\u0130\u015fitme kayb\u0131, toplumlarda b\u00fcy\u00fck pop\u00fclasyonlar\u0131 etkileyen, para, i\u015f g\u00fcc\u00fc kayb\u0131 ve hayat kalitesinde azalmaya neden olan maj\u00f6r bir sa\u011fl\u0131k problemidir. Sadece g\u00fcr\u00fclt\u00fc ve travmaya ba\u011fl\u0131 olarak ABD’de 10 milyon ki\u015fi kal\u0131c\u0131, geri d\u00f6n\u00fc\u015fs\u00fcz i\u015fitme kayb\u0131na sahiptir. \u0130\u015fitme kayb\u0131 artrit ve hipertansiyondan sonra en s\u0131k kar\u015f\u0131la\u015f\u0131lan kronik sorundur. En s\u0131k kar\u015f\u0131la\u015f\u0131lan i\u015fitme kayb\u0131 ya\u015fa ba\u011fl\u0131 i\u015fitme kayb\u0131 veya presbikuzidir, bunu g\u00fcr\u00fclt\u00fcye ba\u011fl\u0131 i\u015fitme kay\u0131plar\u0131 takip etmektedir. \u0130\u015fitme kay\u0131plar\u0131n\u0131 pop\u00fclasyonlara, etiolojiye veya risk fakt\u00f6rlerine g\u00f6re incelemi\u015f olan \u00e7ok say\u0131da epidemiolojik \u00e7al\u0131\u015fma bulunmamaktad\u0131r.<\/p>\n
Cruickshanks ve arkada\u015flar\u0131 yay\u0131nlad\u0131klar\u0131 bir epidemiolojik \u00e7al\u0131\u015fmada 48-92 ya\u015flar\u0131 aras\u0131ndaki i\u015fitme kayb\u0131 olan pop\u00fclasyonda odyometri ve timpanometri ile i\u015fitme kay\u0131plar\u0131n\u0131 taram\u0131\u015flard\u0131r25. Bu \u00e7al\u0131\u015fmaya g\u00f6re verilen ya\u015f gurubunda i\u015fitme kayb\u0131 prevalans\u0131 %45.9 olarak bildirilmi\u015ftir. \u0130\u015fitme kayb\u0131 prevalans\u0131 ya\u015f artt\u0131k\u00e7a artmaktad\u0131r ve erkeklerde daha s\u0131k izlenmektedir. \u0130\u015fitme kayb\u0131n\u0131n 18 ya\u015f alt\u0131nda g\u00f6r\u00fclme s\u0131kl\u0131\u011f\u0131 17\/1000 olarak bildirilmektedir. \u0130\u015fitme kay\u0131plar\u0131n\u0131n bir\u00e7ok farkl\u0131 nedeninin alt\u0131nda yatan molek\u00fcler ve h\u00fccresel patofizyolojinin, s\u0131kl\u0131klar\u0131n\u0131n, risk fakt\u00f6rlerinin ve hangi pop\u00fclasyonlar\u0131 etkilediklerinin daha iyi anla\u015f\u0131lmas\u0131 sonucunda hastalara \u00e7ok daha iyi bir tedavi ve rehabilitasyon \u00f6nerilebilecektir.<\/p>\n
\u0130\u015fitme kay\u0131plar\u0131 bir\u00e7ok nedene ba\u011fl\u0131 olu\u015fmaktad\u0131r. Bunlardan bir\u00e7o\u011fu hakk\u0131nda yeterli epidemiolojik veri bulunmamaktad\u0131r. Bu yaz\u0131da baz\u0131 s\u0131k g\u00f6r\u00fclen i\u015fitme kay\u0131plar\u0131n\u0131n epidemioljik veriler \u0131\u015f\u0131\u011f\u0131nda, s\u0131kl\u0131klar\u0131, risk fakt\u00f6rleri, etiolojileri ele al\u0131nm\u0131\u015ft\u0131r. A\u015fa\u011f\u0131da i\u015fitme kay\u0131plar\u0131n\u0131n etiolojileri g\u00f6r\u00fclmektedir.<\/p>\n
\u0130letim tipi i\u015fitme kayb\u0131 nedenleri:<\/strong><\/p>\n Kond\u00fcktif i\u015fitme kayb\u0131 , d\u0131\u015f kulak kanal\u0131n\u0131n a\u011fz\u0131 ile koklean\u0131n t\u00fcyl\u00fc h\u00fccreleri aras\u0131nda yer alan, temelde i\u015fitsel uyaran\u0131n koklear resept\u00f6r h\u00fccrelere iletiminin engellenmesidir.<\/p>\n D\u0131\u015f kulak yolu kaynakl\u0131 patolojiler<\/p>\n Bu\u015fon<\/p>\n Yabanc\u0131 cisim<\/p>\n Kongenital aplazi veya atrezi<\/p>\n Ekzositoz<\/p>\n T\u00fcm\u00f6rler<\/p>\n Osteom<\/p>\n Kistler<\/p>\n Otitis eksterna<\/p>\n Orta kulak kaynakl\u0131 patolojiler<\/p>\n Akut otitis media ve ef\u00fczyonlu otitis media<\/p>\n Kronik otitis media ve kolesteatoma<\/p>\n Timpanoskleroz<\/p>\n Orta kulak travmas\u0131<\/p>\n Kemik zincir anomalileri<\/p>\n Otoskleroz<\/p>\n T\u00fcm\u00f6rler<\/p>\n Ge\u00e7irilmi\u015f orta kulak operasyonlar\u0131<\/p>\n Sens\u00f6rin\u00f6ral i\u015fitme kayb\u0131 nedenleri:<\/strong> Presbiakuzi<\/p>\n G\u00fcr\u00fclt\u00fcye ba\u011fl\u0131 i\u015fitme kayb\u0131<\/p>\n Ototoksisite<\/p>\n Ani idyopatik i\u015fitme kayb\u0131<\/p>\n Otoimm\u00fcn i\u00e7 kulak hastal\u0131\u011f\u0131<\/p>\n Meniere hastal\u0131\u011f\u0131<\/p>\n Kongenital sens\u00f6rin\u00f6ral i\u015fitme kay\u0131plar\u0131<\/p>\n Travma<\/p>\n Sifiliz<\/p>\n Menenjit<\/p>\n Multiple skleroz<\/p>\n Migren<\/p>\n Diabetes Mellitus<\/p>\n Paget Hastal\u0131\u011f\u0131<\/p>\n \u0130letim tipi i\u015fitme kay\u0131plar\u0131<\/p>\n D\u0131\u015f kulak kaynakl\u0131 patolojiler<\/p>\n Bu\u015fon:<\/strong> Muhtemelen en s\u0131k g\u00f6r\u00fclen iletim tipi i\u015fitme kayb\u0131 sebebidir. D\u00fczce \u00dcniversitesi T\u0131p Fak\u00fcltesi taraf\u0131ndan bir okulda yap\u0131lan kulak muayene bulgular\u0131nda kulak kiri en yayg\u0131n patoloji olarak g\u00f6r\u00fclm\u00fc\u015ft\u00fcr ( \u00c7ocuklar\u0131n % 39,4 \u00fcnde tesbit edilmi\u015ftir )45.<\/p>\n Yabanc\u0131 Cisim:<\/strong> Daha \u00e7ok \u00e7ocuklarda ve d\u0131\u015f kulak yolunda g\u00f6r\u00fclebilmekle birlikte, litarat\u00fcrde orta kulakta g\u00f6r\u00fcnt\u00fclenebilen yabanc\u0131 cisim yay\u0131nlar\u0131na da rastlanmaktad\u0131r46.<\/p>\n DKY Aplazisi ve DKY Stenozu : Embriyolojik geli\u015fimleri g\u00f6z \u00f6n\u00fcne al\u0131nd\u0131\u011f\u0131nda genellikle birlikte g\u00f6r\u00fclen bu iki deformite nadiren i\u00e7 kulak deformitesi i\u00e7erir. \u00dclkemizde M.Kebap\u00e7\u0131 ve arkada\u015flar\u0131n\u0131n yay\u0131nlad\u0131\u011f\u0131 \u0091’ Konjenital Aural Atrezililerde HRCT bulgular\u0131 konulu makalede bunu desteklemektedir47. Mikrotia %0.03 canl\u0131 do\u011fum s\u0131kl\u0131\u011f\u0131nda g\u00f6r\u00fcl\u00fcr. Bu hastalar\u0131n yar\u0131s\u0131nda ilgili bir sendrom bulunmaktad\u0131r55. Daha s\u0131k olarak erkeklerde ve sa\u011f kulakta g\u00f6r\u00fclmektedir.<\/p>\n DKY Egzostozisi :<\/strong> \u00d6zellikle y\u00fcz\u00fcc\u00fclerde g\u00f6r\u00fclen DKY kanal\u0131na do\u011fru kemik \u00e7\u0131k\u0131nt\u0131lar\u0131n\u0131n olu\u015fmas\u0131 \u015feklinde tan\u0131mlanan bu patoloji iletim tipi i\u015fitme kayb\u0131 sebeplerindendir. Avusturalya’da 300 s\u00f6rf tahtas\u0131 kullan\u0131c\u0131lar\u0131nda ger\u00e7ekle\u015ftirilen prevelans \u00e7al\u0131\u015fmas\u0131nda 90 erkek ve 10 bayan s\u00f6rf\u00e7\u00fcde anlaml\u0131 derecede ( DKY nun 2\/3 veya daha fazlas\u0131n\u0131 ) t\u0131kayacak kadar egzostoz saptanm\u0131\u015ft\u0131r. D\u00fczenli y\u00fczen ( 20 y\u0131ldan fazla ) her iki erkek s\u00f6rf\u00e7\u00fcden birinde ve her yedi bayan s\u00f6rf\u00e7\u00fcden \u00fc\u00e7\u00fcnde zamanla DKY kanal\u0131nda t\u0131kan\u0131kl\u0131\u011fa neden olacak derecede egzostoz geli\u015fti\u011fide bildirilmi\u015ftir48.<\/p>\n DKY T\u00fcm\u00f6rleri :<\/strong> Squam\u00f6z h’li Ca , Hollanda \u0091da yap\u0131lm\u0131\u015f bir \u00e7al\u0131\u015fmada bildirildi\u011fi \u00fczere d\u0131\u015f kulak yolu kanal\u0131n\u0131n nadir g\u00f6r\u00fclen bir hastal\u0131\u011f\u0131d\u0131r ve 5 y\u0131ll\u0131k survey % 35 ila % 65 aras\u0131ndad\u0131r50. Avusturalya’dan bildirilmi\u015f ba\u015fka bir makalede bu surveyi desteklemektedir. Burada DKY nun ve temporal kemik malignensisinin yayg\u0131n olmad\u0131\u011f\u0131 belirtilmi\u015f ve Prince \u0091deki Wales Hastanesinde 1974 \u00961995 y\u0131llar\u0131 aras\u0131nda tedavi edilen 59 hastal\u0131k seride 5 y\u0131ll\u0131k survey %54 olarak bildirilmi\u015ftir. Genellikle bu t\u00fcm\u00f6rler 40-60 ya\u015flar aras\u0131nda g\u00f6r\u00fcl\u00fcrler.<\/p>\n Osteomlar :<\/strong> Nadir benign t\u00fcm\u00f6rlerdendir. Genellikle tesad\u00fcfi olarak bulunur ve semptom vermez49.<\/p>\n Kistler: D\u0131\u015f kulak yolunda nadiren iletim tipi i\u015fitme kayb\u0131na neden olabilen kistlere rastlanabilir.<\/p>\n Otitis Externa :<\/strong> Tayland \u0091ta ya\u015flar\u0131 60-96 aras\u0131nda de\u011fi\u015fen 980 ki\u015filik ya\u015fl\u0131 pop\u00fclasyonda kulak hastal\u0131klar\u0131 prevelans\u0131na bak\u0131lm\u0131\u015f ve kulak kirinden sonra (% 8) ikinci en yayg\u0131n patoloji olarak otitis externa ( % 4.3) bildirilmi\u015ftir. Bir ba\u015fka \u00e7al\u0131\u015fmada otitis eksterna s\u0131kl\u0131\u011f\u0131 y\u0131lda 4\/1000 oran\u0131nda bildirilmi\u015ftir57.<\/p>\n Orta kulak kaynakl\u0131 patolojiler:<\/strong> Otitis media s\u0131kl\u0131\u011f\u0131 iklimden ba\u011f\u0131ms\u0131z olarak, kalabal\u0131k ortamlarda daha fazla bulunmaya ba\u011fl\u0131 olarak k\u0131\u015f aylar\u0131nda artmaktad\u0131r.<\/p>\n Teele taraf\u0131ndan belirlenen otitis media i\u00e7in risk fakt\u00f6rleri erkek cinsiyet, erken otitis media ata\u011f\u0131 ge\u00e7irmek, biberonla beslenme ve otitis media ata\u011f\u0131 ge\u00e7irmi\u015f bir akrabaya sahip olmak olarak s\u0131ralanabilir28. Daha sonralar\u0131 Pulander, Karma ve Sipil allerjiyi, sosyoekonomik durumu, ge\u00e7irilen viral enfeksiyonlar\u0131, annenin sigara i\u00e7iyor olmas\u0131n\u0131 ve ebeveynlerinde otitis media ataklar\u0131 olmas\u0131n\u0131 da risk fakt\u00f6rleri olarak g\u00f6stermi\u015flerdir. D\u00fc\u015f\u00fck do\u011fum a\u011f\u0131rl\u0131\u011f\u0131 bir risk fakt\u00f6r\u00fc de\u011fildir. Anne s\u00fct\u00fc ise sadece al\u0131nd\u0131\u011f\u0131 d\u00f6nemde koruyucu bir rol oynar, bunun d\u0131\u015f\u0131nda ileri d\u00f6nemler i\u00e7in bir koruyuculuk sa\u011flamaz.<\/p>\n Akut otitis media ve Ef\u00fczyonlu otitis media i\u00e7in risk fakt\u00f6rleri birlikte \u00e7al\u0131\u015f\u0131lm\u0131\u015ft\u0131r. \u00c7\u00fcnk\u00fc bu iki hastal\u0131k otitis media adl\u0131 hastal\u0131\u011f\u0131n 2 farkl\u0131 d\u00f6nemini simgelemektedirler. Ayr\u0131ca farkl\u0131 farkl\u0131 yap\u0131lan \u00e7al\u0131\u015fmalarda bu iki hastal\u0131\u011f\u0131n da ayn\u0131 risk fakt\u00f6rlerine sahip oldu\u011fu g\u00f6sterilmi\u015ftir.<\/p>\n Marmara \u00fcniversitesi T\u0131p Fak\u00fcltesi KBB A.D. da S. \u0130nanl\u0131 ve arkada\u015flar\u0131n\u0131n \u00dcsk\u00fcdar b\u00f6lgesinde yapt\u0131klar\u0131 bir \u00e7al\u0131\u015fmada okul \u00f6ncesi ve okul \u00e7a\u011f\u0131ndaki \u00e7ocuklarda sekretuar otitis media prevelans\u0131 ara\u015ft\u0131r\u0131lm\u0131\u015ft\u0131r54. Burada \u00e7al\u0131\u015fmaya al\u0131nan 539 \u00e7ocukta genel SOM prevelans\u0131 % 9 iken bu oran 3-6 ya\u015f grubunda %13.6 \/ 6-9 ya\u015f grubunda %7 olarak tesbit edilmi\u015ftir. Danimarka’da yap\u0131lan kapsaml\u0131 bir \u00e7al\u0131\u015fmada ef\u00fczyonlu otitis media epidemiolojisi \u00e7al\u0131\u015f\u0131lm\u0131\u015f ve ef\u00fczyonlu otitis median\u0131n timpanometrik inceleme ile kan\u0131tlanan prevalans\u0131 ara\u015ft\u0131r\u0131lm\u0131\u015ft\u0131r. Sonu\u00e7lar\u0131na g\u00f6re 1 ya\u015f\u0131ndaki bebeklerde Tip B veya Tip C2 timpanometrinin g\u00f6r\u00fclme s\u0131kl\u0131\u011f\u0131 %24 bulunmu\u015ftur33. Bununla birlikte timpanometrilerin en s\u0131k Tip B olarak kar\u015f\u0131m\u0131za \u00e7\u0131kt\u0131\u011f\u0131 ya\u015f gurubu 2-4 ya\u015f olarak kar\u015f\u0131m\u0131za \u00e7\u0131km\u0131\u015ft\u0131r. Timoanometri ile kan\u0131tlanan ef\u00fczyonlu otitis media prevalans\u0131 6-7 ya\u015flar\u0131ndan sonra azalmaya ba\u015flamaktad\u0131r.<\/p>\n Tarihsel olarak otitis media \u00f6staki t\u00fcp fonksiyonuna ba\u011fl\u0131 bir hastal\u0131k olarak g\u00f6r\u00fclmektedir. Temelde \u00f6staki borusu 3 \u00f6nemli fonksiyona sahiptir ve bunlar orta kulak havalanmas\u0131, temizlenmesi ve enfeksiyondan korrunmas\u0131d\u0131r. \u00d6nceki \u00e7al\u0131\u015fmalarda akut otitis media etilojisinde t\u0131kal\u0131 \u00f6staki borusunun enfeksiyona yatk\u0131nl\u0131k yaratt\u0131\u011f\u0131ndan bahsedilirken, son \u00e7al\u0131\u015fmalarda akut otitis median\u0131n primer olarak bakterial enfeksiyona ba\u011fl\u0131 oldu\u011fu ve \u00f6staki disfonksyonunun buna sekonder olarak ortaya \u00e7\u0131kt\u0131\u011f\u0131ndan bahsedilmektedir. Akut otitis media etiolojisinde \u00fcniversal olarak ayn\u0131 patojenler etken olarak g\u00f6r\u00fclmektedir. En s\u0131k etkeni S.pn\u00f6monia’d\u0131r ve s\u0131ras\u0131yla H.influenza ve B.catarrhalis’e ba\u011fl\u0131 olarak g\u00f6r\u00fclmektedir. Ef\u00fczyonlu otitis media da ise \u00f6staki disfonksiyonu, patofizyolojinin tam merkezinde yer almaktad\u0131r. Ancak \u00f6staki disfonksiyonu primer bir problem olmaktan \u00e7ok inflamatuar bir duruma sekonder olarak olu\u015fmaktad\u0131r.<\/p>\n Kronik otitis media ve Kolesteatoma: KOM prevelans\u0131 \u0130srail de yap\u0131lan bir ara\u015ft\u0131rmada 100 000 ki\u015fide 39 olarak bildirilmi\u015ftir53. Hastal\u0131\u011f\u0131n genetik yap\u0131 ve sosyoekonomik seviye ile ili\u015fkili oldu\u011fu kabul edilir. Kolesteatoman\u0131n ger\u00e7ek prevalans\u0131 bilinmemektedir. 4.2\/100000 ki\u015fide kolesteatomal\u0131 kronik otitis media ve 13.8\/100000 ki\u015fide kolesteatomas\u0131z kronik otitis media g\u00f6r\u00fclmektedir40. Baz\u0131 \u00e7al\u0131\u015fmalarda kolesteatoma’l\u0131 kronik otitis media’n\u0131n \u00e7ocuklarda 3\/100000, eri\u015fkinlerde ise 12.6\/100000 oran\u0131nda g\u00f6r\u00fcld\u00fc\u011f\u00fc bildirilmi\u015ftir42. Kolesteatoma etiyolojisinde invajinasyon, epitelyal invazyon, bazal h\u00fccre hiperplazisi ve skuam\u00f6z metaplazi teorileri ayr\u0131 ayr\u0131 destek\u00e7iler bulmu\u015ftur. Kolesteatomas\u0131z kronik otitis media’da ise etiolojide son y\u0131llarda biofilmler tart\u0131\u015f\u0131lmaktad\u0131r.<\/p>\n Timpanoskleroz: Travmaya sekonder yada otitis media’n\u0131n bir komplikasyonu olarak ortaya \u00e7\u0131kmaktad\u0131r. \u00c7o\u011fu hastada bu kalsifiye hyalin plaklar i\u015fitme kayb\u0131na neden olmaz veya \u00e7ok hafif, klinik olarak \u00f6nemsiz i\u015fitme kayb\u0131na neden olurlar. Timpanosklerozdaki i\u015fitme kayb\u0131n\u0131n nedeni kemik zincirdeki fiksasyondur. Kronik otitis media’da timpanoskleroz insidans\u0131 %9-38 olarak bildirilmi\u015ftir. Kinney yapt\u0131\u011f\u0131 bir \u00e7al\u0131\u015fmada kronik otitis media nedeniyle opere edilen 1495 hastan\u0131n %20’sinde timpanoskleroz saptam\u0131\u015ft\u0131r3. Daly yay\u0131nlad\u0131\u011f\u0131 bir \u00e7al\u0131\u015fmada, 4 y\u0131ll\u0131k takipte, 5-15 ya\u015f aras\u0131 \u00e7ocuklar\u0131n ortalama %10’unda timpanoskleroz insidans\u0131 bildirmi\u015ftir1. Hussl ve Mueller yapt\u0131klar\u0131 \u00e7al\u0131\u015fmada timpanosklerozun kronik ef\u00fczyonlu otitis median\u0131n s\u0131k bir komplikasyonu oldu\u011funu bildirmi\u015flerdir2. Bu \u00e7al\u0131\u015fmada ef\u00fczyonlu otitis media i\u00e7in yerle\u015ftirilen ventilasyon t\u00fcplerinden 6-8 y\u0131l sonra kulak zarlar\u0131n\u0131n %19.7’sinde timpanoskleroz saptam\u0131\u015flard\u0131r. Ayr\u0131ca s\u0131k tekrarlayan akut otitis media sonras\u0131nda da timpanoskleroz g\u00f6r\u00fcld\u00fc\u011f\u00fcn\u00fc bildirmi\u015flerdir. Tos ve Stangerup ventilasyon t\u00fcp\u00fc tak\u0131lan kulaklarda (%59), sadece miringotomi yap\u0131lan kar\u015f\u0131 kulaklara g\u00f6re (%13) daha fazla timpanoskleroz saptam\u0131\u015flard\u0131r5. Magat ve arkada\u015flar\u0131 timpanostomi t\u00fcp\u00fc tak\u0131lan 1274 hastada yapt\u0131klar\u0131 bir \u00e7al\u0131\u015fmada timpanoskleroz insidans\u0131n\u0131 %23.6 olarak bildirmi\u015flerdir4.<\/p>\n Kulak travmas\u0131: Kulak travmalar\u0131 sonucunda iletim tipi i\u015fitme kayb\u0131 timpanik membran\u0131n perforasyonu sonucunda, k\u00fcnt bir travma sonras\u0131 olu\u015fabilecek olan hemotimpanum veya ossik\u00fcler dislokasyon sonras\u0131nda g\u00f6r\u00fclebilir. Ayr\u0131ca temporal kemik k\u0131r\u0131klar\u0131na ba\u011fl\u0131 olu\u015fan i\u00e7 kulak hasar\u0131nda da sens\u00f6rin\u00f6ral i\u015fitme kayb\u0131 g\u00f6r\u00fclebilir. T\u00fcm kulak travmalar\u0131na ba\u011fl\u0131 olu\u015fan i\u015fitme kayb\u0131 etiolojisi bu ba\u015fl\u0131k alt\u0131nda incelenmi\u015ftir. Eskiden motorlu ta\u015f\u0131t kazalar\u0131n\u0131n %75’ine kafa travmas\u0131 e\u015flik ediyordu. Son y\u0131llarda kasklar\u0131n ve emniyet kemerlerinin kullan\u0131ma girmesinden sonra bu oran azalm\u0131\u015ft\u0131r.<\/p>\n E\u011fer travma kafa kemiklerinde k\u0131r\u0131\u011fa yol a\u00e7abilecek kadar b\u00fcy\u00fckse %14-22 hastada temporal kemik frakt\u00fcr\u00fc g\u00f6r\u00fclmektedir6,7. Temporal kemik k\u0131r\u0131klar\u0131 i\u00e7in bug\u00fcne kadar yay\u0131nlanm\u0131\u015f en b\u00fcy\u00fck seride t\u00fcm temporal kemik k\u0131r\u0131klar\u0131n\u0131n %31’i motorlu ta\u015f\u0131t kazalar\u0131na ba\u011fl\u0131d\u0131r8. Temporal kemik k\u0131r\u0131klar\u0131 genellikle erkeklerde (3:1) ve gen\u00e7 ve orta ya\u015fl\u0131 eri\u015fkinlerde g\u00f6r\u00fclmektedir. Temporal kemik frakt\u00fcrlerinin %8-29’unun bilateral oldu\u011fu rapor edilmi\u015ftir. Eskiden temporal kemik k\u0131r\u0131klar\u0131 longitudinal veya transvers olarak s\u0131n\u0131fland\u0131r\u0131l\u0131rd\u0131 ancak \u00e7o\u011fu frakt\u00fcr\u00fcn oblik veya mikst olmas\u0131 dolay\u0131s\u0131yla bu klasifikasyon yerine otik kaps\u00fcl\u00fc i\u00e7ine alan k\u0131r\u0131klar veya almayan k\u0131r\u0131klar olarak yeni bir klasifikasyon olu\u015fturuldu8,9. Eski klasifikasyona g\u00f6re longitudinal k\u0131r\u0131klar %70-90 ve transvers k\u0131r\u0131klar %10-30 oran\u0131nda g\u00f6r\u00fclmektedir. Yeni klasifikasyona g\u00f6re k\u0131r\u0131klar\u0131n %2.5-5.8’i otik kaps\u00fcl\u00fc i\u00e7ine alan k\u0131r\u0131klar olarak bildirilmi\u015ftir8,10.<\/p>\n Otik kaps\u00fcl\u00fc ilgilendiren k\u0131r\u0131klar\u0131n \u00e7o\u011fu longitudinal planda saptanm\u0131\u015ft\u0131r10. Otik kaps\u00fcl\u00fc ilgilendiren k\u0131r\u0131klar\u0131n tamam\u0131na yak\u0131n\u0131 sens\u00f6rin\u00f6ral i\u015fitme kayb\u0131yla sonu\u00e7lan\u0131yor olsa da her zaman olmad\u0131\u011f\u0131n\u0131 bildiren yay\u0131nlar da vard\u0131r. Otik kas\u00fcl\u00fc i\u00e7ine almayan k\u0131r\u0131klar ise genellikle iletim tipi veya mikst tip i\u015fitme kayb\u0131yla sonu\u00e7lanmaktad\u0131r8. Hemotimpanum veya kanl\u0131 otore neredeyse t\u00fcm temporal kemik k\u0131r\u0131klar\u0131nda g\u00f6r\u00fclmektedir. Travmatik timpanik membran perforasyonlar\u0131 genellikle spontan olarak iyile\u015fmektedir ve acil m\u00fcdehale gerektirmemektedir. Yap\u0131lan \u00e7al\u0131\u015fmalar sonucunda travmatik timpanik membran perforasyonu prevelans\u0131 ortalama y\u0131lda 1.4-8.6\/100000 oran\u0131nda bildirilmi\u015ftir. Temporal kemik k\u0131r\u0131klar\u0131 genellikle rivinus \u00e7enti\u011fi civar\u0131nda timpanik membran\u0131 y\u0131rtmaktad\u0131r. Bu k\u0131r\u0131klarda %20 oran\u0131nda ossik\u00fcler zincir ayr\u0131lmas\u0131 g\u00f6r\u00fclmektedir11. En s\u0131k g\u00f6r\u00fclen patoloji inkudostapedial eklem ayr\u0131lmas\u0131d\u0131r12. Temporal kemik travmalar\u0131 sonras\u0131 olu\u015fan iletim tipi i\u015fitme kayb\u0131 %80 oran\u0131nda herhangibir m\u00fcdehale gerektirmeden spontan olarak iyile\u015fmektedir13. E\u011fer iletim tipi i\u015fitme kayb\u0131 d\u00fczelmiyorsa muhtemelen kemik zincir patolojisi mevcuttur.<\/p>\n Kemik zincir anomalileri:<\/strong> Orta kulak kemik\u00e7ikleri i\u00e7inde geli\u015fimi en ge\u00e7 tamamlanan ve en \u00e7ok malformasyon g\u00f6r\u00fclen kemik\u00e7ik stapestir. Di\u011fer kemik\u00e7iklerin geli\u015fimi h\u0131zl\u0131d\u0131r.<\/p>\n Otoskleroz: De\u011fi\u015fken penetrans oranlar\u0131yla birlikte otozomal dominant ge\u00e7i\u015f karekteristi\u011fi g\u00f6steren herediter bir bozukluktur. Hastalar\u0131n 2\/3’\u00fc kad\u0131nd\u0131r. Genellikle i\u015fitme kayb\u0131 ge\u00e7 10’lu ya\u015flar ve erken 20’li ya\u015flarda ba\u015flasa da baz\u0131 hastalarda i\u015fitme kayb\u0131n\u0131n ba\u015flang\u0131c\u0131 40 ya\u015f\u0131na kadar gecikebilmektedir. Cerrahi olarak tan\u0131 alan en k\u00fc\u00e7\u00fck otoskleroz hastas\u0131 6 ya\u015f\u0131ndad\u0131r. Gebelik ve \u00f6strojen kullan\u0131m\u0131 ile k\u00f6t\u00fcle\u015febilmektedir. Otoskleroz’un prevalans\u0131 \u0131rklara g\u00f6re farkl\u0131l\u0131k g\u00f6stermektedir. Beyaz \u0131rkta erkeklerde %7.3, kad\u0131nlarda ise %10.3 oran\u0131nda g\u00f6r\u00fclmektedir44. Histopatolojik olarak otoskleroz tan\u0131s\u0131 alm\u0131\u015f hastalar\u0131n ancak %12.3’\u00fcnde stapes fikse olarak izlenmektedir. % 70 hastada hastal\u0131k bilateral olarak g\u00f6r\u00fclmektedir. Hamilelikte k\u00f6t\u00fcle\u015fti\u011fi bilinen hastal\u0131\u011f\u0131n hamilelikte ba\u015flamas\u0131 s\u0131kl\u0131\u011f\u0131 %10-17 aras\u0131nda bildirilmi\u015ftir. Eri\u015fkinlerde g\u00f6r\u00fclen herediter i\u015fitme kayb\u0131n\u0131n en s\u0131k nedeni olarak g\u00f6sterildi\u011fi bir \u00e7al\u0131\u015fmada, i\u015fitme kayb\u0131 olan se\u00e7ilmi\u015f pop\u00fclasyonda %2 oran\u0131nda bulunmu\u015ftur65.<\/p>\n T\u00fcm\u00f6rler: Orta kula\u011f\u0131 ilgilendiren primer benign ve malign bir\u00e7ok nadir t\u00fcm\u00f6r mevcuttur. Bunlar\u0131n i\u00e7inde baz\u0131lar\u0131 daha s\u0131k kar\u015f\u0131la\u015f\u0131lan problemler oldu\u011fundan \u00f6nem kazanmaktad\u0131r. Rabdomiyosarkom orta kulak ve mastoid b\u00f6lgenin \u00e7ocuklardaki en s\u0131k t\u00fcm\u00f6r\u00fcd\u00fcr. Paragangliomalar akustik n\u00f6rinomdan sonra en s\u0131k kar\u015f\u0131la\u015f\u0131lan temporal kemik t\u00fcm\u00f6rleridir.<\/p>\n Sens\u00f6rin\u00f6ral i\u015fitme kay\u0131plar\u0131:<\/strong> G\u00fcr\u00fclt\u00fcye ba\u011fl\u0131 i\u015fitme kayb\u0131:<\/strong> \u0130\u015fitme kayb\u0131n\u0131n en s\u0131k nedenlerinden birisidir. 1966-1971 y\u0131llar\u0131 aras\u0131nda incelenen 30.000 Macar’da g\u00fcr\u00fclt\u00fcye ba\u011fl\u0131 i\u015fitme kayb\u0131 %20 oran\u0131nda bulunmu\u015ftur15. Amerika Birle\u015fik Devletlerinde 30 milyon ki\u015fi g\u00fcr\u00fclt\u00fcye maruz kalmakta ve bunlardan 10 milyonunda i\u015fitme kayb\u0131 g\u00f6r\u00fclmektedir16.<\/p>\n Ototoksisite: Ototoksisite ge\u00e7ici veya kal\u0131c\u0131 i\u00e7 kulak disfonksyonuna neden olan kimyasal ajanlar veya ila\u00e7lar\u0131 i\u00e7ermektedir. Bir\u00e7ok kimyasal madde bu hasara neden olabilmektedir. Burada baz\u0131 s\u0131k kar\u015f\u0131la\u015f\u0131lan maddeler hakk\u0131nda epidemiolojik verilerden bahsedilecektir. Aminoglikozidler uzun y\u0131llard\u0131r ciddi enfeksiyonlar\u0131n tedavisinde kullan\u0131lan antibiyotiklerdir. Aminoglikozidlere ba\u011fl\u0131 ototoksisite, t\u00fcm ajanlar g\u00f6z \u00f6n\u00fcne al\u0131nd\u0131\u011f\u0131nda total olarak, %20 oran\u0131nda g\u00f6r\u00fclmektedir17. Bu ajanlar\u0131n toksik etkileri kullan\u0131m\u0131ndan g\u00fcnler veya haftalar sonra ortaya \u00e7\u0131kmaktad\u0131r. Aminoglikozidler ba\u015fta y\u00fcksek frekanslar\u0131 etkilemektedir, kullan\u0131m devam ederse konu\u015fma frekanslar\u0131 da etkilenmektedir. Aminoglikozidler i\u00e7 kulak ile etkile\u015ferek serbest oksijen radikali olu\u015fumu sonras\u0131 \u00f6zellikle d\u0131\u015f t\u00fcyl\u00fc h\u00fccrelerde toksisiteye neden olmaktad\u0131rlar.<\/p>\n Sisplatin bir\u00e7ok malign t\u00fcm\u00f6r\u00fcn tedavisinde kullan\u0131lan potent bir antineoplastik ajand\u0131r. Yap\u0131lan bir \u00e7al\u0131\u015fmada testis kanseri nedeniyle sisplatin verilen hastalar\u0131n %20’sinde kal\u0131c\u0131 i\u015fitme kayb\u0131 saptanm\u0131\u015ft\u0131r ve y\u00fcksek dozda sisplatin alan hastalarda i\u015fitme kayb\u0131 insidans\u0131 %50 olarak saptanm\u0131\u015ft\u0131r18. Pediatrik hastalarda sisplatin ototoksisitesini daha s\u0131k g\u00f6rmekteyiz. Furasemid ile ototoksisite yap\u0131lan bir \u00e7al\u0131\u015fmada %6 oran\u0131nda g\u00f6r\u00fclm\u00fc\u015ft\u00fcr19. Furosemidin neden oldu\u011fu ototoksisite plazmadaki serbest fraksiyonuyla do\u011fru orant\u0131l\u0131d\u0131r. Salisilatlar da i\u015fitme kayb\u0131na neden olmaktad\u0131rlar. Plazmadaki serbest salisilat miktar\u0131 i\u00e7 kulaktaki sens\u00f6rial h\u00fccrelerde e\u015fik potansiyeli art\u0131\u015f\u0131na neden olmaktad\u0131r ve serbest miktar artt\u0131k\u00e7a i\u015fitme kayb\u0131n\u0131n derinli\u011fi de artmaktad\u0131r20. Malarya tedavisinde kullan\u0131lan Kinin’e ba\u011fl\u0131 i\u015fitme kayb\u0131 kullanan hastalar\u0131n %20’sinde bildirilmi\u015ftir. Makrolid antibiyotikler ve Vankomisin de ototoksik antibiyotiklerden baz\u0131lar\u0131d\u0131r.<\/p>\n Ani idyopatik i\u015fitme kayb\u0131:<\/strong> Ortalama insidans\u0131 y\u0131lda 1\/5000 ile 1\/20000 ki\u015fi aras\u0131nda de\u011fi\u015fmektedir. Her ya\u015fta g\u00f6r\u00fclebilmekteyse de en s\u0131k olarak 50-60 ya\u015flar aras\u0131 g\u00f6r\u00fclmektedir. Erkek kad\u0131n oran\u0131 farkl\u0131l\u0131k g\u00f6stermemektedir. Simultane olarak bilateral g\u00f6r\u00fclme olas\u0131l\u0131\u011f\u0131 \u00e7ok d\u00fc\u015f\u00fckt\u00fcr. Etiolojide viral enfeksiyonlar, vask\u00fcler t\u0131kan\u0131kl\u0131k, otoimm\u00fcnite ve intrakoklear zar y\u0131rt\u0131klar\u0131 su\u00e7lan\u0131yor olsa da en s\u0131k idyopatik olarak g\u00f6r\u00fclmektedir. Ani i\u015fitme kay\u0131pl\u0131 hastalar\u0131n %28’i hikayede son 1 ayda ge\u00e7irilmi\u015f viral \u00dcSYE tan\u0131mlamaktad\u0131rlar. Vask\u00fcler nedenler de etiyolojide incelenmi\u015ftir ancak ger\u00e7ekte \u00e7ok az hastada ger\u00e7ekten vask\u00fcler etiyoloji ortaya konabilmi\u015ftir.<\/p>\n Otoimm\u00fcn i\u00e7 kulak hastal\u0131\u011f\u0131: Primer otoimm\u00fcn i\u00e7 kulak hastal\u0131\u011f\u0131 nadir bir durumdur. Kesin tan\u0131 koydurabilen bir tan\u0131 metodu olmad\u0131\u011f\u0131ndan ger\u00e7ek insidans\u0131 bilinmemektedir. Ancak y\u0131lda 1\/5000-1\/20000 insidans\u0131nda g\u00f6r\u00fclen ani i\u015fitme kayb\u0131ndan daha nadir bir hastal\u0131kt\u0131r. Multisistemik otoimm\u00fcn hastal\u0131klarda kulak tutulumu Wegener gran\u00fclomatozu ve Cogan hastal\u0131\u011f\u0131 haricinde nadirdir. Wegener gran\u00fclomatozu tan\u0131s\u0131 olan hastalar\u0131n %30-50’sinde kulak tutulumu g\u00f6r\u00fclmektedir.<\/p>\n Meniere hastal\u0131\u011f\u0131: Meniere hastal\u0131\u011f\u0131 insidans\u0131 bir\u00e7ok \u00e7al\u0131\u015fmada farkl\u0131 olarak bildirilmi\u015ftir. \u0130ngiltere’de 157\/100000, \u0130sve\u00e7’te 46\/100000, Fransa’da 7.5\/100000 olarak saptanm\u0131\u015ft\u0131r. Meniere hastal\u0131\u011f\u0131 genellikle beyaz \u0131rk\u0131 etkilemektedir ve kad\u0131nlarda bir miktar daha s\u0131k g\u00f6r\u00fclmektedir. Genelde tek tarafl\u0131 olan hastal\u0131k daha nadiren bilateral de olabilir.<\/p>\n Kongenital sens\u00f6rin\u00f6ral i\u015fitme kay\u0131plar\u0131: Kongenital sens\u00f6rin\u00f6ral i\u015fitme kayb\u0131n\u0131n g\u00f6r\u00fclme s\u0131kl\u0131\u011f\u0131 1-3\/1000 canl\u0131 do\u011fum olarak bulunmu\u015ftur. Derin kongenital sens\u00f6rin\u00f6ral i\u015fitme kayb\u0131 olan ki\u015filerin oran\u0131 ise 1\/1000 canl\u0131 do\u011fumdur. Connely ve arkada\u015flar\u0131 yapt\u0131klar\u0131 \u00e7al\u0131\u015fmada risk fakt\u00f6r\u00fc olmayan pop\u00fclasyonda yenido\u011fanlarda i\u015fitme kayb\u0131 s\u0131kl\u0131\u011f\u0131n\u0131 1\/811 ve risk fakt\u00f6r\u00fc olan pop\u00fclasyonda bu oran\u0131 1\/75 olarak bulmu\u015flard\u0131r58. Bu durumun %30 nedeni sendromik sens\u00f6rin\u00f6ral i\u015fitme kay\u0131plar\u0131 iken % 70 nedeni non sendromik i\u015fitme kay\u0131plar\u0131d\u0131r. Non sendromik i\u015fitme kay\u0131plar\u0131n\u0131n %18’i otozomal dominant, %80’i otozomal resesif ve %2’si ise X-linked veya mitokondrial kal\u0131t\u0131m \u00f6zelli\u011fi g\u00f6stermektedir. T\u00fcrkiye’de \u0130stanbul ve Zonguldak’ta i\u015fitme kayb\u0131 olan \u00e7ocuklar aras\u0131nda yap\u0131lan epidemiolojik bir \u00e7al\u0131\u015fmada, i\u015fitme kay\u0131plar\u0131n\u0131n %62.9’unun genetik k\u00f6kenli oldu\u011fu bulunmu\u015ftur59. Bu \u00e7al\u0131\u015fmada geli\u015fmekte olan \u00fclkelerde kongenital i\u015fitme kay\u0131plar\u0131n\u0131n geli\u015fmi\u015f \u00fclkelerden \u00e7ok daha s\u0131k oldu\u011fu vurgulanm\u0131\u015ft\u0131r.<\/p>\n 200’\u00fcn \u00fczerinde sendrom kongenital i\u015fitme kayb\u0131yla alakal\u0131 olarak bulunsa da bunlardan r\u00f6latif olarak daha s\u0131k g\u00f6r\u00fclenlerin epidemiolojik verileri a\u015fa\u011f\u0131da s\u0131ralanm\u0131\u015ft\u0131r.<\/p>\n BRANK\u0130O-OTO-RENAL SENDROM:<\/strong> Otozomal dominant kal\u0131t\u0131m g\u00f6sterir. Prevalans\u0131 1\/40000 yenido\u011fand\u0131r. Derin i\u015fitme kayb\u0131 olan \u00e7ocuklar\u0131n %2’sini olu\u015fturmaktad\u0131r. Mutasyon EYA-1 genindedir.<\/p>\n N\u00d6ROF\u0130BROMATOZ\u0130S T\u0130P 2:<\/strong> Otozomal dominant kal\u0131t\u0131m g\u00f6sterir. Prevalans\u0131 1\/40000 ile 1\/90000 do\u011fumdur34. 22. kromozomda merlin proteinini kodlayan gende mutasyon mevcuttur.<\/p>\n ST\u0130CKLER SENDROMU:<\/strong> Otozomal dominant kal\u0131t\u0131m g\u00f6stermektedir. Prevalans\u0131 1\/10000 do\u011fumdur35. COL2A1, COL2A2 veya CO11A1 genlerindeki mutasyona ba\u011fl\u0131 olarak olu\u015fmaktad\u0131r. Bu genler kollajen tip 2 veya tip 11’i kodlamaktad\u0131rlar.<\/p>\n WAARDENBURG SENDROMU: Otozomal dominant kal\u0131t\u0131m \u00f6zelli\u011fi g\u00f6stermektedir. Prevalans\u0131 1\/10000 ile 1\/20000 aras\u0131nda de\u011fi\u015fmektedir. Tip 1 Waardenburg sendromu PAX3 geni, Tip 2 MITF geni, Tip 3 PAX3 geni ve Tip 4 Waardenburg Sendromu da EDN3, EDNRB ve SOX10 genleri mutasyonlar\u0131 sonucunda olu\u015fmaktad\u0131r.<\/p>\n TREACHER-COLL\u0130NS SENDROMU: Otozomal dominant kal\u0131t\u0131m g\u00f6stermektedir. Treacle proteinini kodlayan TCOF geni mutasyonu sonucunda olu\u015fmaktad\u0131r.<\/p>\n PENDRED SENDROMU: Otozomal resesif kal\u0131t\u0131m \u00f6zelli\u011fi g\u00f6stermektedir. En s\u0131k olarak kongenital i\u015fitme kayb\u0131 nedeni olan sendromdur. Prevalans\u0131 1\/10000 ki\u015fidir. Herediter sa\u011f\u0131rl\u0131k vakalar\u0131n\u0131n %10’unu olu\u015fturmaktad\u0131r39. SLL26A4 gen mutasyonu sonucunda olu\u015fmaktad\u0131r.<\/p>\n USHER SENDROMU: Otozomal resesif kal\u0131t\u0131m \u00f6zelli\u011fi g\u00f6stermektedir. Prevalans\u0131 1\/20000 ile 1\/25000 ki\u015fi aras\u0131nda de\u011fi\u015fmektedir. Herediter i\u015fitme kay\u0131plar\u0131n\u0131n %5’ini olu\u015fturmaktad\u0131r. Hem sa\u011f\u0131r hem k\u00f6rlerin toplumda %50’sinin nedeni olarak kar\u015f\u0131m\u0131za \u00e7\u0131kmaktad\u0131r. En s\u0131k mutasyonlar\u0131n MYO2A ve USH2A genlerinde oldu\u011fu heterojen bir grubu temsil etmektedir.<\/p>\n ALPORT SENDROMU: X’e ba\u011fl\u0131 kal\u0131t\u0131m \u00f6zelli\u011fi g\u00f6stermektedir. COL4A5 gen mutasyonu sonucunda olu\u015fmaktad\u0131r. Bu gen mutasyonu 1\/5000 do\u011fumda bir g\u00f6r\u00fclmektedir.<\/p>\n Non sendromik i\u015fitme kay\u0131plar\u0131 bir\u00e7ok gen mutasyonuna ba\u011fl\u0131 olu\u015fan, i\u015fitme kayb\u0131na ba\u015fka anomalilerin e\u015flik etmedi\u011fi hastal\u0131k grubunu olu\u015fturmaktad\u0131r.<\/p>\n DFNB1 MUTASYONU: Non sendromik herediter i\u015fitme kay\u0131plar\u0131nda g\u00f6r\u00fclen en s\u0131k mutasyondur. Otozomal resesif ge\u00e7i\u015f \u00f6zelli\u011fi g\u00f6stermektedir. Connxin 26’y\u0131 kodlayan GJB’ gen mutasyonu sonucunda olu\u015fmaktad\u0131r. Otozomal resesif ge\u00e7i\u015fli i\u015fitme kay\u0131plar\u0131n\u0131n %50’sini olu\u015fturmaktad\u0131r36. Irklara g\u00f6re ta\u015f\u0131y\u0131c\u0131l\u0131k oran\u0131 de\u011fi\u015fmekle birlikte mutasyonun ortalama g\u00f6r\u00fclme s\u0131kl\u0131\u011f\u0131 %3 civar\u0131ndad\u0131r.<\/p>\n Menenjit: Geli\u015fmekte olan \u00fclkelerde menenjit s\u0131k g\u00f6r\u00fclen bir hastal\u0131kt\u0131r. Menenjitin en s\u0131k n\u00f6rolojik sekeli i\u015fitme kayb\u0131 olmaktad\u0131r. Etiyopya kaynakl\u0131 bir \u00e7al\u0131\u015fmada menenjit sonras\u0131 taburcu edilen \u00e7ocuklarda i\u015fitme kayb\u0131n\u0131n s\u0131kl\u0131\u011f\u0131 %25 olarak bildirilmi\u015ftir60. Hollanda’da 628 non-Hib menenjit ge\u00e7iren hastada yap\u0131lan bir \u00e7al\u0131\u015fmada i\u015fitme kayb\u0131 s\u0131kl\u0131\u011f\u0131 %7 olarak bulunmu\u015ftur62. Bu da g\u00f6stermektedir ki d\u00fc\u015f\u00fck sosyoekonomik d\u00fczey nedeniyle i\u015fitme kayb\u0131 sekeli daha s\u0131k olarak ortaya \u00e7\u0131kmaktad\u0131r.<\/p>\n Kistik Fibrozis: \u0130spanya’da Kistik fibrozis nedeniyle takip edilen hastalar aras\u0131nda yap\u0131lan bir epidemiolojik \u00e7al\u0131\u015fmada i\u015fitme kayb\u0131 prevalans\u0131 %28.56 olarak bulunmu\u015ftur63. Burada ototoksik antibiyotiklerin kullan\u0131m\u0131n\u0131n bu oran\u0131 artt\u0131raca\u011f\u0131 da vurgulanm\u0131\u015ft\u0131r.<\/p>\n Sifiliz: Kongenital veya akkiz sifiliz sens\u00f6rin\u00f6ral i\u015fitme kayb\u0131 ile ili\u015fkili bulunmu\u015ftur. Kongenital sifilizde %17, ge\u00e7 latent sifilizde %25 ve semptomatik n\u00f6rosifilizde %80 s\u0131kl\u0131kta i\u015fitme kayb\u0131 bildirilmi\u015ftir21.<\/p>\n Multiple skleroz: Multiple skleroz hastalar\u0131n\u0131n %4 ile %10’u oran\u0131nda sens\u00f6rin\u00f6ral i\u015fitme kayb\u0131 g\u00f6r\u00fclmektedir22,23. Bilateral, unilateral , ani ba\u015flang\u0131\u00e7l\u0131 veya yava\u015f ba\u015flang\u0131\u00e7l\u0131 olabilir. Bayanlarda daha s\u0131kt\u0131r ve 20-30 ya\u015flar en s\u0131k g\u00f6r\u00fcld\u00fc\u011f\u00fc d\u00f6nemdir.<\/p>\n Migren: Migren hastalar\u0131nda semptomlara baz\u0131 odyovestibular \u015fikayetler e\u015flik edebilir. \u00d6zellikle baziler migren alt tipinde bilateral i\u015fitme kayb\u0131 insidans\u0131 %46 olarak saptanm\u0131\u015ft\u0131r, tek tarafl\u0131 i\u015fitme kayb\u0131 insidans\u0131 da %34 olarak saptanm\u0131\u015ft\u0131r24.<\/p>\n Diabetes Mellitus:<\/strong> Diabetes Mellitus hastalar\u0131nda artm\u0131\u015f vask\u00fcler patoloji riski nedeniyle artm\u0131\u015f i\u015fitme kayb\u0131 insidans\u0131 beklense de bunun b\u00f6yle oldu\u011funu kan\u0131tlayan hi\u00e7bir delil elde edilememi\u015ftir.<\/p>\n Paget Hastal\u0131\u011f\u0131: Paget hastal\u0131\u011f\u0131 40 ya\u015f\u0131ndaki pop\u00fclasyonun %3’\u00fcn\u00fc, 80 ya\u015f\u0131ndaki pop\u00fclasyonun %11’ini etkileyen s\u0131k bir hastal\u0131kt\u0131r. Paget hastal\u0131\u011f\u0131nda i\u015fitme kayb\u0131 %5-%44 oran\u0131nda g\u00f6r\u00fclmektedir ve genelde sens\u00f6rin\u00f6ral veya mikst tiptedir56.<\/p>\n Beh\u00e7et Hastal\u0131\u011f\u0131: T\u00fcrkiyede nispeten s\u0131k g\u00f6r\u00fclen bir hastal\u0131k olan Beh\u00e7et Hastal\u0131\u011f\u0131 i\u015fitme kayb\u0131na neden olabilmektedir. T\u00fcrkiye’de yap\u0131lan bir \u00e7al\u0131\u015fmada Beh\u00e7et Hastal\u0131\u011f\u0131nda i\u015fitme kayb\u0131n\u0131n s\u0131kl\u0131\u011f\u0131 %55 olarak bulunmu\u015ftur ve bunun \u00e7o\u011fu y\u00fcksek frekanslar\u0131 ilgilendiren kay\u0131pt\u0131r61.<\/p>\n Referanslar<\/strong> \u0130\u015fitme kayb\u0131, toplumlarda b\u00fcy\u00fck pop\u00fclasyonlar\u0131 etkileyen, para, i\u015f g\u00fcc\u00fc kayb\u0131 ve hayat kalitesinde azalmaya neden olan maj\u00f6r bir sa\u011fl\u0131k problemidir. Sadece g\u00fcr\u00fclt\u00fc ve travmaya ba\u011fl\u0131 olarak ABD’de 10 milyon ki\u015fi kal\u0131c\u0131, geri d\u00f6n\u00fc\u015fs\u00fcz i\u015fitme kayb\u0131na …<\/p>\n","protected":false},"author":1,"featured_media":3724,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[18],"tags":[656,40,158,36,37],"class_list":["post-3723","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-kulak-burun-bogaz","tag-656","tag-calisma","tag-hastaligi","tag-isitme-kaybi","tag-yas"],"_links":{"self":[{"href":"https:\/\/odyova.com\/haberler\/wp-json\/wp\/v2\/posts\/3723","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/odyova.com\/haberler\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/odyova.com\/haberler\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/odyova.com\/haberler\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/odyova.com\/haberler\/wp-json\/wp\/v2\/comments?post=3723"}],"version-history":[{"count":1,"href":"https:\/\/odyova.com\/haberler\/wp-json\/wp\/v2\/posts\/3723\/revisions"}],"predecessor-version":[{"id":3725,"href":"https:\/\/odyova.com\/haberler\/wp-json\/wp\/v2\/posts\/3723\/revisions\/3725"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/odyova.com\/haberler\/wp-json\/wp\/v2\/media\/3724"}],"wp:attachment":[{"href":"https:\/\/odyova.com\/haberler\/wp-json\/wp\/v2\/media?parent=3723"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/odyova.com\/haberler\/wp-json\/wp\/v2\/categories?post=3723"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/odyova.com\/haberler\/wp-json\/wp\/v2\/tags?post=3723"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}
Sensorin\u00f6ral i\u015fitme kayb\u0131 ya koklean\u0131n sensoryal u\u00e7 organdaki ya da merkezi sinir sistemine uzanan n\u00f6ral iletim yolundaki defektlere ba\u011fl\u0131d\u0131r. Bu defekt, ya i\u00e7 kulak duyu organ\u0131n\u0131n akustik enerjiyi elektrik enerjisine d\u00f6n\u00fc\u015ft\u00fcrmesi veya n\u00f6ral impulslar\u0131n merkeze iletimi s\u00fcrecinde ortaya \u00e7\u0131kar.<\/p>\n
Akut ve ef\u00fczyonlu otitis media: Kulakta en s\u0131k g\u00f6r\u00fclen hastal\u0131klardan birisidir. Amerika Birle\u015fik Devletlerinin g\u00fcneyinde yap\u0131lan bir \u00e7al\u0131\u015fmada, \u00e7al\u0131\u015fmaya kat\u0131lan \u00e7ocuklar\u0131n %84’\u00fcnde en az bir otitis media ata\u011f\u0131, %50’sinde 3 veya daha fazla otitis media ata\u011f\u0131 ve %25’inde 6 veya daha fazla otitis media ata\u011f\u0131 ge\u00e7irdikleri g\u00f6r\u00fclm\u00fc\u015ft\u00fcr26. B\u00fcy\u00fck Boston Otitis Media \u00e7al\u0131\u015fmas\u0131nda \u00e7ocuklar\u0131n %93’\u00fcnde en az bir Otitis media ata\u011f\u0131, %74’\u00fcnde en az 3 veya daha fazla otitis media ata\u011f\u0131 ge\u00e7irdikleri saptanm\u0131\u015ft\u0131r27. ABD’de son y\u0131llarda prevalans\u0131n giderek artmakta oldu\u011fu g\u00f6r\u00fclmektedir. En y\u00fcksek prevalans ilk 2 ya\u015fta g\u00f6r\u00fclmektedir ve otitis media s\u0131kl\u0131\u011f\u0131 ya\u015f artt\u0131k\u00e7a azalmaktad\u0131r.<\/p>\n
Presbiakuzi: Bir etiolojinin ortaya konamad\u0131\u011f\u0131 ya\u015fl\u0131l\u0131k ile ili\u015fkili i\u015fitme kayb\u0131d\u0131r. Genellikle i\u015fitme kayb\u0131 sens\u00f6rin\u00f6raldir ve y\u00fcksek frekanslarda yo\u011funla\u015fmaktad\u0131r. Bu konuda epidemiolojik \u00e7al\u0131\u015fma yapmak \u00e7ok g\u00fc\u00e7t\u00fcr, \u00f6zellikle g\u00fcr\u00fclt\u00fcye ba\u011fl\u0131 i\u015fitme kay\u0131plar\u0131n\u0131 \u00e7al\u0131\u015fma gruplar\u0131ndan ay\u0131klamak neredeyse imkans\u0131zd\u0131r. \u0130\u015fitme kayb\u0131n\u0131n en s\u0131k nedenidir. 65 ya\u015f \u00fcst\u00fc pop\u00fclasyonda %30 oran\u0131nda g\u00f6r\u00fclmektedir14. 75 ya\u015f \u00fczeri pop\u00fclasyonda %50’ye \u00e7\u0131kmaktad\u0131r. Ya\u015fl\u0131l\u0131\u011fa ba\u011fl\u0131 i\u015fitme kayb\u0131 erkek hastalarda daha ciddi olmaktad\u0131r. Kore’de yap\u0131lan bir \u00e7al\u0131\u015fmada 65 ya\u015f \u00fczeri risk fakt\u00f6r\u00fc olmayan pop\u00fclasyonda presbiakuzi g\u00f6r\u00fclme s\u0131kl\u0131\u011f\u0131 %37.8 olarak bulunmu\u015ftur64.<\/p>\n
Daly K: Risk factors for otitis media sequelae and chronicity, Ann Otol Rhinol Laryngol 103:39, 1994.
Hussl B, Mueller K: Physiology and pathophysiology of eustachian tube and middle ear, New York, 1980, Thieme-Stratton.
Kinney SE: Postinflammatory ossicular fixation in tympanoplasty, Laryngoscope 88:821, 1978.
Magat KS, Morrison GA, Ganniwala TM: T-tubes: a retrospective review of 1274 insertion over a 4-year period, Int J Ped Otorhinolaryngol 25:119, 1993.
Tos M, Stangerup SE: Hearing loss in tympanosclerosis caused by grommets, Arch Otolaryngol 115:931, 1989.
Nageris B and others: Temporal bone fractures, Am J Emerg Med 12:211, 1995.
Virapongse and others: Radiography of the abnormal ear, Philadelphia, 1987.
Brodie HA, Thompson TC: Management of complications from820 temporal bone fractures, Am J Otol 18:188, 1997.
Kelly KE and others: Temporal bone and skull trauma, Neurootology, 1994.
Dahiya R and others: Temporal bone fractures, J Trauma 47:1079, 1999.
Cannon CR and others: Temporal bone fractures, Arch Otolaryngol 109:285, 1983.
Hough JVD and others: Middle ear injuries in skull trauma, Laryngoscope 78:899, 1968.
Tos M: Course of and sequela to 248 petrousal fractures, acta Otolaryngol 75:353, 1973.
Dobie RA: Medical-legal evaluation of hearing loss, New York, 1993.
Surjan L and others: Epidemiology of hearing loss, Audiology 12:396-410.
American Speech-Language Hearing Association (1991)
Forge A, Schacht J: Aminoglycoside antibiotics, Audiol Neuro-Otol 5:3-22, 2000.
Bokemeyer C and others: Analysis of risk factors for cisplatin induced ototoxicity in patients with testicular cancer, Br J Cancer 77:1355, 1998.
Tuzel IJ: Comparison of adverse reactions to bumetanide and furosemide, J Clin Pharmacol 21:615, 1981.
Myers EN and others: Salicylate ototoxicity, Arch Otolaryngol 82:483, 1965.
Schuknecht HF: Pathology of the ear, 1993.
Grenman R: \u0131nvolvement of the audiovestibular system in multiple sclerosis, Acta Otolaryngol Suppl 420:1, 1985.
Noffsinger D and others: Auditory and vestibular aberrations in multiple sclerosis, Acta Otolaryngol Suppl 303:1, 1972.
Olsson JE: Neurotologic findings in basilar migraine, Laryngoscope 101:1, 1991.
The epidemiology of hearing loss study: Cruickshanks KJ et al., Am J Epidemiol. 1998 Nov 1;148(9):879-86.
Brownlee RC Jr and others: Otitis media in children, J Pediatr 75:636-642,1969.
Casselbrant ML and others: Otitis media in a population of black and white American infants, \u0130nt J Pediatr Otorhinolaringol 33:1-16, 1995.
Teele DW and others: Epidemiolgy of otitis media during the first seven years of life in children, J \u0130nfect Dis 160:83-94, 1989.
Center for disease control: Vital and Health statistics, Series 10: Data from the national health survey #190, pp 95-1518.
Henderson FW and others: A longitudinal study of respiratory viruses and bacteria in acut otitis media with effusion, N Eng J Med 306:1377-1383, 1982.
Howie VM and others: The otitis prone condition Am J Dis Child 129:676-678, 1975.
Ingvarsson L and others: Epidemiology of acute otitis media in children, Acta Otolaryngol Suppl 388:1-52, 1982.
Tos M and others: Spontaneous course and frequency of secretory otitis media, Arch Otolaryngol 108:4-10, 1982.
Kang BS and others: The structure of FERM domain of merlin, Neurofibromatosis type2 product, Acta Crystallogr D Biol Crystallogr 58:382, 2002.
Admiraal RJ and others: Hearing impairment in Stickler syndrome, Adv Otorhinolaryngol 61:216, 2002.
Smith RJ and others: Genetic testing for deafness GJB2 and SLC26A4 as causes of deafness, J Comm Disord 35:367, 2002.
Newton VE and others: Clinical features of Waardenburg syndromes, Adv Otorhinolaryngol 61:201, 2002.
Morton N: Genetic epidemiology of hearing impairment, Ann NY Acad Sci 630:16, 1991.
Stinckens C and others: Pendred Syndrome Redefined, Adv Otorhinolaryngol 61:131, 2002.
Harker LA: Cholesteatoma: An incidence study, Cholesteatoma first international congress 1977.
Ruben RJ: The Disease in society: Evaluation of chronic otitis media Cholesteatoma and mastoid surgery, 1982.
Tos M: \u0130ncidence, etiology and pathogenesis of cholesteatoma in childeren Ann Otol Rhinol Larygol 40:110, 1988.
House JW and others: stapedectomy in children, Laryngoscope 90:1804, 1980.
Altmann FN and others: The incidence of otosclerosis, Ann Otol Rhinol Laryngol 76:377, 1967.
Ear examination findings at the Yeditepe School for the Deaf , Egeli E.ve ark. ( \u0130nt j.Pediatr Otorhino \u0096 laryngol 2003 Aug ; 67(8) : 905-910
High resolution CT of the petrous bone for locating a foreign body in the middle ear. Becker C. And att all. ( Article in German \u0096 Rontgenpraxis. 1995 Aug.; 48 (8) : 245-246.
Ear diseases and hearing in the Thai elderly population . Bunnag C., Department of Otolarngology , Fakulty of Medicine Siriraj Hospital , Mahidol Univesity , Bangkok , Thailand-( J. Med Assoc. Thai. 2002 May ; 85 (5) : 521-531
HRCT findings in congenital aural atresia . Kebapc\u0131 M, Kaya T, Adap\u0131nar B, \u00d6zkan R, Osmangazi \u00dcTF Radyoloji A.D.Eski\u015fehir ( Tan\u0131 Giri\u015fim Radyol.2003 mart; 9(1) : 47-53 )
Prevelance of external auditory canal exostoses in australian surfboard riders. Hurst W, Department of Otolaryngology , Frankstan Hospital . ( J. Laryngol Otol . 2004 . May ; 118(5) : 348-351
Osteoma of the ear canal presenting with headocha Shenay P, Paulose KO, Department of Ear, Nose and Throat , Bahrein Defence Force Hospital, State of Bahrein. (J. Laryngol Otol .1989 Jul; 103(7) 683-684
Squamous carcinoma of the external auditory canal : a different approach . Knegt PP, The Department of Otolaryngology and Head Neck Surgery . University Hospital Rotterdam, The Netherlands . ( Clin Otolaryngol. 2002 Jun ; 27(3) : 183-187
Malignancies of the external auditory canal and temporal bone ; a review . Yeung P, \/ Department of Otolaryngology Head and Neck Surgery, Prince of Waks Hospital , Randwick , New Sauth Wales , Australia ( ANZ J. Surg. 2002 Feb ; 72(2) : 114-120)
Prof. Dr. Recep \u00dcnal KOM Semineri
\u0130nanl\u0131 s ve arkada\u015flar\u0131, Turk Arch ORL , 2000 ; 38 (1) 9: 16.
Schuknecht HF: Congenital aural atresia and congenital middle ear cholesteatoma, New York, 1993.
Davies DG: Paget’s disease of the temporal bone, Acta Otolaryngol Suppl 242:1, 1968.
Guthrie RM: Diagnosis and treatment of otitis externa, Ann Otol Rhinol Laryngol Suppl 176:1, 1999.
Connolly JL, Carron JD, Roark SD: Universal newborn hearing screening, Laryngoscope. 2005 Feb;115(2):232-6.
Silan F, Demirci L, Egeli A, Egeli E, Onder HI, Ozturk O, Unal ZS: Syndromic etiology in children at schools for the deaf in Turkey, Int J Pediatr Otorhinolaryngol. 2004 Nov;68(11):1399-406.
Melaku A: Sensorineural hearing loss in children with epidemic meningococcal meningitis at Tikur Anbessa Hospital, Ethiop Med J. 2003 Apr;41(2):113-21.
AK E, Harputluoglu U, Oghan F, Baykal B: Behcets disease and hearing loss, Auris Nasus Larynx. 2004 Mar;31(1):29-33.
Koomen I, Grobbee DE, Roord JJ, Donders R, Jennekens-Schinkel A, van Furth AM: Hearing loss at school age in survivors of bacterial meningitis: assessment, incidence, and prediction, Pediatrics. 2003 Nov;112(5):1049-53.
Piltcher OB, Teixeira VN, de Oliveira MW, Scattolin I, Piltcher SL: The prevalence of neurosensorial hearing loss among cystic fibrosis patients from Hospital de Clinicas de Porto Alegre, Int J Pediatr Otorhinolaryngol. 2003 Sep;67(9):939-41.
Kim HN, Kim SG, Lee HK, Ohrr H, Moon SK, Chi J, Lee EH, Park K, Park DJ, Lee JH, Yi SW: Incidence of presbycusis of Korean populations in Seoul, Kyunggi and Kangwon provinces, J Korean Med Sci. 2000 Oct;15(5):580-4.
Sakihara Y, Christensen B, Parving A: Prevalence of hereditary hearing impairment in adults, Scand Audiol. 1999;28(1):39-46.<\/p>\n","protected":false},"excerpt":{"rendered":"