022 yllausu ,ycneuqerf niat -rec a ta enot a stime eborp ehT .eborp larua-artni na htiw derusaem eb nac enarbmem cinapmyt dna lanac rae lanretxe eht fo ecnadepmi citsuoca ehT :elpicnirP stseT gniraeH evitcejbO 4.8 raE III 481
  • 194. :yawhtap xelfer eht ni setis suoirav ta nois -el a yb desuac eb yam xelfer eht rof dlohserht desaerc -ni na ro xelfer laidepats eht fo ecnesbA :noitaterpretnI º.rae sulumitsª eht morf tne -reffid si ºrae esnopserª ro ºrae eborpª eht ,elpicnirp emas eht swollof hcihw ,gnitset laretalartnoc roF · .dlohserht xelfer laidepats eht ot lauqe si enot eborp eht ot esnopser ni dedrocer egnahc ecnadepmi tsrif ehT .dlohserht gniraeh eht evoba Bd 09±07 era taht slevel erusserp dnuos latnemercni ta ilumits dnab -daorb htiw ro zH 00 04 ot 005 ta seslup enot htiw detalumits si ºrae eborpª eht ,gnitset laretalispi roF · :euqinhceT .xelfer laidepats eht tset ot red -ro ni tneserp eb tsum margonapmyt C ro A epyt A .noitalitnev rae elddim deriapmi htiw tnetsisnoc ,aPad 001 ± woleb noiger erusserp evitagen eht ni kaep a sah margonapmyt C epyt ehT c .sisat -celeta cinapmyt ro rae elddim eht ni diulf ot eud eb yam hcihw ,enarbmem cinapmyt eht fo ytilibommi setacidni sihT .kaep dednuor ,wol yrev a sah ro talf si margonapmyt B epyt ehT b .aPad 001 ± dna 001 + neewt -eb kaep prahs ,tnenimorp a sah margonapmyt lamron ehT a – 200 – 100 0 + 100 + 200 + 300 (daPa or mm H2O) Compliance – 200 – 100 + 100 + 200 + 300 (daPa or mm H2O) 0 + 100 + 200 + 300 (daPa or mm H2O) Compliance – 200 – 100 Compliance 581 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. – 300 c Type C: negative pressure peak – 300 0 b Type B: flat curve – 300 a Type A: normal finding snrettap margonapmyt lamronba dna lamroN .giF .ecnadepmi enarbmem cinapmyt ni egnahc elbarus -aem a ecudorp ot dedeen level erusserp dnuos mum -inim eht si dlohserht xelfer laidepats ehT .xelfer laidep -ats laretalartnoc ro dessorc eht dellac si edis etisoppo eht no dedrocer xelfer ehT .xelfer laidepats laretalispi ro dessorcnu eht dellac si edis detalumits yllacitsuoca eht no xelfer laidepats ehT .cra xelfer laicafocitsuoca eht aiv tcartnoc sedis htob no selcsum suidepats eht ,rae eno ylno ot dereviled si dnuos nehW :snoitinifeD .rewol Bd 02±01 yletamixorppa slevel dnuos ta xelfer eht ekove ilumits dnab-daorB .xelfer laidepats eht ekove ot tneiciffus si LH Bd 09±08 yletamixorppa fo enot a ,gniraeh lamron htiW .ytisnetni niatrec a fo ilumits citsuoca ot esnopser ni xelfer a sa stcartnoc elcsum suidepats ehT .lanac rae eht ni decalp eborp a htiw derusaem eb nac egnahc ecnadepmi eht dna ,enarb -mem cinapmyt dna rae elddim eht fo ecnadepmi eht segnahc sihT .sutarappa noitcudnoc dnuos eht gni -neffits fo tceffe eht sah noitcartnoc sti dna ,sepats eht no stresni elcsum suidepats ehT :)02.8 .giF( ygoloisyhP )RS( xelfeR laidepatS .skaep elpitlum tibihxe osla yam margonapmyt eht ,ytiunitnocsid ralucisso na ro enarbmem cinapmyt eht fo yhporta laitrap htiW .)c±a 91.8 .giF( sepahs margonapmyt suoirav htiw yllac -inilc setalerroc hcihw ,ecnailpmoc ni egnahc a ot dael rae elddim dna enarbmem cinapmyt eht ni segnahc ci -golohtaP .aPad ro O2Hmm 0 03  fo egnar a revo deirav yllausu era serusserp ehT .lanac rae eht ni delaes yl -lacitemreh eb eborp larua-artni eht taht seriuqer sihT .egnar evitisop-ot-evitagen a revo deirav si erusserp ria deilppa eht sa segnahc ecnailpmoc fo noitatneserper cihparg a si margonapmyt ehT .ecnailpmoc ro noitpros -ba dnuos sti rewol eht dna ,enarbmem cinapmyt eht fo ºssenffits citsuocaª eht retaerg eht ,lanac rae eht ni erusserp evitagen ro evitisop eht retaerg ehT .tseb dnuos sbrosba erofereht dna )ecnatsiser( ecnadep -mi tsewol eht sah enarbmem cinapmyt eht ,noitidnoc siht nI .erusserp cirehpsomta eht ot dnopserroc dna lauqe era rae elddim dna lanac rae eht ni serusserp ria eht yllamroN .enarbmem cinapmyt eht morf de -tcelfer si dnuos erom ,siht fo tluser a sA .lanac rae eht ni ecnadepmi citsuoca eht gnisaercni ybereht ,rae eld -dim eht fo gnineffits a sesuac lanac yrotidua lanretxe eht ni erusserp ria eht gnirewol ro gnisiar ylevitceleS yrtemonapmyT .ecnadepmi fo egnahc dekove yllac -itsuoca na secudorp hcihw ,)RS( xelfer laidepats ehT · dna ;lanac rae lanretxe eht ni erusserp ria deilppa yb desuac segnahc ecnadepmi eht fo noitat -neserper cihparg a sedivorp hcihw ,yrtemonapmyT · )gnitseT y rotiduA( ygoloiduA 8
  • 195. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. -ivitca GEE tnednepedni-sulumits( sulumits yrotidua eht htiw etalerroc ton od taht slaitnetop dnuorgkcab demit ylmodnar ,detnawnu ecuder ot sdnet osla noit -ammus sihT .tnemges GEE eht fo gnimmus evititep -er eht yb deifilpma eb nac dna emit emas eht ta ruc -co syawla hcihw ,lavretni emit siht gnirud slaitnetop mrofinu ,cificeps sekove sulumits tnettimretni ehT .sul -umits citsuoca evititeper ,tnatsnoc a dna dezylana eb ot tnemges GEE eht neewteb deniatniam si pihsnoital -er laropmet tnatsnoc a taht niatrec gnikam ,retupmoc a ni tnemges GEE trohs a fo noitammus evitareti eht sevlovni tI .esion ni deirub era taht segnahc laitnet -op llams yrev drocer ot elbissop ti sekam gnigarevA .SNC eht fo ytivitca latot eht ot evitaler llams os si edutilpma rieht esuaceb ecart GEE yranidro na ni elbatceted ton era metsys yrotidua eht yb desuac segnahc laitnetop ehT .euqinhcet siht yb ylsuoenatlumis dedrocer era sllec ynam morf slait -netop eht ,)GEE( margolahpecneortcele na ni sA .sed -ortcele ecafrus ro eldeen gnisu placs eht morf dedroc -er era )sPEA( slaitnetop dekove yrotiduA :euqinhceT .noitcnuf yrotidua fo gnitset evitcejbo eht ni dezil -itu eb nac segnahc laitnetop esehT .)SNC( metsys suov -ren lartnec dna ,evren yrotidua ,aelhcoc eht ni ecalp ekat taht segnahc laitnetop cirtceleoib ynam taerg a sevlovni gniraeh fo ssecorp cigoloisyhp ehT :elpicnirP )sPEA( slaitnetoP dekovE yrotiduA .)tnemtiurcer zreM ro ºevitcejboª( dlohserht yrot -idua eht evoba Bd 01 ylno ta xelfer laidepats eht ekove ot elbissop eb yam ti ,tnemtiurcer lamronba dna ssol gniraeh raelhcoc htiw stneitap nI .stcejbus gniraeh -lamron ni erom ro Bd 06 si ecnereffid sihT .tnemtiurc -er gnitaulave rof erusaem a sedivorp dlohserht xelf -er laidepats eht dna dlohserht gniraeh evitcejbus eht neewteb ecnereffid eht ,revoeroM .ssol gniraeh raelhc -ocorter dna raelhcoc morf ssol gniraeh rae elddim gni -taitnereffid ni lufesu era snrettap xelfer laidepats suo -irav ehT .sexelfer dessorcnu dna dessorc eht htob rof sedis htob no denimreted eb dluohs dlohserht xelfer laidepats ehT .sredrosid gniraeh suoremun fo noitagit -sevni eht rof lufesu si tI .yrtemonapmyt retfa demrof -rep syawla si xelfer laidepats eht fo tnemerusaeM .enarbmem cinapmyt eht fo noitanimaxe cipocs -oto htiw noitcnujnoc ni deterpretni eb syawla dluohs dna ,revewoh ,flesti yb eulav ronim fo si tI .ygoloht -ap rae elddim gnisongaid ni desu si yrtemonapmyT stnemerusaeM ecnattimmI fo snoitacilppA )sivarg ainehtsaym ,.g.e( elcsum suidepats eht fo esaesiD )492 .p ,2.41 ees ,yslap evren laicaf cihtapoidi ,.g.e( evren laicaf eht fo noiseL )egahrromeh ,sisorelcs elpitlum ,.g.e( metsniarb eht fo noiseL )803 .p ,3.51 ees ,amonnawhcs ralubitsev ,.g.e( tnemriapmi raelhc -ocorter ro raelhcoc htiw tneitap a ni evren yrotid -ua ro/dna aelhcoc eht yb noitpecer dnuos lamronbA )352±152 .pp ,4.11 ees ,sisorelcsoto ot eud gni -neffits ro noitpursid ,.g.e( ygolohtap niahc ralucissO · · · · · .metsniarb eht ni ielcun evren laicaf eht dna xelpmoc yravilo roirepus eht ot suelcun raelhcoc eht morf sdnetxe cra xelfer ehT .noitalumits citsuoca larehpirep yb dekove si xelfer laidepats ehT Stapedius muscle Stapedius muscle Sound Auditory nerve Auditory nerve Cochlea Middle ear Cochlea Cochlear nucleus Superior olivary complex Cochlear nucleus Facial nerve Middle ear Facial nerve Facial nerve nucleus Facial nerve nucleus Brainstem Ipsilateral reflex Contralateral reflex xelfer laidepatS .giF raE III 681
  • 196. 781 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .aiseht -sena lareneg rednu yllanoisacco dna detades ro gni -peels elihw detset eb tsum nerdlihc llams dna stnaf -ni ,ytluciffid tuohtiw stluda ni derusaem eb yllausu nac RBA eht elihW .snoitidnoc noitanimaxe teiuq evah ot tnatropmi si ti ,nerdlihc llams ni sdlohserht gniraeh gninimreted ni tseretni fo era sdlohserht laitnetop esuaceB .)202 .p ,2.9 ees( ygoloidua cirt -aidep ni gnitset dlohserht rof tnatropmi si RBA ehT · .).cte ,snoisel metsniarb cimehcsi ,sisorelcs elpitlum( sesaesid cigoloruen fo sisongaid eht ni tnatropmi eb osla nac RBA ehT · .)852 .p ,gnigamI citsongaiD ,1.21 ees( snoitagitsevni reht -ruf tpmorp dluohs dna ssol gniraeh raelhcocorter fo ngis a si ycnetal kaepretni degnolorp A .lanac yrotid -ua lanretni ro elgna enitnopolleberec eht ni romut a fo noisulcxe eht dna ssol gniraeh raelhcocorter fo sisongaid eht ni tnatropmi era )ssel ro sm 3.4 yletam -ixorppa si ycnetal kaepretni lamron( V dna I sevaw neewteb doirep tnetal eht dna ).cte ,sevaw tcnitsid -ni ,sevaw fo ecnesba( evruc eht fo epahs eht htoB · .dlohserht gniraeh eht fo tnemerusaem evitcejbo eht ni dna ssol gniraeh raelhcocorter dna raelhcoc neewt -eb gnitaitnereffid ni era esnopser metsniarb yrot -idua eht fo snoitacilppa lacinilc niam ehT :snoitacidnI .RBA lamronba na htiw enod eb tonnac sihT .)12.8 .giF( serutcurts lacimotana cificeps ot dengissa ylhguor eb .sessecorp evitingoc fo noitaulave eht ni lufesu era hcihw ,)sPCE( slaitnetop detalerroc-tneve lacipyt ekove osla nac sulumits a fo tnetnoc noitamrofni ehT .dlohserht y rotidua fo noitanimreted cificeps-sulumits ,evitcejbo eht rof desu eb nac taht sesnopser detalerroc-sulumits ot dael ,RLMA dna )RBA( esnopser metsniarb y rotidua ni sa ,sulumits eht fo seit -reporp lacisyhp ehT .sulumits citsuoca evititeper yna yb de -ticile eb ,elpicnirp ni ,nac )PEC( slaitnetop dekove lacitroC .terpretni ot tluciffid erom meht gnikam ,slaitnetop eseht tceffa aisehtsena lareneg dna peels larutaN .egnar ycneuqerf -wol eht ni dlohserht gniraeh eht enimreted ot desu eb nac yrtemoidua )RLMA( esnopser ycnetal elddim yrotiduA .)402 .p ,3.9 ees( stnalpmi raelhcoc rof stneitap fo noita -ulave citsongaid eht ni dna )582±382 .pp ,4.31 ees( esaesid er›inØM fo sisongaid eht ni desu si yhpargoelhcocortcelE .euqinhcet siht htiw dedrocer eb nac slaitnetop raelhcoc sa llew sa slaitnetop evren yrotiduA .lanac rae eht otni detres -ni eb nac sedortcele dengised yllaiceps ro ,yrotnomorp eht ot enarbmem cinapmyt eht hguorht dessap eb yam sedort -cele eldeeN .elbissop sa aelhcoc eht ot esolc sa decalp eb edortcele na taht seriuqer yhpargoelhcocortcelE .)PS = lait -netop noitammus ,MC = scinohporcim raelhcoc( laitnetop raelhcocodne eht ni stfihs dna slaitnetop rotpecer sa llew sa slaitnetop evren serusaem )GhcoCE( yhpargoelhcocortcelE slaitnetop dekove yrotidua rehto fo snoitacilppA 4.8 nac sevaw laudividni eht ,esnopser metsniarb lamron a htiW .tteweJ yb debircsed sa IV ot I morf derebmun sevaw xis ro evif fo ecneserp eht yb deziretcarahc si tI .)nerdlihc llams ni tnatropmi( aisehtsena lareneg red -nu dna peels gnirud neve degnahcnu yllautriv si taht mrofevaw lacipyt a drocer nac diotsam eht revo dna xetrev eht no decalp sedortcele ecafrus evisehdA .dega -reva era sesnopser GEE eht dna semit 00 02 ot 0001 morf detaeper eb tsum sulumits eht ,RBA eht drocer oT .murtceps ycneuqerf daorb a sah dna sdnocesillim wef a ylno stsal taht sulumits kcilc a yb dekove yllausu si tI .detneserp si sulumits citsuoca na retfa sm 01 tsrif eht tuoba gnirud srucco RBA ehT .esnopser metsniarb yrotidua eht sa ot derrefer yllausu ,slaitnetop mets -niarb eht era sesoprup citsongaid rof dedrocer ylnom -moc tsom era taht slaitnetop dekove yrotidua ehT )RBA( esnopseR metsniarB yrotiduA .PEA rof mynonys a sa ygoloidua ni desu net -fo si )ARE( ºyrtemoidua esnopser lacirtceleª mret ehT .sm 0001±001 fo ycnetal a htiw slaitnetop serusaem :)yrtemoidua esnopser lacirtcele lacitroc sa nwonk osla( )PEC( slaitnetop dekove lacitroC · .xetroc yrotidua yramirp dna sumalaht eht ni etanigiro taht sm 001 ±01 fo ycnetal a htiw slaitnetop serusaem :yrt -emoidua )RLMA( esnopser ycnetal elddim yrotiduA · .sm 01 yletamixorppa ot pu ycnetal a htiw ,serutcurts metsniarb dna evren yrot -idua eht ni gnisira slaitnetop eht serusaem :)yrtem -oidua esnopser lacirtcele metsniarb sa nwonk os -la( yrtemoidua )RBA( esnopser metsniarb yrotiduA · .detneserp si sulumits eht retfa sm 3±1 yletamixorppa rucco slaitnetop esehT .evren yrotidua dna aelhcoc eht ni gnisira slaitnet -op eht serusaem :)GhcoCE( yhpargoelhcocortcelE · :sPEA eht fo seicnetal dna nigiro fo setis tnereffid eht no desab dehsiugnitsid era yrtemoidua esnopser lacirtcele fo sepyt lareveS .sulu -mits eht ot ylkciuq yrev dnopser taht serutcurts morf etanigiro dna sulumits eht retfa yltrohs yrev rucco yc -netal trohs a htiw sPEA .)sdnocesillim ni( ycnetal rieht ro ,sulumits citsuoca eht fo noitatneserp retfa rucco yeht hcihw ta emit eht no yltrap dneped )sPEA( slait -netop dekove yrotidua fo sepahs dna seitreporp ehT slaitnetoP dekovE yrotiduA fo ygolonimreT dna noitacifissalC .slaitnetop dekove yrotidua sa sulumits citsuoca eht ot yllaropmet dengis -sa eb nac slaitnetop deyalpsid eht ,degareva era seirt -ne demmus eht nehW .snoitammus fo rebmun egral yltneiciffus a retfa tuo lecnac yeht ,rehtegot dedda era slaitnetop dnuorgkcab evitagen dna evitisop ecniS .)yt )gnitseT y rotiduA( ygoloiduA 8
  • 197. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. :sulumits eht fo erutan eht no desab sepyt lareves otni deifissalc era snoissime citsuocaotO .)sEAO dekove( snoissime dna snoitarbiv raelhcoc ecudni yltnetsisnoc lliw ytisnetni etaredom ot wol fo sulumits citsuoca na ,emit emas eht tA .)sEAO suoen -atnops( sulumits lanretxe na tuohtiw aelhcoc eht ni ylsuoenatnops esira nac snoitarbiv ,reifilpma raelhcoc eht fo ytivitisnes hgih eht ot gniwO :noitacifissalC evitisnes A .lanac rae lanretxe eht otni sevaw dnuos sa snoitarbiv eht gnittime ,rekaepsduol a fo enarb -mem eht ekil stca hcihw ,enarbmem cinapmyt eht ot selcisso eht ssorca noihsaf edargorter ni dettimsnart era ,sulumits citsuoca na ot esnopser ni ro ylsuoenat -nops rehtie ,)361±161 .pp ,2.7 ees( aelhcoc eht fo reif -ilpma lacinahcemoib eht yb decudorp snoitarbiv ehT )sEAO( snoissimE citsuocaotO y rotidua dna evren y rotidua eht fo ytivitca decudni yllacitsuoca eht tcelfer slaitnetop ehT .)IV hguorht I derebmun( sevaw 6 ro 5 fo stsisnoc hcihw ,mrofevaw RBA lacipyt eht swohs evruc ehT .serutcurts lacimotana suoirav eht ni srotareneg elopid yb decudorp era sevaw ehT .snoruen .gniraeh ycneuqerf-wol no noitam -rofni niatbo ot tluciffid erom si tI .)zHk 1 >( seicneuq -erf hgih dna elddim ta gniraeh stset ylniam RBA ehT .gniraeh rotinom ot ylevitarepoartni de -tset osla era slaitnetop metsniarb dekove yrotiduA · .enarbmem cinapmyt eht ot dettimsnart eb ton dluow snoitarbiv raelhcoc eht esiw -rehto rof ,noitcnuf rae elddim lamron nopu tnegnit -noc si lanac rae eht ni sEAO fo noitceted ehT .devlovni ton si evren yrotidua eht ;sEAO fo ecruos tnatropmi yl -ralucitrap a era sllec riah retuo ehT .aelhcoc eht fo ytir -getni lanoitcnuf eht tcelfer snoissime ehT º.reifilpma raelhcocª eht fo noitcnuf eht tset ot desu eb nac yeht taht ni tnatropmi yllacinilc era snoissime citsuocaotO .)sEAO( snoissime citsuocaoto dellac era hcihw ,snoitarbiv raelhcoc evitca eseht tcet -ed nac lanac rae eht otni detresni eborp enohporcim .dlohserht gni -raeh eht evoba Bd 01 tuoba ylno ta detceted eb nac V evaw ,yllamroN .V evaw fo noitceted eht rof dlohserht eht dna sevaw eht neewteb slavretni emit eht era RBA eht fo sretemarap tnatropmi tsom ehT :noitaterpretnI 0 1 2 3 4 5 6 7 8 Time after acoustic stimulus (ms) 9 10 11 – 0,5 Amplitude (μV) II 0 + 0,5 VI I III V IV Cochlea Auditory nerve Superior olivary complex Cochlear nucleus Rhomboid fossa Lateral lemniscus Inferior colliculus esnopser metsniarb yrotiduA .giF raE III 881
  • 198. 981 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .)snoitacidem cixototo gnisu stneitap ,.g.e( spuorg ksir ni noitcnuf raelhcoc ssessa ot dna ,stluda ni sgnidnif cirtemoidua yfitcejbo ot ,ssol gni -raeh cinagronon etagitsevni ot desu eb osla nac sEAO .desu eb dluohs yrtemoidua laroivaheb dna slaitnetop dekove yrotidua sa hcus stset cigoloidua lanoitidda ,sEAO fo ecnesba eht nI .snoissime citsuocaoto gnizylana yb denimreted eb ton -nac eerged sti dna )laruenirosnes ro rae elddim( ssol gniraeh eht fo noitacol ehT .ygoloite raelhcoc a evah puorg ega siht ni sredrosid gniraeh fo ytirojam ehT .smelborp gniraeh fo noitceted ylrae eht gnitatilicaf suht ,aisehtsena lareneg ro noitades tuohtiw noitcnuf raelhcoc tset ot yaw elpmis dna tsaf a edivorp sEAOPD dna sEAOET .)202 .p ,2.9 ees( nerdlihc llams dna ,stnaf -ni ,snrobwen ni noitcnuf raelhcoc gnineercs rof si snois -sime citsuocaoto fo noitacilppa tnatropmi tsom ehT snoissimE citsuocaotO fo noitacilppA .sEAOET rof sa emas eht era sEAOPD rof snoitacidni lacinilc ehT .derus -aem era sEAOET nehw stcafitra etanimile ot reisae si ti ,dnah rehto eht nO .segnar ycneuqerf etercsid ni reifilpma raelhcoc eht fo esnopser eht erusaem ylkciuq ot desu eb nac smetsys gnirusaem detamotuA .deriap -mi si reifilpma raelhcoc eht fo noitcnuf eht nehw neve sEAOPD tceted ot elbissop eb llits yam ti ,tlus -er a sA .sEAOET htiw elbissop era naht slevel dnuos rehgih ta dna egnar ycneuqerf reworran a nihtiw stnemerusaem rof swolla senot suounitnoc fo esu ehT .meht ot lacitnedi ton era tub seicneuqerf sulu -mits eht ot pihsnoitaler dexif a raeb taht senot ecneref -retni sa rucco stcudorp noitrotsid ,detceles ylreporp era seicneuqerf sulumits owt eht nehW .)32.8 .giF( senot suounitnoc owt htiw noitalumits yb dekove era taht snoissime citsuocaoto eht gnirusaem sevlov -ni tset ehT .gnitset lacinilc ni desu osla era sEAOPD )sEAOPD( snoissimE citsuocaotO tcudorP noitrotsiD .stluda ni naht edutilpma retaerg a evah yllausu stnafni gniraeh-lamron ni dedrocer sEAOET .esaercni dlohserht Bd 03 yletamixorppa na htiw ssol gniraeh raelhcoc a ro esae -sid rae elddim htiw stneitap ni rucco ton od sEAOET .rae elddim dna aelhcoc eht fo ytirgetni lanoitcnuf eht smrifnoc siht ,syawla tsomlA .)22.8 .giF( gniraeh lamron htiw stcejbus ni )EAOET( esnopser citsuoca raelhcoc a sekove yltnetsisnoc kcilc ehT :noitaterpretnI .)681 .p ees( slaitnetop dekove yrotidua ni slangis cirtceleoib eht sa yaw ralimis a ni degareva era hcihw ,slangis citsuoca eht drocer nac lanac rae lanretxe eht otni detresni eborp enohporc -im A .sulumits eht fo murtceps eht tcelfer dna )kcilc( sulumits feirb a ot esnopser ni dedrocer era sEAOET )sEAOET( snoissimE citsuocaotO dekovE tneisnarT .ecnacifingis lacinilc elttil evah yehT .sEAOPD dna sEAOET naht tceted ot tluciffid erom era snoissime esehT .ycneuqerf emas eht fo snoissime lanot sekove enot evaw-enis a htiw noitalumitS :)sEAOFS( snoissime citsuocaoto ycneuqerf sulumitS .yduts cirtemoidua evitcejbo desu yltneuqerf rehtona si sEAOPD fo tnemerusaem ehT .seicneuqerf tnecajda tub tnereffid evah taht senot suounitnoc owt htiw noitalumits yb detceted eb nac reifilpma raelhcoc eht ni snoitrotsid citsuocA :)sEAOPD( snoissime citsuocaoto tcudorp noitrotsiD .dohtem tset cirtemoidua evitcejbo desu ylnommoc a si sEAOET fo tnemerus -aem ehT .)681 .p ees( slaitnetop dekove yrotidua rof debircsed taht ot ralimis euqinhcet gnigareva na gnisu detceted era yehT .noitcnuf raelhcoc lamron htiw stcejbus ni )kcilc( sulumits feirb a ot esnops -er ni detceted yltnetsisnoc era snoissime esehT :)sEAOET( snoissime citsuocaoto dekove tneisnarT .ecnatropmi lacinilc elttil evah yehT .senot suounitnoc ,level-wol sa elbatceted era dna stcej -bus gniraeh-lamron fo %05 yletamixorppa ni sulu -mits citsuoca lanretxe na tuohtiw rucco snoissime esehT :)sEAOS( snoissime citsuocaoto suoenatnopS · · · · )gnitseT y rotiduA( ygoloiduA 8
  • 199. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .)c ees( lanac rae eht ni dedrocer sesnopser erusserp dnuos eht rof elacs eht naht retaerg semit 0001 si )aP( erusserp dnuos sulumits eht fo elacs eht taht etoN .sm 2 yletamixorppa stsal hcihw ,sulumits eht fo mrofevaW b .rekaepsduol dna enohp -orcim htiw eborp gnirusaem :sEAOET gnirusaem rof puteS a 5 .esion stneserper ecart egnaro ehT .)elprup( sEAOET eht fo noitubirtsid ycneuq -erf eht gnitacidni ,)c morf( esnopser dekove eht fo murtcepS d .sEAOET eht fo erusserp dnuos eht fo edutilpma dna esruoc emit eht stcelfer sulumits eht fo noitaitini retfa sm 5.2 dedrocer mrofevaw ehT c 0 10 Time (ms) 15 20 0 –1 1 500 3 000 4 500 6 000 Frequency (Hz) – 20 5 – 0,5 Pressure (Pa) Level (dB SPL) 1 2 3 4 Time (ms) Pressure (mPa) 0 – 0,3 0 0 0,5 + 0,3 b 1 c – 10 0 10 d 20 TEOAEs Noise Microphone Loudspeaker a )sEAOET( snoissime citsuocaoto dekove tneisnarT .giF raE III 091
  • 200. 2 3 4 Frequency (kHz) Sound pressure in ear canal (dB SPL) f1 5 6 f2 f2 191 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. 1 – 20 0 DPOAE 2f1 – f2 20 40 60 Loudspeakers .EAOPD a sa aelhcoc eht ni setanigiro enot sihT .dedrocer si 2f±1f 2 fo ycneuq -erf a htiw enot lanoitidda na ,2f dna 1f senot sulumits eht sediseB .langis enohporcim eht fo murt -ceps ycneuqerf eht stneserper evruc ehT .2f dna 1f senot yramirp htob fo erusserp dnuos eht dna esnopser eht fo erusserp dnuos dettime eht htob gnitceted ,lanac rae lanretxe eht ni erusserp dnuos eht sdrocer enohporcim A .eborp a yb dereviled ,2f dna 1f ,senot owt htiw detalumits si aelhcoc ehT f1 Microphone )sEAOPD( snoissime citsuocaoto tcudorp noitrotsiD .giF )gnitseT y rotiduA( ygoloiduA 8
  • 201. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .noitaulave cigoloidua dna yrotsih etarucca na fo sisab eht no denimreted eb tsum ycadidnac ,dia gniraeh a htiw dettif si tneitap eht erofeB :ycadidnac gninimreteD :spets fo seires a sevlovni ,stneitap deriap -mi-gniraeh ynam rof noitatilibaher larua fo snaem tnatropmi na si hcihw ,dia gniraeh a fo gnittif ehT .stnemeriuqer dna ssol gniraeh laudiv -idni stneitap eht ot dia gniraeh eht roliat ot elbissop ti sekam dna langis citsuoca eht fo gnissecorp deta -itnereffid rof swolla ygolonhcet latigid dna pihcorciM .evren yrotidua eht ot ti yaler dna langis dessecorp dna deifilpma eht eviecer ot elba eb tsum aelhcoc eht ,ylreporp krow ot dia gniraeh a roF .rae eht ot rekaeps -duol a yb dettimsnart dna ,deifilpma ,enohporcim a yb deviecer si tnemnorivne eht morf dnuoS .)42.8 .giF( reifilpma citsuoca fo epyt laiceps a si dia gniraeh ehT stludA ni gnittiF diA gniraeH .gnieb-llew tneitap dna gninoitcnuf laicos rof laic -urc si hcihw ,noitacinummoc larua fo noitarotser mumixam a eveihca ot si noitatilibaher fo laog ehT hceeps rieht gnivorpmI · daer pil ot gninraeL · secived evitsissa rehto dna sdia gniraeh fo esu reporp ehT · )gni -niart yrotidua ,scitcat gninetsil( gninetsil evitceleS · :ni deniart eb nac stneitap deriapmi-gniraeH :gniniarT .tenretni eht dna ,gnigassem txet ,sexaf sa hcus secived noitacinummoc latigid dna ,senohpdaeh noisivelet ,senohpelet txet ,sreifilpma enohpelet ,srehsalf thgil ,smrala pu-ekaw gnitarbiv ro lacitpo edulcni secived esehT .stneit -ap deriapmi-gniraeh rof noitacinummoc evorpmi nac secived evitsissa fo yteirav A :secived evitsissa rehtO .sregnif ro tsirw eht ot dettimsnart era taht snoitarbiv ot detrevnoc dna enohporcim a yb pu dekcip era slangis citsuocA :sdia elitcatorbiV .sedortcele raelhcocartni htiw evren yrotid -ua eht etalumits yltcerid taht seslupmi lacirtcele otni sevaw dnuos mrofsnart nac ecived detnalpmi yllacig .3.9 ni deweiver era nerdlihc ni erac dia gniraeh fo selpicnirp cisab dna snoitacidni ehT .dia gniraeh a fo gnittif etarucca eht sa tnatropmi sa tsuj era daer pil ot gninrael dna gniniart yrotidua sa hcus serusaem yral -licnA .ssenfaed ro ssol gniraeh dnuoforp htiw stneitap -rus siht ,noitcnuf raelhcoc fo ecnesba etelpmoc tsom -la ro etelpmoc a htiw stneitap nI :tnalpmi raelhcoC .niahc ralucisso ro enob lainarc eht ot yltcerid dettimsnart era snoitarbiv ehT .snoit -arbiv lacinahcem otni sevaw dnuos smrofsnart hcihw detnalpmi si reifilpma nA :stnalpmi rae elddim evitcA .)dia ETI( lanac rae eht edisni ro )dia ETB( rae eht dniheb nrow eb yam dia gniraeh ehT .)42.8 .giF( slangis yrot -idua seifilpma ylevitceles dia gniraeh A :sdia gniraeH .)252 .p ees ,sisorelcsoto ni yregrus sepats ,.g.e( ssol gniraeh evitcudnoc htiw stneitap ni gniraeh fo noitarotser lanoitcnuf edivorp nac gniraeh evorpmi ot noitarepo lacigrus A :yregruS .sesopmi ti taht pacidnah fo eerged eht dna ssol gniraeh eht fo eerged dna erutan eht no gnidnep -ed ,elbaliava era snoitpo evitatilibaher fo yteirav A .noit -avirped yrotidua ot gnitaler ytilibasid rehtruf tnev -erp nac dna lufsseccus erom si ega reilrae na ta noit -atilibaher esuaceb ,ssol gniraeh rieht yb delbasid ylevitcejbus era ohw stneitap ni deyaled gnol eb ton dluohs serusaem evitatilibaher ,dnah rehto eht nO .noitavitom fo kcal a ot eud gnidrawernu eb yllareneg lliw serusaem evitatilibaher ,ssol eht yb deppacidnah ton si dna tnemriapmi gniraeh evitcejbus ecneirepxe ton seod ssol gniraeh htiw tneitap eht fI .sesac erar ni ylno ssol gniraeh rof noitpo na si tnemtaert lacideM .pacidnah gnitluser eht dna ytilibasid yrotidua laudividni eht tnuocca otni ekat osla dluohs tub ssol gniraeh cirtemoidua no yleritne desab eb ton dluohs ecnamrofrep yrotidua evorpmi ot serusaem ,suhT .sdnamed dna stnemeriuqer yrotidua laudividni sa llew sa ssol gniraeh eht fo eerged eht edulcni taht srotcaf no sdneped efil yadyreve ni gnilbasid si ssol gniraeh rehtehW .tneitap eht fo ytirgetni lacisyhp eht sesimorpmoc syawla ti ,.e.iкtnemriapmiª na syaw -la si yrtemoidua yb elbarusaem si taht ssol gniraeH noitatilibaheR yrotiduA fo seitilibissoP dna snoitacidnI ni desu eb yam )stnalpmi rae renni( stnalpmi raelhcoc elihw ,ssol gniraeh ereves ot etaredom rof debircs -erp yltneuqerf era sdia gniraeH .stnemeriuqer laicos ro laudividni rehto dna ,tneitap eht fo sdeen eht ,ssol gniraeh fo eerged eht ot deroliat era serusaem evitat -ilibaher cificepS .noitacinummoc yrotidua evorpmi ro erotser ot si noitatilibaher yrotidua fo laog lareneg ehT sdiA gniraeH dna noitatilibaheR 5.8 raE III 291
  • 202. .tneserp si esion dnuorgkcab nehw noitingocer hceeps ni niag yrotcafsitas a edivorp ton od netfo sdia gniraeh ,tluser a sA .tnemnorivne ysion a ni elbaeciton ylralucitrap eb nac snoitatimil esehT .snoitcnuf yrotidua lartnec laitnesse ro aelhcoc eht fo noit -uloser ycneuqerf enif eht evorpmi yllaitnatsbus ro ecalper tonnac taht dia gninetsil larehpirep a llits si dia gniraeh a ,ygolonhcet detacitsihpos eht etipseD .noitaulave cigoloidua na ot noitidda ni gniniarT rednu evoba detsil stniop eht sedulcni nemiger pu-wollof ehT :erac pu-wolloF .tifeneb mumitpo evir -ed ot redro ni secudorp ti noitasnes yrotidua eht dna ecived eht ot demotsucca emoceb tsum tneitap eht ,gnittif eht retfA .noitceles lanif eht troppus )stnemerus -aem utis ni( lanac rae eht ni stnemerusaem citsuoca dna ,tneitap eht fo noisserpmi yrotidua evitcejbus eht ,esion dnuorgkcab tuohtiw dna htiw gnitset cirtem -oidua hceepS .slairt lacitcarp ni ylno enod eb nac reif -ilpma eht fo gninut-enif dna noitceles lanif ehT .morf esoohc ot secived lareves tneitap eht reffo dluohs tsilaiceps dia gniraeh ehT :noitceles dia gniraeh laniF .laeuqs dehctip-hgih a gnisuac ,rekaeps -duol dna enohporcim eht neewteb rucco ot kcabdeef citsuoca wolla yam dlomrae gnittif ylroop A .dlom -rae wen a fo noitcurtsnoc eht eriuqer yam )yregrus ot eud ,.g.e( lanac rae ro elcirua eht ni segnahC .dlom -rae detacirbaf-motsuc a htiw lanac yrotidua stneitap eht ot delpuoc yllacitsuoca dna yllacisyhp si )ecived rae-eht-ni ro rae-eht-dniheb a yllausu( dia gniraeh ehT .)tsilaiceps dia gniraeh ro tsigoloidua( tsilaiceps deniart a yb enod si dia gniraeh eht fo gnittiF .sisab lairt a no detceles si dia gniraeh a ,tneitap eht fo serised eht dna sgnidnif cigoloidua dna lacinilc eht no desaB :lairt dia gniraeH .)3.8 ees( gnilacs egnar cimanyd yb ,.g.eÐegnar cimanyd eht fo noitanimreted a dna ,yrte -moidua hceeps ,yrtemoidua enot-erup edulcni dluohs noitanimaxe cigoloidua ehT :noitanimaxe cigoloiduA .yregrus yb gniraeh stneitap eht gnivorpmi fo tcepsorp elbanosaer on eb dluohs erehT -ed neht dna ,dessecorp dna deifilpma ,enohporcim a yb deviec -er si langis citsuoca ehT .reifilpma citsuoca na sa snoitcnuf dia gniraeh ehT .dia gniraeh a fo margaid citamehcs lanoitcnuF .seitreporp citsuoca tnatropmi sah dna dia gniraeh eht fo trap largetni na si dlom -rae detacirbaf-motsuc ehT .rekaepsduol a yb rae eht ot derevil .dia gniraeh eht niatniam dna esu ot elba dna gnilliw eb tsum tneitap ehT · .LPS Bd 56 ta noitingocer drow ciballysonom rof sesnops -er tcerroc rewef ro %08 ,yrtemoidua hceeps nI · .zH 00 03 ot 0 05 morf egnar eht ni ycneuqerf eno tsael ta rof derusaem ,yrtemoidua enot-erup yb rae retteb eht ni erom ro LH Bd 03 fo ssol gniraeH · :dia gniraeh a fo noitpircserp eht rof ynamreG ni dehsilbat -se neeb evah snoitidnoc gniwollof eht ,elpmaxe roF .rae dedianu eht fo noitavirped yrotidua tneverp osla lliw gnittif laruaniB .esion dnuorgkcab ni noitingocer hceeps evorpmi dna ,gniraeh lanoitcer -id wolla ,)noitammus laruanib( niag tnacifingis a ediv -orp lliw eseht sa ,sdia laruanib htiw dettif eb dluohs ssol gniraeh lacirtemmys ylegral a htiw stneitaP Miniature loudspeaker (sound emission) 391 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. Amplifier: – Uses filters – Amplifies soft sounds more than loud ones – Limits maximum loudness level (compression) – Amplifies frequency bands selectively – Suppresses noise and feedback Earmold (custom-fitted) Microphone (sound reception) dia gniraeH .giF )gnitseT y rotiduA( ygoloiduA 8
  • 203. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. sdia gniraeh eht fo tnemtsujda mumitpo etips -ed gnittif dia gniraeh laruanib morf tifeneb fo kcaL · 402 .p ,3.9 ees ,)ssenfaed laugnilerp( nerdlihc ni ssenfaed deriuqca ylrae ro latinegnoC · yawhtap yrotidua lartnec tcatni dna evren yrot -idua lanoitcnuf a htiw )ssenfaed laugniltsop( ssen -faed raelhcoc yltnanimoderp ,laretalib ,deriuqcA · :swollof sa era tnalp -mi raelhcoc a gnibircserp rof airetirc ehT :noitacidnI .tnalpmi eht morf tifeneb tsetaerg eht evired noitarud trohs fo ssenfaed htiw stneitap ,stluda nI .ssenfaed eht fo noitarud dna tesno fo emit eht yb decneulfni yltrap si tnalpmi raelhcoc a fo sseccus ehT .)metsys sserdda cilbup a ro enohpelet eht revo ,.g.e( seuc lausiv no gniyler tuohtiw hceeps detaidem-IC dnatsrednu nac yeht ,.e.iÐnoisneh -erpmoc hceeps nepo eveihca nac %05 naht erom dna ,IC a morf tifeneb etinifed evired stneitap fo %09 revO .daer pil ot stneitap eht gnihcaet yb detroppus rehtruf si noitingocer hceepS .hceeps sa seslupmi lacirtcele eht terpretni ot nrael stneitap eht ,srehcaet deriapmi-gni -raeh ro/dna stsipareht hceeps fo ecnadiug eht rednU .gniniart yrotiduA · dna ;rossecorp hceeps eht gnitsujda dna gnikcehC · noitcnuf IC fo kcehc lacinhcet A · :sedulc -ni margorp pu-wollof ehT .shtnom lareves rof stsal yllareneg dna noitarepo eht retfa skeew lareves snig -eb rossecorp hceeps eht fo tnemtsujdA :erac pu-wolloF .erar osla era ,noitcnuflam elbissop gnidulcni ,snoitac -ilpmoc retaL .stceffe edis wef ylevitaler sah taht erud -ecorp dezidradnats ,efas a si yregrus noitatnalpmi ehT .)tset yrotnomorp evitisop( noisserpmi yrot -idua na ecudorp lliw tset siht ,tneserp era srebif evren yrotidua tcatni fI .edortcele cinapmytsnart a htiw detalumits yltcerid si )yrotnomorp( nrut raelhcoc tse -wol eht hcihw ni ,tset yrotnomorp eht yb noitatnalp -mi ot roirp detset eb nac evren yrotidua eht fo ssen -evisnopser lacirtcele ehT .sedortcele raelhcocartni eht yb noitalumits ot evisnopser si taht evren yrotidua lanoitcnuf yllaitrap a seriuqer tnalpmi raelhcoc ehT tnalpmi eht fo ecnanetniam dna noitarepo eht nrael ot gnilliw tneitap detavitom A · .tneitap hcae rof yllaudividni ,rossecorp hceeps eht yb slangis hceeps eht fo gnissecorp eht suht dna ,noitalumits lac -irtcele eht tsujda ot yrassecen ti sekam sihT .tneserp llits era taht sllec noilgnag dna srebif evren laudis -er fo rebmun eht ni dna sedortcele raelhcocartni eht fo noitisop eht ni rucco secnereffid laudividni dekraM .langis citsuoca yna ekil gnissecorp lartnec rehtruf seogrednu lan -gis eht ,)Ã( evren yrotidua eht gnitalumits retfA .)Â( sedortcele raelhcocartni suoirav eht setalumits dna ,reviecer detnalpmi eht ot niks eht hguorht langis eht stimsnart ,noitingocer hceeps rof tnatropmi era taht stnenopmoc dnuos lufesu eht stcartxe rossecorp sihT .)Á( dia gniraeh a ekil rae eht dniheb nrow yllausu si hcihw ,rossecorp hceeps lanretxe na yb dessecorp si )À 52.8 .giF( rae eht dniheb nrow enohporcim lanoitcer -id a yb deviecer si taht langis citsuoca ehT .sllec riah raelhcoc eht gnissapyb yllanoitcnuf ,noilgnag larips dna evren yrotidua eht etalumits yltcerid sedortcele ehT .aelhcoc eht otni detresni yarra edortcele na ot de -tcennoc si reviecer ehT .niks eht rednu enob laropmet eht otni detnalpmi si reviecer cinortcele nA .52.8 .giF ni nwohs si IC eht fo elpicnirp lanoitcnuf ehT :elpicnirP .sesac eseht rof noitpo na si )IC( tnalpmi raelhcoc ehT .noitacinummoc larua evorpmi ot elbanu eb lliw noitacifilpma citsuoca gnitanimircsid tsom dna tsegnorts eht neve ,slangis cirtceleoib otni noitarbiv a mrofsnart ot elba sllec riah on ro wef sniatnoc aelhcoc eht nehW .ereves erom semoceb ssol gniraeh fo eerg -ed eht sa stimil rieht hcaer sdia gniraeh tseb eht nevE stludA ni tnalpmI raelhcoC .)srettimsnart MF ,tupni oid -ua( dia gniraeh eht ot enohporcim srekaeps eht morf noissimsnart langis-oidar tcerid si noitpo rehtonA .sehcruhc dna sllah erutcel ynam otni tliub era dnik siht fo slioc noitcudnI .dia gniraeh eht fo tnenopmoc enohporcim eht gnissapyb ,lioc noitcudni na gnisu langis citengamortcele na sa dettimsnart yltcerid eb nac langis enohporcim eht ,elpmaxe roF .desu gnieb si enohporcim a erehw sllah erutcel ni esion dnuorg -kcab nepmad nac serusaem lacinhcet lanoitiddA raE III 491
  • 204. 591 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .ecruos rewop etarapes a eriuqer ton seod flesti tnalpmi eht ;dettimsnart osla si ylppus rewop yras -secen ehT . )lioc gniviecer( IC eht fo noitrop detnalpmi eht ot niks eht hguorht seicneuqerf oidar sa seslupmi eht stimsnart rae eht dniheb nrow lioc gnittimsnart A .Á seslupmi lacirtcele fo seires a otni meht strevnoc dna ,noisneherpmoc rof yrasse -cen era taht stnenopmoc hceeps eht stcartxe ,langis enohporc -im eht sessecorp ,yllanretxe nrow si hcihw ,rossecorp hceeps ehT .À langis golana na sa rossecorp hceeps eht ot def dna rae eht no nrow enohporcim lanoitcerid a yb deviecer si dnuos ehT Speech processor – Selects and processes the acoustic signal – Transforms the acoustic signal into electrical impulses Intracochlear electrodes (stimulate the auditory nerve) Microphone (sound reception) Implant = receiver (receives the electrical impulses) Magnet (to secure the transmitting coil) Sound Transmitting coil (transmits electrical impulses to the implant) Stimulus path )IC( tnalpmi raelhcoC .giF )gnitseT y rotiduA( ygoloiduA 8
  • 205. 9 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 206. III Ear 7 8 9 10 11 12 13 14 15 Anatomy and Physiology of the Ear Audiology (Auditory Testing) The External Ear The Middle Ear Inner Ear and Retrocochlear Disorders Vestibular Disorders Facial Nerve Lateral Skull Base Hearing Disorders in Children— Pediatric Audiology 9.1 Causes and Effects of Pediatric Hearing Disorders 198 Causes of Pediatric Hearing Disorders 198 Hearing Impairment in Newborns 198 Hearing Impairment in Infants and Small Children 200 Effects of Hearing Loss in Children 201 9.2 9.3 Treatment of Pediatric Hearing Disorders 204 Auditory Devices 204 Education Services 205 Detection and Investigation of Pediatric Hearing Disorders 202 Screening 202 Diagnostic Methods in Pediatric Audiology 202 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license.
  • 207. Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .sred -rosid deriuqca yllatanirep dna latinegnoc neewteb hsiugnitsid ot tluciffid erom neve ti sekam sisongaid ni yaled A .nerdlihc deneercsnu ynam ni tnemriapmi gniraeh fo ngis tseilrae eht yletanutrofnu si tnempolev -ed hceeps deyaled ,snrobwen ni suoivbo ton si snoit -amroflam ro sredrosid rehto htiw detaicossanu ssol gniraeh esuaceB .ssol gniraeh deriuqca yllatanirep dna latinegnoc a neewteb hsiugnitsid ot tluciffid netfo si tI snrobweN ni tnemriapmI gniraeH ssol gniraeh laruenirosnes dna ,hteet nosni -hctuH ,sititarek laititsretni htiw silihpys latinegnoC · ssol gniraeh laruenirosnes dna yslap larb -erec diotehta htiw emordnys aimeniburilibrepyH · aimlaht -hporcim dna ,noitadrater latnem ,sisonets yranom -lup ,ssol gniraeh raelhcoc htiw emordnys allebuR · :sa hcus ,yl -latanirep ro oretu ni deriuqca eb nac taht semordnys latinegnoc emos era ereht ,semordnys citeneg sediseB .stnaf -ni dna snrobwen ni ssol gniraeh deriuqca fo sesuac tneuqerf tsom eht stsil 2.9 elbaT .)yllatantsop( htrib retfa ro ,)yllatanirep( htrib gnirud ,)yllatanerp ,eni -retuartni( htrib erofeb deriuqca eb yam ssol gniraeH ssoL gniraeH deriuqcA .elbissop sa htrib ret -fa noos sa tnemriapmi gniraeh rof detset yllacificeps eb dluohs emordnys eseht htiw nerdlihc ,yltneuqes -noC .stnafni era nerdlihc eseht nehw redrosid gniraeh a ot noitnetta llac taht sngis tcerid on era ereht ,lanac rae ro elcirua eht fo ylamona na htiw sesac morf edisA yb deinapmocca tnemriapmi gniraeh ni gnitluser de -tceffa era semosomorhc ro icol eneg elpitlum ,yleraR semordnyS citeneG ni ssoL gniraeH .puorg ega cirtaidep eht ot denif -noc ton era yeht esuaceb )062 .p( 2.21 ni derevoc era ssol gniraeh citeneg citamotpmysonom fo smrof ehT .tnempoleved hceeps lamronba ot eud retal detceted netfo si ,gnineercs tuohtiw ,dna sesac eseht ni suoivbo ton si tnemriapmi gniraeh ehT .evitagen yllausu si yrotsih ylimaf eht os dna ,tiart evissecer-lamosotua na sa detirehni era sred -rosid gniraeh eseht fo tnecrep yteniN .lamron si dlihc eht ,tnemriapmi gniraeh eht rof tpecxE .citamotpmys -onom sa debircsed era dna gniraeh ylno tceffa esuac citeneg a ot eud sredrosid gniraeh fo ytirojam ehT ssoL gniraeH citeneG citamotpmysonoM retal ro yllatantsop deriuqcA ± yllatanirep deriuqcA ± )latinegnoc osla( oretu ni deriuqcA ± sesuac deriuqcA · retal ro yllatantsop gnirruccO ± latinegnoC ± sesuac citeneg yratidereH · :seirogetac lareves otni llaf ssol gniraeh doohdlihc ylrae fo sesuac ehT :noitacifissalC sredrosiD gniraeH cirtaideP fo sesuaC -wen dna stnafni ni deretnuocne osla era sesuac lat -anirep laiceps ,stluda ni sa sesuac emas eht evah nac nerdlihc ni sredrosid gniraeh elihW .redlo si dlihc eht litnu detcetednu og netfo dna ezingocer ot tluciffid eb nac nerdlihc llams dna stnafni ni sredrosid gniraeH .tnempoleved ytilanosrep dna egaugnal fo smret ni secneuqesnoc cificeps evah nac doirep evitamrof siht gnirud sredrosid gniraeh dna ,ytiliba gniraeh ot detaler ylesolc si hceeps fo tnempoleved ehT .tnereffid osla si sesuac eht fo noitubirtsid ycneuqerf ehT .snrob .nerd -lihc fo %4±3 yletamixorppa ni srucco siht ;aidem sit -ito ot yradnoces ssol evitcudnoc yraropmet a yllausu si ,revewoh ,puorg ega siht ni tnemriapmi gniraeH .sreloohcserp dna nerdlihc llams ni tnelaverp erom hcum era sredrosid gniraeH .%05±03 yb sesir nerd -lihc deriapmi-gniraeh fo rebmun eht os dna ,nerdlihc 0 0 02±00 01 ni eno ni spoleved ,laruenirosnes yllausu ,ssol gniraeh tnenamrep ,efil fo sraey tsrif eht gniruD .tnemriapmi raelhcoc ot eud ssol gniraeh laruenirosnes evlovni sesac eseht fo tsoM .snrobwen 0 0 01 ni eno yletamixorppa ni htrib ta tne -serp si tnemriapmi gniraeh tnacifingiS :ygoloimedipE .seussit ro snagro detceffa eht ot gnidrocca deifissalc era yehT .ssol gniraeh htiw deta -icossa era taht semordnys nwonk 003 naht erom eht fo lareves sweiver 1.9 elbaT .emordnys latinegnoc a fo erutaef eno si ssol gniraeh eht ,suhT .smotpmys rehto .semordnys eseht htiw nerdlihc fo noitatilibaher dna tnempoleved rehtruf eht stceffa yldnuoforp ssol gniraeh fo ecneserp ehT sredrosiD gniraeH cirtaideP fo stceffE dna sesuaC 1.9 raE III 891
  • 208. 991 Probst-Grevers-Iro, Basic Otorhinolaryngology© 2006 Thieme All rights reserved. Usage subject to terms and conditions of license. .tinu erac-evisnetni na ni tnem -taert eriuqer taht snrobwen lla fo %4 yletamixorppa ni tneserp si tnemriapmi gniraeh ,llarevO .ksir hgih ylralucitrap ta era stnafni erutamerp dna ,drager siht ni rotcaf tnatropmi na si nrobwen eht fo ytirutam ehT .esion dna ,)scitoibitna( stnega cixot ,aixopyh ot elb ro X ro X )ereves( X X -arenluv yllanoitpecxe si snrobwen ni aelhcoc eht taht deveileb osla si tI .serutcurts lartnec ot egamad esuac doolb eht ni slevel niburilib hgih hcihw ni ,suretcin -rek si elpmaxe lacipyt A .doirep latanoen eht gnirud semit niatrec ta secneulfni lufmrah ot elbitpecsus ylral -ucitrap era metsys yrotidua eht fo serutcurts niatreC ro )tneuqerf( X cidaropS ro )tneuqerf( 12 ymosirT emordnys X cidaropS -lamosotuA TQ degnolorP evissecer lav retni X renruT±hcirllU ro X emordnys grubnedraaW evissecer-lamosotuA -lamosotuA ralubitsev tnetaP evissecer ,tcudeuqa X )noitcnufsyd dioryht( emordnys derdneP etnaruD±leppilK ,rronK±nietsnethciL X sitirhpen cinorhC elbairaV ,enyakcoC ,.g.E emordnys t roplA tnanimod-lamosotuA · emordnys trepA seilamona caidraC seilamona yratnemgip dna suoenatuC )emordnys retnuH( II sisodirahc -casylopocuM snoitcnufsyd cilobatem dna enircodnE )aixata htiw( sredrosid metsys suovreN tnemriapmi noitcnuf laneR )smrof suoirav( atcefrepmi sisenegoetsO · emordnys nozuorC tnanimod -lamosotuA seitilamronba emosomorhC emordnys nesleiN±egnaL±llev reJ suhtnacelet ,sidiri X tnanimod aimorhcoreteh ro -lamosotuA ,kcolerof etihW X X retiog elbissop )ereves( elbairaV X )evissergorp( X X X :sisotsonysoinarC sredrosid lateleksolucsuM ssol gniraeh noitareneged )evissergorp( laruenirosnes dna -lamosotuA III±I epyT evissecer laniter X rae lanretxe eht X fo seilamonA asotnemgip sitiniter :emordnys rehsU seilamona raluco dna noitareneged laniteR seilamona rae ,aisalpopyh latineg ,htworg dedrater ,ean -aohc fo aiserta ,tcef h ,amoboloc :emordnys EGRAHC -ed trae cidaropS )emordnys laruenirosneS dexiM X X ro ro X -lamosotuA fo seilamonA tnanimod rae lanretxe eht rae elddim X r o-oihcarb( emordnys ROB lane ot )emordnys snilloC -lamosotuA fo seilamonA tnanimod dna lanretxe eht sisotsosyd laicafolubidnaM ±rehcaerT( rae lanretxe eht fo seilamonA evitcudnoC ssol gniraeh fo epyT serutaef lacipyT ecnatirehnI emordnyS seilamona yb noitacifissalC ssol gniraeh htiw detaicossa era taht semordnys latinegnoC 1.9 elbaT ygoloiduA cirtaidePÐnerdlihC ni sredrosiD gniraeH 9