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LAPORAN KASUS Seorang anak laki-laki usia 4 tahun dibawa oleh orangtuanya datang ke poli THT pada tanggal

17/02/2012 dengan No.Rekam Medis 59.21.82 Pasien dibawa oleh orang tua pasien ke poliklinik THT RSMH dengan keluhan bengkak belakang telinga kanan sejak 2 minggu yang lalu, bengkak makin meluas hingga ke pipi dan daerah mata kanan menjadi sembab. Bengkak disertai keluar cairan terus menerus dari telinga kanan, cairan berbau busuk, demam ada, pasien menjadi rewel dan terus-terusan menangis. Sejak 7 bulan yang lalu pasien mengalami keluar cairan dari telinga kanan, cairan kental berwarna putih dan berbau, nyeri (+), demam (+) hilang timbul, pasien hanya dibawa berobat ke bidan di kampung, diberi obat tetes telinga. Keluhan keluar cairan dari telinga kanan tidak berkurang. Riwayat keluhan yang sama dialami pasien sejak berumur 2 tahun , keluhan keluar cairan disertai demam hilang timbul. Pada pemeriksaan fisik : Keadaan umumnya tampak sakit sedang, kesadaran kompos mentis, RR; 35x/menit. Pemeriksaan Telinga kanan : bengkak sebesar bola kasti di daerah mastoid dan retro auricula kanan bengkak sebesar bola kasti, hiperemis, tidak berbatas tegas, nyeri tekan, fluktuatif. Liang telinga sempit, edema ada, hiperemis ada, sekret kental putih kekuningan, bau busuk (+), sagging (+), membran timpani belum dapat dinilai. Pemeriksaan telinga kiri : liang telinga lapang, serumen minimal, sekret (-), membran timpani intak, reflek cahaya (+). Pemeriksaan hidung kanan dan kiri : kavum nasi lapang, sekret (-), konka inferior eutrofi, mucosa merah muda, septum deviasi (-). Pada pemeriksaan tenggorok dalam batas normal. Pasien di diagnosis dengan OMSK tipe maligna fase aktif AD dengan komplikasi abses mastoid. Pasien dikonsulkan ke kamar 20 Poliklinik THT dan dilakukan tindakan apirasi didapatkan pus (+), kemudian dilakukan incisi dan drainase abses. Didapatkan pus bercampur darah sekitar 20 cc. Pus diambil untuk dilakukan kultur dan resistensi mikro organisme. Dipasang drain pada luka incisi untuk mengalirkan pus. Pasien tampak lebih tenang dan bisa tertidur. Pasien dirawat di bangsal. Terapi yang diberikan adalah IVFD RL mikro gtt xx/menit, injeksi Ampicillin 3 x 500 mg, injeksi Metronidazole 3 x 250 mg, injeksi Gentamisin 3 x 25 mg, Ibuprofen syrup 3 x 1, cuci telinga dengan H2O2 3 % 3ddgtt III AS , diet bubur biasa. Ganti perban dan kompres rivanol 2 x sehari. Periksa darah rutin dan darah kimia, Ro mastoid, Ro thorax PA.

Pada tanggal 18/02/2012 dilakukan follow up pada pasien ini. Keluhan keluar pus dari tempat incisi (+), didapatkan pus sekitar 10 cc, demam (-), Pemeriksaan fisik Telinga kanan : liang telinga sempit sekret (+), sagging (+), membran timpani belum dapat dinilai. Luka incisi di belakang telinga kanan pus bercampur darah (+) masih mengalir dari drain. Hidung dan tenggorok dalam batas normal. Hasil Laboratorium Hb 12, eritrosis 4.620.000. Hematokrit 36. MCH 26, MCV 78, MCHC 33, Leukosit 21.200, retikulosit 0,9 Trombosit 63.000, hitung jenis 0/0/2/74/17/7 waktu perdarahan 1 waktu pembekuan. BSS 51, Ureum 10, creatinin 0,6 protein total 6,1 albumin 2,7 globulin 3,4, SGOT 42, SGPT 20, Na 143, K 4,9. Hasil Ro. mastoid : tampak lesi radiopaque pada mastoid dekstra et sinistra, tak tampak destruksi tulang. Kesan : Mastoiditis dekstra et sinistra. Hasil Ro thorax, kesan : proses spesifik, asmatik/empisematous. Terapi diteruskan, pasien dikonsulkan kebagian Anak dan rencana CT-scan mastoid. Pada tanggal 19/02/2012 dilakukan follow up didapatkan keluhan keluar nanah dari tempat incisi (+), keluar cairan dari telinga kanan (+), demam (-), pemeriksaan fisik telinga kanan liang telinga sempit sekret (+), sagging (+), membran timpani belum dapat dinilai. Luka incisi di belakang telinga kanan pus bercampur darah (+) masih mengalir dari drain. Hidung dan tenggorok dalam batas normal. Terapi yang diberikan adalah IVFD RL mikro gtt xx/menit, injeksi Ampicillin 3 x 500 mg, injeksi Metronidazole 3 x 250 mg, injeksi Gentamisin 3 x 25 mg, Ibuprofen syrup 3 x 1, albumin 20% 50 cc cuci telinga dengan H2O2 3 % 3ddgtt III AS , diet bubur biasa. Ganti perban dan kompres rivanol 2 x sehari. Pada tanggal 20/02/2012 dilakukan follow up didapatkan keluhan keluar nanah dari tempat incisi (+), keluar cairan dari telinga kanan (+), demam (-), pemeriksaan fisik telinga kanan liang telinga sempit sekret (+), sagging (+), membran timpani belum dapat dinilai. Luka incisi di belakang telinga kanan pus bercampur darah (+) masih mengalir dari drain sekitar 5 cc. Hidung dan tenggorok dalam batas normal. Terapi injeksi Ampicillin 3 x 500 mg, injeksi Metronidazole 3 x 250 mg, injeksi Gentamisin 3 x 25 mg, Ibuprofen syrup 3 x 1, albumin 20% 50 cc cuci telinga dengan H2O2 3 % 3ddgtt III AS , diet bubur biasa. Ganti perban dan kompres rivanol 2 x sehari. Pada tanggal 21/02/2012 dilakukan follow up didapatkan keluhan keluar nanah dari tempat incisi minimal, keluar cairan dari telinga kanan minimal, demam (-), pemeriksaan fisik telinga kanan liang telinga sempit sekret (+), sagging (+), membran

timpani belum dapat dinilai. Luka incisi di belakang telinga kanan pus bercampur darah (+) masih mengalir dari drain. Hidung dan tenggorok dalam batas normal. Terapi injeksi Ampicillin 3 x 500 mg, injeksi Metronidazole 3 x 250 mg, injeksi Gentamisin 3 x 25 mg, Ibuprofen syrup 3 x 1,cuci telinga dengan H2O2 3 % 3ddgtt III AS , diet bubur biasa. Ganti perban dan kompres rivanol 2 x sehari. Pada tanggal 21/02/2012 dilakukan follow up didapatkan keluhan keluar nanah dari tempat incisi (+) , keluar cairan dari telinga kanan (+), demam (-), pemeriksaan fisik telinga kanan liang telinga sempit sekret (+), sagging (+), membran timpani belum dapat dinilai. Luka incisi di belakang telinga kanan pus bercampur darah (+) masih mengalir dari drain. Hidung dan tenggorok dalam batas normal. Hasil lab darah rutin dan kimia darah tgl 22/02/2012 HB 9,3 Eritrosit 3.530.000 Ht. 29, Leukosit 7.900, LED 8, retikulosit 1,9 trombosit 439.000, hitung jenis 0/11/0/42/40/7, ureum 12, creatinin 0,6, protein total 6,1, albumin 3,1, globulin 3,0 bilirubin total 0,39 Bilirubin direk 0,10 bilirubin indirek 0,29 SGOT 31, SGPT 14, Natrium 146, Kalium 4,6, calsium 1,62. Terapi IVFD Rl mikro gtt xx/menit injeksi Ampicillin 3 x 500 mg, injeksi Metronidazole 3 x 250 mg, injeksi Gentamisin 3 x 25 mg, Ibuprofen syrup 3 x 1,cuci telinga dengan H2O2 3 % 3ddgtt III AS , diet bubur biasa. Ganti perban dan kompres rivanol 2 x sehari. Pada tanggal 23/02/2012 dilakukan follow up didapatkan keluhan keluar nanah dari tempat incisi (+) , keluar cairan dari telinga kanan (+), demam (-), pemeriksaan fisik telinga kanan liang telinga sempit sekret (+), sagging (+), membran timpani belum dapat dinilai. Luka incisi di belakang telinga kanan pus bercampur darah (+) masih mengalir dari drain. Hidung dan tenggorok dalam batas normal. Terapi Terapi IVFD Rl mikro gtt xx/menit injeksi Ampicillin 3 x 500 mg, injeksi Metronidazole 3 x 250 mg, injeksi Gentamisin 3 x 25 mg, Ibuprofen syrup 3 x 1,cuci telinga dengan H2O2 3 % 3ddgtt III AS , diet bubur biasa. Ganti perban dan kompres rivanol 2 x sehari. Hasil kultur dan resistensi mikro organisme didapatkan Proteus Vulgaris dengan antibiotik yang sensitif adalah Cefotaksim. Pada tanggal 23/02/2012 dilakukan follow up didapatkan keluhan keluar nanah dari tempat incisi (+) , keluar cairan dari telinga kanan (+), demam (-), pemeriksaan fisik telinga kanan liang telinga sempit sekret (+), sagging (+), membran timpani belum dapat dinilai. Luka incisi di belakang telinga kanan pus bercampur darah (+) masih mengalir dari drain. Hidung dan tenggorok dalam batas normal. Terapi IVFD Rl mikro gtt xx/menit, Injeksi

Cefotaksim 2 x 250 mg, injeksi Metronidazole 3 x 250 mg, Ibuprofen syrup 3 x 1, cuci telinga dengan H2O2 3 % 3ddgtt III AS, diet bubur biasa. Ganti perban dan kompres rivanol 2 x sehari. Pada tanggal 24/02/2012 dilakukan follow up didapatkan keluhan keluar nanah dari tempat incisi (-) , keluar cairan dari telinga kanan (+), demam (-), pemeriksaan fisik telinga kanan liang telinga sempit sekret (+), sagging (+), membran timpani belum dapat dinilai. Luka incisi di belakang telinga kanan mengering, Hidung dan tenggorok dalam batas normal. Terapi IVFD Rl mikro gtt xx/menit, Injeksi Cefotaksim 2 x 250 mg, injeksi Metronidazole 3 x 250 mg, Ibuprofen syrup 3 x 1, cuci telinga dengan H2O2 3 % 3ddgtt III AS, diet bubur biasa. Ganti perban dan kompres rivanol 2 x sehari. Pada tanggal 25/02/2012 dilakukan follow up didapatkan keluhan keluar nanah dari tempat incisi (+) , keluar cairan dari telinga kanan (+), demam (-), pemeriksaan fisik telinga kanan liang telinga sempit sekret (+), sagging (+), membran timpani belum dapat dinilai. Luka incisi di belakang telinga kanan pus bercampur darah (+) masih mengalir dari drain sekitar 5 cc. Hidung dan tenggorok dalam batas normal. Terapi IVFD Rl mikro gtt xx/menit. Injeksi Cefotaksim 2 x 250 mg, injeksi Metronidazole 3 x 250 mg, Ibuprofen syrup 3 x 1, cuci telinga dengan H2O2 3 % 3ddgtt III AS, diet bubur biasa. Ganti perban dan kompres rivanol 2 x sehari. Konsul ke Bagian Anak untuk pembacaan hasil Mantoux test dan evaluasi HB 9,3 gr/dl. Kesan TB paru belum bisa ditegakkan, Susp. Anemia defisiensi. Saran : pemeriksaan darah perifer lengkap SI, TIBC, konsul ulang jika ada hasil. Saat ini tidak diperlukan transfusi darah karena tidak ditemukan adanya gangguan oksigenasi. Mantoux test indurasi 0, saran: mantoux test 2 minggu lagi. Keluarga cek sputum BTA. Antibiotik sesuai TS. Pada tanggal 26/02/2012 dilakukan follow up didapatkan keluhan keluar nanah dari tempat incisi (-) , keluar cairan dari telinga kanan (+), demam (-), pemeriksaan fisik telinga kanan liang telinga sempit sekret (+), sagging (+), membran timpani belum dapat dinilai. Luka incisi di belakang telinga baik, pus (-). Hidung dan tenggorok dalam batas normal. Terapi IVFD Rl mikro gtt xx/menit Injeksi Cefotaksim 2 x 250 mg, injeksi Metronidazole 3 x 250 mg, Ibuprofen syrup 3 x 1, cuci telinga dengan H2O2 3 % 3ddgtt III AS, diet bubur biasa. Ganti perban dan kompres rivanol 2 x sehari.

Pada tanggal 27/02/2012 dilakukan follow up didapatkan keluhan keluar nanah dari tempat incisi (+), keluar cairan dari telinga kanan (+), demam (-), pemeriksaan fisik telinga kanan liang telinga sempit sekret (+), sagging (+), membran timpani belum dapat dinilai. Luka incisi di belakang telinga kanan baik, pus (-). Hidung dan tenggorok dalam batas normal. Hasil lab darah tgl 27/02/2012 Hb 10,5, Eritrosit 3.910.000, hematokrit 32, MCH 32, MCV 26, MCHC 82, Leukosit 12.700, LED 97, Retikulosit 0,9, trombosit 307.000, hitung jenis 0/7/3/23/61/6. Gambaran darah tepi, kesan: anemia normositik normokrom disertai leukositosis. TIBC 300 g/dl, Fe 74 g/dl. Terapi IVFD RL mikro gtt xx/menit, Injeksi Cefotaksim 2 x 250 mg, injeksi Metronidazole 3 x 250 mg, Ibuprofen syrup 3 x 1, cuci telinga dengan H2O2 3 % 3ddgtt III AS, diet bubur biasa. Ganti perban dan kompres rivanol 2 x sehari. Pada tanggal 28/02/2012 dilakukan follow up didapatkan keluhan keluar nanah dari tempat incisi (-) , keluar cairan dari telinga kanan (+), demam (-), pemeriksaan fisik telinga kanan liang telinga sempit sekret (+), sagging (+), membran timpani belum dapat dinilai. Luka incisi di belakang telinga kanan pus bercampur darah (+) masih mengalir dari drain. Hidung dan tenggorok dalam batas normal. Terapi IVFD RL mikro gtt xx/menit, Injeksi Cefotaksim 2 x 250 mg, injeksi Metronidazole 3 x 250 mg, Ibuprofen syrup 3 x 1, cuci telinga dengan H2O2 3 % 3ddgtt III AS, diet bubur biasa. Ganti perban dan kompres rivanol 2 x sehari. Pada tanggal 29/02/2012 dilakukan follow up didapatkan keluhan keluar nanah dari tempat incisi (+) , keluar cairan dari telinga kanan (+), demam (-), pemeriksaan fisik telinga kanan liang telinga sempit sekret (+), sagging (+), membran timpani belum dapat dinilai. Luka incisi di belakang telinga kanan pus bercampur darah (+) masih mengalir dari drain sekitar 5 cc. Hidung dan tenggorok dalam batas normal. Terapi IVFD RL mikro gtt xx/menit, Injeksi Cefotaksim 2 x 250 mg, injeksi Metronidazole 3 x 250 mg, Ibuprofen syrup 3 x 1, cuci telinga dengan H2O2 3 % 3ddgtt III AS, diet bubur biasa. Ganti perban dan kompres rivanol 2 x sehari. Pada tanggal 30/02/2012 dilakukan follow up didapatkan keluhan keluar nanah dari tempat incisi (-) , keluar cairan dari telinga kanan (+), demam (-), pemeriksaan fisik telinga kanan liang telinga sempit sekret (+), sagging (+), membran timpani belum dapat dinilai. Luka incisi di belakang telinga kanan pus bercampur darah (+) masih mengalir dari drain

sekitar 5 cc. Hidung dan tenggorok dalam batas normal. Terapi Terapi IVFD RL mikro gtt xx/menit, Injeksi Cefotaksim 2 x 250 mg, injeksi Metronidazole 3 x 250 mg, Ibuprofen syrup 3 x 1, cuci telinga dengan H2O2 3 % 3ddgtt III AS, diet bubur biasa. Ganti perban dan kompres rivanol 2 x sehari. Pada tanggal 01/03/2012 dilakukan follow up didapatkan keluhan keluar nanah dari tempat incisi (+) , keluar cairan dari telinga kanan (+), demam (-), pemeriksaan fisik telinga kanan liang telinga sempit sekret (+), sagging (+), membran timpani belum dapat dinilai. Luka incisi di belakang telinga kanan pus bercampur darah (+) masih mengalir dari drain sekitar 5 cc. Hidung dan tenggorok dalam batas normal. Terapi IVFD RL mikro gtt xx/menit, Injeksi Cefotaksim 2 x 250 mg, injeksi Metronidazole 3 x 250 mg, Ibuprofen syrup 3 x 1, cuci telinga dengan H2O2 3 % 3ddgtt III AS, diet bubur biasa. Ganti perban dan kompres rivanol 2 x sehari. Pada tanggal 02/03/2012 dilakukan follow up didapatkan keluhan keluar nanah dari tempat incisi (+) , keluar cairan dari telinga kanan (+), demam (-), pemeriksaan fisik telinga kanan liang telinga sempit sekret (+), sagging (+), membran timpani belum dapat dinilai. Luka incisi di belakang telinga kanan pus bercampur darah (+) masih mengalir dari drain sekitar 5 cc. Hidung dan tenggorok dalam batas normal. Terapi Terapi IVFD RL mikro gtt xx/menit, Injeksi Cefotaksim 2 x 250 mg, injeksi Metronidazole 3 x 250 mg, Ibuprofen syrup 3 x 1, cuci telinga dengan H2O2 3 % 3ddgtt III AS, diet bubur biasa. Ganti perban dan kompres Rivanol 2 x sehari. Dilakukan CT-Scan Mastoid. Pada tanggal 03/03/2012 dilakukan follow up didapatkan keluhan demam (+) , keluar cairan dari telinga kanan (+), demam (-), pemeriksaan fisik nadi 122 x menit, RR 32 x menit temperatur 37,9C. Status lokalis : telinga kanan liang telinga sempit sekret (+), sagging (+), membran timpani belum dapat dinilai. Luka incisi di belakang telinga kanan baik. Hidung dan tenggorok dalam batas normal. Terapi IVFD RL mikro gtt xx/menit, Injeksi Cefotaksim 2 x 250 mg, injeksi Metronidazole 3 x 250 mg, Ambroxol syrup 3 x 1 cth , Tripolidin syrup 3 x1 cth cuci telinga dengan H2O2 3 % 3ddgtt III AS, diet bubur biasa. Ganti perban dan kompres Rivanol 2 x sehari, Rencana BERA dan OAE, Konsul Anak Subdivisi Tumbuh kembang.

FREQUENCY OF INTRA CRANIAL COMPLICATIONS IN CHRONIC OTITIS MEDIA

Ajmal Hussain, Arif Raza Khan*


Department of ENT, PGMI, Lady Reading Hospital and *Department of ENT, Khyber Teaching Hospital, Peshawar

Background: Chronic Otitis Media can lead to intracranial complications, which were more common in pre-antibiotic era as compared to the present antibiotic era. Patients of Chronic Otitis Media with intracranial complications usually present very late due to ignorance and lack of primary health care. The aim of this study was to investigate, the frequency, mortality and morbidity of intracranial complications of chronic otitis media admitted in Ear Nose and Throat Unit of Lady Reading Hospital Peshawar. Methods: This study was conducted in Government Lady Reading Hospital Peshawar for a period of two years from October 2001 to October 2003. All the patients diagnosed as intracranial complications of chronic otitis media were included in the study. Result: The total number of patients reporting with intracranial complication due to chronic Otitis media (Unsafe ear) was 20. Meningitis and brain abscess were present in 8 cases each (40%). In 3 cases (15%) extradural abscess was found while 1 (5%) had lateral sinus thrombosis. Conclusion:Chronic Otitis media is a common disease in our part of the world. Key word: Chronic Otitis Media, Intracranial complications, Brain abscess, Meningitis.

INTRODUCTION
Chronic Otitis Media is very serious disease because it can lead to both intra cranial and extra cranial complications. The use of antibiotics has reduced the incidence, morbidity and mortality of complications due to Chronic Otitis Media. Acute exacerbation in Chronic Otitis Media usually leads to rapid intra cranial extension of disease. 1,2 In most of the cases with the intra cranial complications due to Chronic Otitis Media cholesteatoma was the commonest finding and exoneration of the disease is very important to prevent recurrence. 2 Different routes of spread of infection to cranial cavity are direct erosion of bone, haemetological, through anatomical pathways and previous trauma surgical or non surgical. 1 Mortality has reduced to 5% with use of antibiotics as compared to 35% in pre-antibiotic era, due to intra cranial complications. 2 This study was carried out to assess frequency and presentation of intracranial complications of chronic otitis media in our setting.

MATERIAL AND METHODS


This was a case series conducted at Postgraduate Medical Institute, Lady Reading Hospital, Peshawar Pakistan from October 2001 to October 2003. Patients presenting to Ear Nose Throat Unit and diagnosed as having intra cranial complication due to Chronic Otitis Media were included in the study. History clinical examination and investigation were done. CT scan was done in all patients with suspected intracranial complications. All patients were put on antibiotics and steroids to reduce oedema. Neurosurgical and ophthalmic opinion were taken and followed. Brain abscess and subdural abscess were first treated by neuro-surgical departments and later on mastoid exploration was done in ENT department. In meningitis patients were treated conservatively first with antibiotics and lumbar puncture. After the condition of the patient was stabilized, mastoid exploration was carried out. In extradural abscess mastoid surgery was done immediately. In later sinus thrombosis mastoid exploration with removal of infected thrombosis was done with antibiotic cover.

RESULTS
In twenty patients with intra cranial complications males were 15 (75%), females were 5(25%)(Table-1). Age range was 15-30 years(Table-2). Most of the patients with intra cranial complications were between the age of 15-16 years (15 patients, 75%) between 25-30 years (5 patients, 25%).

Table-1: Gender wise distribution Gender Male Female No. patients 15 5 % 75 25

Table-2: Age wise distribution of intracranial complication Age 1525 years 2530 years No. patients 15 5 % 75 25

All patients with intra cranial complications were having foul smell discharge (Otorrhea) headache, fever and decreased hearing were present in 75% of patients (15). Otalgia in 50% and vertigo was present 15% of the patient (Table-3). The common intra cranial complications were meningitis 40% (8 cases), brain abscess 40% (8 cases), extradural abscess 15% (3 cases) and lateral sinus thrombosis 5% (1 case) (Table-4). Table-3: Clinical Symptoms Symptoms Otorrhea Headache Fever Decreased Hearing Otalgia Vertigo No. patients 20 20 15 15 10 5 % 100 100 75 75 50 25

In our study morbidity occur in three cases. There was epilepsy hemipersis, cerebellar ataxia one case each.(Table-5). In our study 2 patients died and both were from brain abscess due to very late presentation. Overall mortality rate was 10%. The major operative findings in the middle ear were cholesteatoma in 80% and granulation tissue in 20%. Table-4: Distribution of Intracranial complications Complications Meningitis Brain Abscess Extradural Abscess Lat. Sinus thrombosis Subdural abscess No. patients 8 8 3 1 0 % 40 40 15 5 0

Table-5: Morbidity of Intracranial complications Morbidity Epilepsy Hemiperises Cerebellar ataxia No. patients 1 1 1 % 5 5 5

DISCUSSION
With advent of antimicrobial agents, the frequency of intracranial complication of chronic otitis media has reduced but still serious complications exist with high mortality.3-6 The advent of high resolution CT scan and I/V high doses of proper antibiotic has decreased the mortality and morbidity in otitis media.7 In pre-antibiotic era the incidence of intracranial complications were 2.3% of cases, but with effective antibiotic and with recent surgical technique, those have been greatly reduced to 0.150.04%.8,9

In our study 75% patients (15) were between age of 15-25 years, while other studies showed that intracranial complication occurred frequently in children of young adults (74%). 6 Meningitis is the most common intra cranial complication. Its incidence was 3477%3,6 but in our study the incidence is 40%. Patient with meningitis usually presents with fever, headache, vomiting, neck stiffness. The diagnosis can be made by CSF examination and culture sensitivity. CT scan is done to exclude multiple complications like brain abscess. Mortality rate is being reduced to 836%. 6,8,10 In our study the mortality rate from meningitis was zero. The most serious otegenic intracranial complications which occur commonly is brain abscess. It needs prompt diagnosis and treatment. The temporal lobe abscess is the commonest followed by cerebellar abcess. 12 The brain abscess was the commonest intracranial complication in other studies 40% (8 patient) almost equal to meningitis. 11,13 Lateral sinus thrombosis may result either from direct spread of infection from the mastoid or from thrombophelibitis of the small veins of the middle ear.6 The incidence of lateral sinus thrombosis has been reported to be 19%6,8 and the mortality 10%. In our study only 1 patient was diagnosed as having lateral sinus thrombosis and mortality rate was zero. In three cases, extradural abscess was found. It is usually present with headache and local tenderness and its diagnosis was made by clinical examination and CT scan. The incidence of extradural abscess in patients with intra cranial complications has been reported to be 16-22%. In our study 15% (1 patient) was having exctradural abscess and no patient died with this complication. Rate of mortality is 14-32.6% in intracranial complication. 6,8,21 In our study mortality rate was 10% (3 cases). The morbidity rate is reported to be between 11.6 and 27.9%. 8,21 In our study morbidity was 15%. Our morbidity and mortality rate is still high because patients usually present late.

CONCLUSION
The otogenic complications are decreasing, however the morbidity and mortality is still high even with the advent of antibiotics and surgical eradication of the disease. In our region, still the otogenic intracranial complications do occur. Therefore, for early diagnosis of disease detailed history and meticulous clinical examination are the most important tools. In otogenic intracranial complication the prominent features are headache, fever, nausea, vomiting, personality change and signs of increased intra cranial pressure and focal neurological signs. A delay in the diagnosis and treatment of intracranial complication can lead to increased morbidity and mortality.

REFERENCES
1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. Austin DF. Complications of acute and chronic Otitis media. In: Ballenger JJ. Snow JB. Eds. Otolaryngology-Head and Neck Surgery. 15th edn. Philadelphia: Williams & Wilkins, 1996: 1037-53. Yaniv E. Pocock R. Complications of ear disease. Clin Otalryngol 1988;13:357-61. Goycoolea MV, Jung TK. Complications of suppurative Otitis media. In: Paperella MM. Shumrick DA, Gluckman JL, Meyerhaff WL. Eds. Otolaryngology 3rd edn. Philladelphia:W.B. Saunders 1991;1381-1404. Myamoto RT, Worth RM. Otogenic cerebellar abscess. Ann Otol Rhinol Laryngol 1986:95 (6 pt1):647-9. Pfalts CR. Complications of Otitis media. ORL Oto-Rhino Laryngol 1982;44(6):301-9. Samuel J, Fernandes CMC, Steinberg JL. Intracranial otogenic complications: a persisting problem. Laryngoscope 1986:96:272-8. Munz M, Farmer JP, Auger L, OGorman AM, Schloss MD. Otitis media and CNS complications. J Otolaryngol 1992:21(3):2246. Kangsanarak J, Fooanant S, Ruckphaopunt K, Navacharoen N, Teotrakul S. Extractanial and intracranial complications of suppurative Otitis media Report of 102 cases. J Laryngol Otol 1993;107:999-1004. Palva T, Virtanen H, Makinen J. Acute and latent mastoiditis in children. J Laryngol Otol 1985;99:127-9. Bluestone CD, Klein JO, Intracranial suppurative complications of Otitis media and mastoiditis. In: Bluestone CD, Stool SE, Scheetz MD, eds. Pediatric Otolaryngology, 2nd edn. Philadelphia: WB. Saunders, 1990:537-46. Murthy PSN, Sukumar R, Hazarika P, Rao AD, Mukulchandj RA. Otogenic brain abscess in childhood. Int J Pediatr Otorhinolaryngol 1991;22:9-17. Neely JG. Complications of temporal bone infection. In: Cummings CW, Fredrickson JM. Harker LA, Krause CJ. Schuller DE, eds. Otolaryngology Head and Neck Surgeyr. 2nd edn. St. Louis: Mosby Year Book, 1993; 2840-64. Rupa V, Raman R. Chronic suppurative Otitis media;complicated versus uncomplicated disease. Acta Otolaryngol (Stockh) 1991;111(3):530-5. Ibrahim AW, Al-Rajeh SM, Chowdhary UM, Ammar A. Brain abscess in Saudi Arabia. Neurosurg Rev 1990;13(2):103-7. Kulali A, Ozatik N, Topcu I. Otogenic intracranial abscess. Acta Neurochir (Wien) 1990;107:140-6. Shamboul KM. An unusual prevalence of complications of chronic suppurative Otitis media in young adults. J Laryngol Otol 1992;106:874-7.

17. 18. 19. 20. 21. 22.

Yen PT, Chan St, Huang TS. Brain abscess: with special reference to otolaryngologic sources of infection. Otolaryngol Head Neck Surg 1995;113:15-22. Ibekwe AO, Okoye BCC. Subperiosteal mastoid abscess in chronic suppurative Otitis media. Ann Otol Rhino Laryngol 1988;97:373-5. Savic DIJ, Djeric DR. Facial paralysis in chronic suppurative Otitis media Clin Otolaryngol 1989;14:515-7. Glasscock ME, Shambaugh GE Jr. Surgery of the ear. 4th edn. Philadelphia: W.B. Saunders, 1990:249-92. Navacharoen W, Soprasuchart A. Intracranial complications of Otitis media; a five-year study. J Infect Dis Antimicrob Agents (Thai) 1984;1:52-7. Panda NK, Sreedharan S, Mann SB, Sharma SC. Prognostic factors in complicated and uncomplicated chronic Otitis media. Am J Otolaryngol 1996;17(6):391-6.

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Address for Correspondence: Dr. Ajmal Hussain, Department of ENT, PGMI Lady Reading Hospital Peshawar, Pakistan

Chronic Otitis Media


ALTERNATIVE NAMES: Secretory otitis media; otitis media with effusion; glue ear. DEFINITION: Among otolaryngologists, who are specialists in the management of ear disease, chronic otitis media has a distinct connotation. By definition it is a perforated eardrum with intermittent or persistent infected ear drainage. The term chronic otitis media, however, has taken on an alternative meaning and has been used to refer to asymptomatic fluid behind the eardrum which has failed to resolve. WHAT IS GOING ON IN MY BODY? The anatomy and physiology are identical to that discussed under acute otitis media. In otitis media with effusion (secretory otitis media), there is persistent fluid which is not resolving spontaneously. From a number of studies, approximately 90% of children who develop fluid behind the eardrum, regardless of its cause, will have it resolve in approximately three months. In otitis media with effusion, part of the reason the fluid fails to resolve is continued swelling and obstruction of the eustachian tube and also continued inflammation of the lining of the middle ear space. The reasons for the continued inflammation vary. When the fluid has been cultured for bacteria, approximately a third of the time it contains organisms commonly associated with acute otitis media, such as Streptococcus pneumonia, non-typable hemophilus, and Moraxella catarrhalis. In another third of patients other bacteria are present that usually are not associated with acute otitis media, and in the other third the fluid collections are sterile. What is thought to occur is that the presence of bacteria or products from their breakdown by the immune system, in addition to some of the

products released by the immune system during the infection, cause a continued inflammatory response behind the eardrum. Part of the response in inflamed mucous membrane is to make an increased volume of a more viscous solution. The mucosal lining of the eustachian tube also becomes swollen and obstructive. The mechanism of chronic otitis media with a perforated eardrum and ear drainage is somewhat different than that of otitis media with effusion, although eustachian tube problems may also exist. In this condition there is usually inflammation in the mastoid or in the channel between the middle ear and mastoid which is a result of chronic bacterial infection. These bacteria are usually different from that causing acute ear infections and often consist of Staphylococcus aureus, Pseudomonas aeruginosa, or a class of bacteria called anaerobes which require low-oxygen environments to thrive. WHAT ARE THE SIGNS AND SYMPTOMS? In otitis media with effusion there is fluid present behind the tympanic membrane which often has very few, if any, symptoms. The main symptom is conductive hearing loss. If the patient is old enough, they may complain that their ear feels plugged or full. There is often no pain or fever as often is seen with the more acute form of infection. In children the signs of hearing loss may be quite difficult to determine. Even deaf children will babble until the age of six months, but the babbling typically stops. If the child "ignores" the parent, sits close to the TV, needs to have words repeated, says "what" frequently, or is not progressing in their speech, hearing loss may exist. It is usually mild in nature, and its effect upon speech is quite subtle. In these milder forms of hearing loss, low-power sounds, such as F, S, or TH are the first to be inaccurately articulated. In otitis media with effusion different kinds of fluid can be present behind the eardrum. It ranges anywhere from the yellow-colored, more liquid type all the way to thick, white, rubber-cement-like material. The more viscous types of fluid are usually a result of more significant degrees of middle ear mucous membrane inflammation. In an individual with chronic otitis media there will be a perforation in the tympanic membrane. Through the perforation the mucous membrane lining of the middle ear can be examined. There may be a small amount of drainage behind the eardrum, and the lining blood vessels may be more prominent, or the lining itself might be thicker and more red than usual. Varying types of fluid may be present in the ear canal. Sometimes it may have a watery, slightly mucous consistency all the way to frank yellow-green, foul-smelling discharge. These individuals often respond to antibiotics, only to relapse with their drainage. They may often complain

of hearing loss. As opposed to acute mastoiditis, there is usually no pain, swelling of the skin overlying the mastoid, or fever. WHAT ARE THE CAUSES AND RISKS? The causes of otitis media with effusion are almost identical to those which cause acute otitis media (see acute otitis media). From large studies of children in daycare centers, up to 70% of them may have fluid behind their eardrums at some point during the course of a year. Usually 90% of the time the fluid resolves spontaneously without treatment. Other causes include chronic sinusitis, chronic or acute allergy, craniofacial abnormalities, or palate dysfunctions. Malignancies around the eustachian tube can give rise to secretory otitis media. Even though these are extraordinarily rare, asymptomatic fluid behind just one eardrum can indicate a cancer. This is particularly true in adults, and therefore, unilateral otitis media with effusion in adults is assumed to be caused by malignancy until proven otherwise. The causes of chronic otitis media are not only eustachian tube dysfunction but also ongoing low-grade infection within the mastoid. Once again individuals who have eustachian tube dysfunction, regardless of the mechanism, are at a greater risk. These causes would include individuals with craniofacial or palatal abnormalities, Down's syndrome, individuals of American Eskimo or Indian descent, slag burns to the tympanic membrane, and patulous eustachian tube. HOW TO PREVENT THE DISEASE: Preventing otitis media with effusion would depend upon preventing the diseases that lead to it, particularly viral upper respiratory illness. This factor and others are discussed in detail under acute otitis media. Preventing chronic otitis media once again depends upon improving overall eustachian tube function. Unfortunately, even with our great technological strides, there is still not a definite test of eustachian tube function. As chronic mastoiditis may be the result of poorly or inadequately treated acute otitis, it is imperative that children with acute otitis who need antibiotics have not only appropriate therapy, but the therapy must be completed. HOW IS IT DIAGNOSED? Otitis media with effusion is diagnosed by three different means. The first method is physical examination, the second is with tympanometry, and the third is with audiometry. Fluid behind the eardrum and poor tympanic membrane movement are present upon examination. Tympanometry is the measure of the amount of eardrum mobility, and in otitis media with effusion it is often severely

impaired, which manifests as a flat line on the tympanogram instead of a peak pattern. On hearing testing a conductive hearing loss will be present of varying degree. There is usually no role for CT scans of the mastoid. In chronic otitis media, diagnosis employs physical examination. On examination there is a perforation in the tympanic membrane and infected material visualized in the middle ear space through the perforation and/or in the external ear canal. Culture of the infected material to try to determine the specific bacteria and to which antibiotics they are sensitive can help guide treatment. Hearing tests are obtained to document the type and degree of hearing loss, and if surgery is contemplated or the diagnosis is not absolutely certain, then a CT scan of the mastoid and temporal bone can yield useful information. WHAT ARE THE LONG-TERM EFFECTS? In otitis media with effusion, the long-term effects depend upon whether or not hearing is restored by draining the fluid, usually with ventilation tubes. In children who have undiagnosed fluid and subsequent conductive hearing loss, speech and learning delays are often present. If the inflammation that gives rise to the fluid behind the tympanic membrane is unresolved, then tympanosclerosis can occur. Tympanosclerosis is scarring of the tympanic membrane or mucous membrane of the middle ear. It is quite firm and in some cases actually calcifies. As a consequence, it can impair eardrum or ossicle (middle ear bone) movement, with a resultant hearing loss. Surgical correction of hearing loss from tympanosclerosis is typically less successful. Some individuals with untreated otitis media with effusion will start to develop retraction pockets of the tympanic membrane because of the constant negative pressure behind the eardrum. These pockets arising from the eardrum begin to push into the middle ear space and can erode the bones for hearing, with hearing loss, and if they get particularly large or infected, can impair their ability to shed the skin forming on their surface. If this skin starts to accumulate within the pocket, it can form a cholesteatoma (see benign ear cyst or tumor). In some patients an adhesive process can develop whereby the drum adheres to the bones for hearing and other middle ear structures. If eustachian tube function then improves and the fluid resolves, the drum is often left adherent. As long as eustachian tube function continues to remain normal, then no further sequelae occur; but if the eustachian tube function is inadequate, then the drum can continue to be pulled into the middle ear space, with erosion of the bones for hearing, perforation, or formation of a cholesteatoma. The long-term effects of chronic otitis media relate mostly to the infectious process. Tympanosclerosis around the ossicles and drum can

occur. Because of the perforation in the eardrum, adhesive otitis may not develop, or if it has already developed, it often will stabilize. The main concern is the damage to the conductive mechanism for hearing, and because of the ongoing infection, these individuals may develop an impairment of hearing nerve function. The greatest concern relates to the infectious process in the mastoid. If chronic otitis media occurs at a fairly young age, mastoid development will be impaired. Chronic otitis media also places the individual at risk for intracranial complications, such as brain abscess and meningitis. AM 1 PUTTING OTHERS AT RISK? No. WHAT ARE THE TREATMENTS? For otitis media with effusion that does not respond to antibiotics and oral steroids, ventilation tubes are effective. In the treatment for chronic otitis media the most important goal is creation of a safe ear. This involves repairing the tympanic membrane and removing any diseased or infected tissue in the mastoid and middle ear. Hearing in surgery for chronic ear disease is a secondary goal. In the individual with chronic otitis media, removal of the diseased lining within the mastoid and middle ear and simultaneous restoration of the air channel between the mastoid and middle ear is performed via mastoidectomy. At the same setting the eardrum perforation is repaired, and if there are abnormalities in the bones for hearing, these are simultaneously reconstructed. WHAT ARE THE SIDE EFFECTS TO THE TREATMENTS? Ventilation tubes have fortunately few, if any, side effects. Persistent perforation occurs in approximately 2 to 3% of patients once the tubes extrude. Average duration of tube life span is 6 to 12 months. Another potential side effect of the tube placement would be the need for another set of tubes, which is necessary in approximately 20% of children. Other complications of tube placement can occur, although they are very rare, such as nerve deafness and cholesteatoma. The side effects to mastoidectomy would be failure to completely eradicate the infection, taste disturbance on that side of the tongue, incomplete restoration of hearing, nerve deafness, vertigo, facial nerve injury, or breakdown of the repaired tympanic membrane. If synthetic materials are used to restore the chain of bones for hearing, these can become dislodged or fail. WHAT HAPPENS AFTER TREATMENT? For otitis media with effusion,

hearing is usually restored quite rapidly. There may be some brief, continued drainage through the ventilation tube. After tubes are placed, some care needs to be taken regarding prevention of contamination of the middle ear space by bacteria. Treated, chlorinated water, such as in swimming pools or out of the tap, will infrequently penetrate the middle ear space through the ventilation tube. Often antibiotic ear drops are used after a child swims or if there is some concern that they have gotten water in their ears. The risk of developing an infection with a tube in place is highest if shampoo or soapy bath water enters the middle ear through the tube. Usually there is a high concentration of intestinal bacteria once the child has bathed, and this water, because of the soap, much more readily enters the middle ear. If an individual with ventilation tubes decides to dive or swim deeply under water, it is prudent to wear custommade ear plugs along with neoprene headbands. In most individuals, after surgical intervention for chronic otitis media, healing is complete within two to three months. If there has been successful treatment of the process, there will be no further infections, and an improvement in hearing. However, if the mastoid infection continues, the tympanic membrane will re-perforate, the drum will be retracted, or fluid will re-develop behind the eardrum. HOW DO I MONITOR THE DISEASE? As the main complaint in otitis media with effusion is hearing loss, diminished audition after an upper respiratory tract infection or treated acute ear infection should prompt a visit to their physician. Continued drainage after tube placement or failure to improve the hearing needs to be investigated. Monitoring the disease in chronic otitis media depends upon the presence of ear drainage. Any individual with intermittent or persisting ear drainage, especially if it is associated with hearing loss or in whom a complication develops, such as dizziness, facial paralysis, or intracranial problems, needs to be evaluated immediately.
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Chronic Suppurative Otitis Media

By Dr. T. Balasubramanian M.S. D.L.O.

Definition: Chronic suppurative otitis media is defined as a chronic infection of the mucosa lining the middle ear cleft. Middle ear cleft include the eustachean tube, hypotympanum, mesotympanum, epitympanum, aditus and mastoid air cell system. Types of chronic suppurative otitis media: Chronic suppurative otitis media is of two types: 1. Tubotympanic disease (safe type) 2. Atticoantral disease (unsafe type) Tubotympanic disease: This is also known as safe disease because it is bereft of any serious complications. The infection is limited to the mucosa and the antero inferior part of the middle ear cleft, hence the name. This disease does not have any risk of bone erosion. The discharge any will flow through a perforation present in the pars tensa portion of the ear drum. This perforation is usually surrounded by a rim of remnant ear drum or atleast the annulus is intact. (Central perforation). The perforation is usually reniform (kidney shaped) because of poor blood supply to the affected portion of the tympanic membrane. The infective activity of safe disease is related to the frequency of upper respiratory tract infections, the discharge tending to increase with increasing freqency of upper respiratory infections.

Aetiology: 1. Could be a sequelae to inadequately treated acute otitis media. 2. Acute suppurative otitis media causing persistant perforation which could be infected from bacteria in the external auditory canal. This condition is knonw as persistant perforation syndrome. Microbiology of CSOM: In all varieties of CSOM the major organism found in the discharge are gram negative bacilli i.e. Ps. aeruginosa, E. coli, and B. proteus. These organisms are not commonly found in the upper respiratory tract, but they are found in the skin of external auditory canal. Clinical features of tubotympanic disease: 1. The discharge in this condition is profuse and mucopurulent in nature. 2. The discharge is not foul smelling. 3. Since the infected area is open at both ends i.e. the eustachean tube end and the perforation in the ear drum, the discharge doesnot accumulate in the middle ear. 4. The ossicular chain is not at risk in this type of disorder, the conductive deafness caused is due to the presence of perforation in the tympanic membrane and thickening of the tympanic membrane. 5. Conductive deafness may also be accentuated by thickening of round window membrane due to the presence of secretions. Hearing loss is usually about 30 - 40 dB. 6. These patients have poorly pneumatised / sclerosed mastoid air cell system. This feature has been attributed to repeated attacks of middle ear infections during childhood causing inadequate pneumatisation of mastoid air cell system. In patients with pneumatised mastoid air cell system repeated middle ear infections can cause sclerosis with evidence of new bone formation. Mastoids in these patients may be sclerotic. 7. Pain in the ear when present is always associated with otitis externa. This commonly occurs when the patient attempts to clean the ear off the purulent secretions with a ear bud or cotton tipped applicator.

Pathology of tubotympanic disease: Pathological changes depend on the stage of the disease. The stages are as follows: Acute stage: This is where the ear is actively discharging. The mucosa of the middle ear cavity is hypertrophied, and congested. Inactive stage: This condition is characterised by dry perfortion of ear drum, commonly in its antero inferior part, close to the eustachean tube orifice. The middle ear mucosa is normal. Quiescent stage: Perforation of ear drum is present, the middle ear is dry and mucosa may be normal or hypertrophied. Healed stage: Here the perforation of ear drum has healed by formation of thin scar. There may even be tympanosclerotic patches / chalky deposits on the ear drum. The ossicular chain is invariably intact. Tuning fork tests show: Rinne - Negative on the affected side Weber - Lateralised to the good ear Absolute bone conduction test - Not reduced Pure Tone audiometry show conductive hearing loss. The hearing loss is invariably under 40 dB. Management of tubotympanic disease: Conservative management: If the disease is active - with active ear discharge Aural toileting - must be done using dry cotton swabs. Suction method can be used to suck out secretions from the external canal and the middle ear cavity. The only disadvantage of this procedure is the risk of noise induced deafness.

Syringing the affected ear with warm saline mixed with acetic acid (1.5%) can be used to syringe the affected ear. This solution not only clears the ear of its purulent secretions, it also helps to remove crusts if present. The presence of weak acetic acid has bacteriostatic effect. Role of antibiotics in the management of tubotympanic disease: Antibiotics can be administered depending on the culture report. The best route of administration is topical because the presence of a large central perforation enables adequate concentration of antibiotics to reach the middle ear mucosa. Ototoxic drugs are to be avoided because the increased vascularity present in the middle ear mucosa will cause easy absorption of the drug into the inner ear fluids causing sensori neural hearing loss. Ciprofloxacillin can be administered topically. Oral amoxycillin in adequate doses or penicillins in adequate doses may be beneficial. Role of antihistamines and nasal decongestants: Is questionable. Their role is to decongest the nasal and naso pharyngeal mucosa, pharyngeal end of eustachean tube. Since there is associated perforation of tympanic membrane, secretions dont tend to accumulate inside the middle ear cavity. Topical nasal decongestants should not be used for more than a week, because of their propensity to cause rhinitis medicamentosa. Precautions: 1. The ear must be kept dry. This can be achieved by keeping the ears plugged when taking head bath. Swimming must be avoided till the perforation heals. 2. Pre existing sinus infections if any must be treated aggressively. 3. Presence of focal sepsis in the throat (tonsils commonly) must be ruled out. Surgical management: 1. Surgical management aims at correcting the causative problems if any. The presence of deviated nasal septum must be corrected as this could predispose to chronic sinus infections.

If focal sepsis is identified in the tonsils and adenoid then adenotonsillectomy needs to be performed. After eradicating the possible focal sepsis only attempt must be made to definitively treat the perforation. If the ear drum has managed to stay dry for more than 6 months myringoplasty can be performed. Temporalis fascia is used as grafting material because of its availability in close proximity, its thickness is more or less similar to that of normal ear drum. One other added advantage is its low basal metabolic rate. If middle ear mucosa is wet and oedmatous then cortical mastoidectomy should be resorted to if conservative management fails. Mastoidectomy can always be combined with myringoplasty in the same sitting. Atiko antral shifting yang dapat dilakukan dengan Atticoantral type of disease (Unsafe type of disease): This is termed as unsafe because dangerous intra cranial and extra cranial complications can occur, proving fatal to the patient. This disease spreads by erosion of the bony wall of the attic. Cholesteatoma is commonly present in this condition. This disease is commonly seen in sclerosed mastoid cavities. Presence of granulation tissue is also common in this disorder. This condition mainly affects the attic region of the middle ear. This region is pretty crowded, with the presence of the head of the malleus and incus. Any disease process involving crowded portions tend to cause more complications. Bone erosion occurs due to the presence of osteitic reaction in the bone tissue. Definition of cholesteatoma: Cholesteatoma is defined as a cystic bag like structure lined by stratified squamous epithelium on a fibrous matrix. This sac contains desquamated squamous epithelium. This sac is present in the attic region. Cholesteatoma is also defined as 'skin in wrong place'. Cholesteatoma is known to contain all the layers of skin epithelium. The basal layer (germinating layer) is present on the outer surface of cholesteatoma sac in contact with the walls of the middle ear cleft. Theories of bone invasion by cholesteatoma:

1. Pressure theory - states that increase in the pressure caused by enlarging cholesteatoma cause bone erosion. Ischemia has been attributed as the cause in this theory. 2. Enzymatic theory: Inside the cholesteatoma are present multinucleated osteoclasts and histiocytes. These cells release acid phosphatase, collagenase and other proteolytic enzymes. These enzymes are known to cause bone erosion. 3. Pyogenic osteitis: Pyogneic bacteria may release enzymes which could cause bone resorption.

Types of cholesteatoma: 1. Congenital cholesteatoma 2. Primary acquired cholesteatoma 3. Secondary acquired cholesteatoma Congenital cholesteatoma: is known to arise from embryonic cell rests present in the middle ear cavity and temporal bone. These cell rests are known to commonly occur in cerebello pontine angle and petrous apex. Infact congenital cholesteatoma is seen as a whitish mass behind an intact tympanic membrane. Derlacki and Clemis laid down the following as criteria to diagnose congenital cholesteatoma: 1. The patient should not have previous episodes of middle ear disease 2. Ear drum must be intact and normal 3. It is purely an incidental finding 4. If discharge and ear drum perforation is present then it should be contrued that congential cholesteatoma has managed to erode the tympanic membrane. Clinical features: The disorder is an incidental finding. The common location of congenital cholesteatoma is the antero superior quadrant of

tympanic membrane, postero superior quadrant being the next common site of involvement. Anteriorly situated congenital cholesteatomas are known to affect the eustachean tube function causing conductive deafness due to middle ear effusion, where as posterior congenital cholesteatoma is known to cause conductive deafness due to impairment of ossicular chain mobility. Staging of congenital cholesteatoma: Staging as suggested by Derlacki and Clemis: They were the first to stage congenital cholesteatoma. They classified congenital cholesteatoma into 1. Petrous pyramid cholesteatoma 2. Cholesteatoma involving the mastoid cavity 3. Cholesteatoma involving the middle ear cavity. Potsic suggested the following staging mechanism: Stage I : Single quadrant involvement with no ossicular / mastoid involvement. Stage II : Multiple quadrant involvement with no ossicular / mastoid involvement Stage III : Ossicular involvement without mastoid involvement Stage IV : Mastoid extension Nelson's staging: Type I : Involvement of mesotympanum without involvement of incus / stapes Type II : Involvement of mesotympanum / attic along with erosion of ossicles without extension into the mastoid cavity Type III : Involvement of mesotympanum with mastoid extension Staging this disease will help in deciding the modality of treatment and in predicting the long term prognosis.

Acquired Cholesteatoma: can be divided into two types, primary acquired and secondary acquired cholesteatomas. Primay acquired cholesteatoma: In this condition there is no history of preexisting or previous episodes of otitis media or perforation. Lesions just arise from the attic region of the middle ear. Secondary acquired cholesteatoma: always follows active middle ear infection which manages to destroy the ear drum along with the annulus. This type of destruction is common in acute necrotising otitis media following exanthematous fevers like measles etc.

Oto endoscopic picture showing attic cholesteatoma Theories to explain pathogenesis of cholesteatoma: Various theories have been postulated to explain the pathogenesis of cholesteatoma. They are: 1. Cawthrone theory: This theory suggested by cawthrone in 1963 suggested that cholesteatoma always originated from congential embryonic cell rests present in various areas of the temporal bone. 2. Theory of immigration: This theory was suggested by Tumarkin. He was of the view that cholesteatoma was derived by immigration of squamous epithelium from the deep portion of the external auditory canal into the middle ear cleft through a marginal perforation or a total perforation of the ear drum as seen in acute necrotising otitis media. 3. Theory of invagination: This theory was suggested by Toss. He theorised that persistent negative pressure in the attic region causes invagination of pars flaccida causing a retraction pocket. This retraction pocket becomes later filled with desquaated epithelial debris which forms a nidus for the infection to occur later. Common organisms known to infect this keratin debris are Psuedomonas, E. coli, B. Proteus etc. Toss also classified attic retraction pockets into 4 grades: 1. Grade I: The retracted pars flaccida is not in contact with the neck of the malleus. 2. Grade II: The retracted pars flaccida is in contact with the neck of the malleus to such an extent that it seems to clothe the neck of the malleus. 3. Grade III: Here inaddition to the retracted pars flaccida being in contact with the neck of the malleus there is also a limited erosion of the outer attic wall or scutum. 4. Grade IV: In this grade in addition to all the above said changes there is severe erosion of the outer attic wall or scutum.

4. Metaplastic theory: This theory was first suggested by Wendt in 1873. He took into consideration the histological changes seen in various portions of the middle ear cavity. The attic area of the middle ear cavity is lined by pavement type of epithelium. This epithelium undergoes metaplastic changes in response to subclinical infection. This metaplastic mucosa is squamous in nature there by forming a nidus for cholesteatoma formation in the attic region.

Of all the above mentioned theories, the theory of invagination appears to be the most plausible one currently explaining the various pathologic features of cholesteatoma. Clinical features of acquired cholesteatoma: Ear discharge: is scanty and foul smelling. Infact the odur is best described as musty in nature. This is due to the presence of saprophytic infection and osteitis. Hearing loss: is commonly conductive in nature. Some patients may even surprisingly have a normal hearing despite the presence of a huge cholesteatoma. This normal hearing could be attributed to the bridging effects of cholesteatomatous mass.

Sensorineural hearing loss if present could be attributed to the absorption of toxins through the round window membrane, or may be due to use of ototoxic antibiotics topically on a long term basis. Ear ache: if present could be attributed to the presence of co existing otitis externa, or presence of extradural abscess. Tinnitus if present may indicate imminent sensorineural hearing loss. Vertigo may be present if there is erosion of lateral semicircular canal by the cholesteatomatous matrix.Fistula test if performed is positive in these patient. Fistula test: This test is positive if there is a third window is present in the laryrinth due to the erosion of the labyrinthine bone. This commonly occurs in the lateral semicircular canal area. This test is performed using a snugly fitting siegles pneumatic speculum and slowly applying pressure by compressing the pneumatic bulb. If labyrinthine fistula is present the patient will feel giddy and will have nystagmus. Facial palsy may indicate erosion of facial nerve canal with involvement of facial nerve. On examiantion: There is destruction of the outer attic wall, with presence of attic perforation. Cholesteatomatous flakes may be seen through the perforation like cotton wool. There is associated sagging of the posterior superior meatal wall. Hearing tests indicate conductive deafness commonly if labyrinth is uninvolved. It may turn out to be sensorineural hearing loss if there is associated erosion of the labyrinth. X ray mastoids may show slcerosis with presence of cavity. Management: Since this is a surgical problem modified radical mastoidectomy is advocated in almost all of these patients.

The aims of the surgical procedure is as follows: 1. To exteriorise the disease 2. To create adequate ventilation to the middle ear cavity 3. To create a permenant skin lined cavity exposed to the exterior. The various modifications of mastoidectomy procedures are discussed elsewhere.

Chronic Otitis Media and Cholesteatoma


Etiology and Diagnosis
A patient with a perforated tympanic membrane can develop chronic otitis media. This is defined as a chronic ear infection with drainage out the ear canal (otorrhea). The long-standing infection slowly erodes the middle ear ossicles, causing ossicular chain discontinuity. Occasionally, the infection can spread to the inner ear causing permanent sensorineural hearing loss, to the facial nerve causing facial nerve paralysis, or to the brain causing meningitis or a brain abscess. Chronic otitis media can also lead to a cholesteatoma. A cholesteatoma is a skin growth that occurs behind the eardrum. It is usually caused by repeated ear infections associated with poor Eustachian tube function. Over time, the cholesteatoma increases in size and destroys the delicate middle ear bones. Eventually, it may erode into the inner ear and cause permanent hearing loss or dizziness. It may grow to involve the facial nerve causing facial paralysis. In some instances, cholesteatomas can expand up into the brain. Chronic otitis median and/or cholesteatoma are a serious conditions that requires prompt treatment. Initially, this involves careful cleaning of the ear, antibiotics, and eardrops. Often, computed tomography (CT scan) is helpful to define the extent of the disease. This also can act as a road map for surgery.

Treatment

Most patients with chronic otitis media and nearly all patients with cholesteatoma require surgery to cure the disease. This involves making an incision behind the ear, drilling out the infection from the mastoid bone behind the ear, and removing cholesteatoma from the middle ear space or mastoid air cells. Also, the eardrum is rebuilt. The surgery is called a tympanoplasty with mastoidectomy. There are two types of mastoidectomies: canal-wall-up and canal-wall-down. A canal-wall-up procedure means that the ear canal is maintained and the location of the eardrum is in its normal location. Thus, when a physician not specialized in ear surgery looks in your ear canal, he may not know that you have had surgery. The downside to having a canal-wall-up tympanoplasty with mastoidectomy is that residual cholesteatoma within the middle ear or mastoid space may grow asymptomatically, until it reaches an ext remely large and dangerous size. So, most physicians who perform canal-wall-up procedures recommend a second-look procedure 6-12 months after the first surgery. This is basically the same as the first surgery but since most of the work has been done, it is usually a somewhat shorter procedure. A canal-wall-down procedure means that the ear canal is removed and opened up into the mastoid cavity behind the ear. This is called a mastoid bowl. In most cases, it is quite obvious to any physician who looks in the ear that surgery has been performed because the ear canal is no longer a tube, it is a large cavity. A standard part of this procedure is a meatoplasty. This means that the ear canal is surgically enlarged, in order to permit proper aeration of the mastoid bowl and reduce the chances of infection. Most patients need to have their mastoid bowl cleaned out by an otolaryngologist every 6-12 months. This is because the normal process of the ear canal to extrude earwax and debris has been disrupted. A second look operation is usually not needed after a canal-wall-down tympanoplasty with mastoidectomy, because any residual cholesteatoma can be easily seen and removed in clinic. With either a canal-wall-up or canal-wall-down, an ossicular chain reconstruction to rebuild the middle ear bones may be considered. This can be done at the time of the first surgery or at a second surgery 6-12 months later. This length of time is preferred because it gives time after the first surgery for the ear to heal. If a second surgery for ossicular chain reconstruction is planned, many surgeons will place a piece of Silastic into the middle ear space. This is a thin sheet of rubbery plastic that prevents scar tissue from forming between the eardrum and the inner ear, simplifying the second surgery.

Results of Surgery
The primary goal of surgery for chronic otitis media and cholesteatoma is to remove all infection and cholesteatoma. Hopefully, this will stop the ear from draining, and prevent further complications later on in life. A good result may be expected in 80-90% of the cases. The secondary goal is to improve your hearing. Failure to improve hearing is not a complication. Success depends almost as much on the ability of the body to heal and preserve the reconstruction as it does on the surgeons skill. Fortunately, even those cases that fail may be revised.
Stanford Medicine School of Medicine Departments Otolaryngology Oghalai Lab Patient Resources

OGHALAI LAB

Childhood otitis media ii. specialist view


Henley C. Harrison, Specialist, Sydney

Summary
Three presentations of otitis media are common in children: acute, recurrent and otitis media with effusion (glue ear). Antimicrobial treatment lessens the duration of pain in acute otitis media and may prevent serious complications. Recurrent otitis media may be managed best by treating each attack, but, if it is severe, preventive treatment may help. Otitis media with effusion usually resolves without surgery, but, if it is chronic, ventilation tubes may be required. These tubes effectively restore hearing and relieve other symptoms, but do not cure the underlying causes. Recurrences can occur when the tube ceases to function and reinsertion may be needed. Otitis media with effusion may have long-term effects on educational performance. Key words: antibiotics, ventilation tubes, glue ear, deafness. Aust Prescr 1994;17:84-7

Introduction Otitis media can be classified as:


acute (suppurative) otitis media otitis media with effusion (glue ear) chronic suppurative otitis media o without cholesteatoma o with cholesteatoma

Acute otitis media and glue ear are closely related and can merge into one another. While acute otitis media has a rapid onset of symptoms and signs of inflammation, in glue ear there is a relatively asymptomatic effusion in the middle ear.

Acute otitis media Diagnosis Not all cases present with the typical picture of significant earache, sleeplessness, pyrexia and a bulging red tympanic membrane. Complaints of earache can be muted and only represented by irritability or bad behaviour. Pyrexia may be minimal and tympanic membrane changes can be almost identical to those of glue car. However, the association of several of these symptoms and signs usually alerts practitioners to the diagnosis, especially if they are familiar with the features of the normal tympanic membrane. In acute otitis media, redness, bulging and apparent opacity of the tympanic membrane will usually be seen. If an otoscope with an attached bulb is used to puff air into the ear canal, the mobility of the tympanic membrane will be reduced or absent. The view may be obscured by wax or by struggling infants, but an accurate clinical diagnosis is usually possible in most cases. Tympanometry may help, but is often unsatisfactory in the difficult situations where it would be of most assistance. Perforation of the tympanic membrane in acute otitis media is the usual cause of discharge in the child's external auditory canal as primary otitis externa is uncommon in young children. Parents can be reassured that perforations usually heal spontaneously. Treatment (Fig. 1) The bacteria most commonly grown from the exudate of acute otitis media are Streptococcus pneumoniae, non-typeable Haemophilus influenzae and Moraxella (Branhamella) catarrhalis1. Unfortunately, vaccines againstHaemophilus influenzae are only effective against type b organisms and I do not believe they will reduce the incidence of otitis media. Most studies report growth in ~ 50% of cases,

but in a recent study which maximised the chances of growth, bacteria were grown in 90%.2 A recent controlled study of antibiotics in otitis media3 showed that treatment failure was 8 times more likely in the placebo group than the treatment group. Antibiotics relieved pain more rapidly than placebo and, the day after entry into the study, the placebo group had a significantly higher incidence of fever. Analgesic consumption, duration of crying and absence from school were also higher in the placebo group. Antimicrobials may also be responsible, at least in part, for the current rarity of serious complications, which had an incidence of up to 20% in the pre-antibiotic era.1 Despite the spread of ampicillin-resistant Haemophilus influenzae, amoxycillin (4050 mg/kg/day) is still, on empirical grounds, an appropriate first choice antimicrobial in Australia (the incidence of beta-lactamase-producing organisms in otitis media in Australia is not known, although high incidences are present in respiratory tract isolates).1Amoxycillin/potassium clavulanate and cefaclor are also satisfactory1 and are especially appropriate if improvement does not occur in a sick child after 24-36 hours of treatment with an antimicrobial such as amoxycillin or in the case of an early recurrence (within one month). These drugs may become more appropriate as first choice medications if the effectiveness of amoxycillin wanes as resistance increases.

Fig. 1 Acute otitis media

Recent concerns about the adverse effects of trimethoprim/ sulfamethoxazole have led to reduced usage of the combination, but it may still be considered if the child is allergic to penicillin.1 The main alternatives in these children are cefaclor and

trimethoprim. Cefaclor has an incidence of cross-sensitivity with penicillin4 so trimethoprim may prove to be the drug of choice in the case of penicillin allergy, although it is comparatively unproven for otitis media. Erythromycin, penicillin, 'first generation' cephalosporins (e.g. cephalexin) and sulphonamides alone do not adequately treat the common organisms.1 Analgesics may also be needed. Myringotomy is rarely used in Australia for acute otitis media. It may have a place if there is severe, persistent pain which does not respond to antimicrobials or if there is concern about a possible complication. Complications The effusion of acute otitis media tends to clear with time, but in 20-40% of cases, patients' ears will still have an effusion (otitis media with effusion) after one month and in 10% of cases after 12 weeks.1 Children should be checked between 3 and 6 weeks after an attack of acute otitis media to make sure that the ears do clear. Recurrent attacks will interfere with natural resolution and make chronic otitis media with effusion more likely. Other sequelae are less common (see Table 1). Recurrent otitis media Recurrent otitis media may be defined as 3 acute attacks in 6 months.1 This is more likely in the presence of otitis media with effusion. Many cases can be managed by general practitioners, but referral to a paediatrician may be indicated if an underlying medical cause is suspected, such as a possible immune deficiency.

Table 1 Complications of acute otitis media Extracranial


chronic tympanic membrane perforation chronic suppurative otitis media cholesteatoma mastoiditis facial palsy suppurative labyrinthitis

Intracranial

meningitis cerebral thrombophlebitis

lateral sinus thrombosis benign intracranial hypertension intracranial abscess

Generalised

septicaemia pyaemia

Preventive treatment, usually prophylactic antibiotics or the insertion of a ventilation tube (grommet), may be worthwhile if the attacks are frequent (e.g. every 2-3 weeks) or severe (e.g. significant pain or sleep loss). In contrast, if the attacks are infrequent (e.g. second monthly) or not severe, prophylactic treatment is probably not worthwhile. This is because, even if prophylaxis is completely successful, it will only prevent one or two attacks in a 3-month course of antimicrobials or 4 attacks in the average duration of action of a ventilation tube (9 months). If a prophylactic antimicrobial is prescribed, amoxycillin 25-50 mg/kg/day is appropriate. Trimethoprim/sulfamethoxazole is an alternative which can reduce recurrences, but the possibility of serious adverse effects from sulphonamides should be taken into account.1 Ventilation tubes are considered if the ears do not clear between attacks (i.e. there is concurrent otitis media with effusion), if antimicrobials are not tolerated (or have failed) or if attacks are very severe. Ventilation tubes usually eliminate or greatly alleviate recurrent otitis media while they are functional, but success cannot be guaranteed. With a ventilation tube in situ, otitis media usually presents with aural discharge which often clears quickly. If discharge persists, pseudomonas could be involved and ear drops (often containing an aminoglycoside) may be necessary. Although there is a theoretical risk of sensori-neural deafness due to the aminoglycoside, I have never seen this complication. Adenoidectomy may help if the above measures fail5, but I rarely use it unless adenoids are enlarged. Tonsillectomy may help in children whose recurrent otitis media is accompanied by tonsillitis. Otitis media with effusion (glue ear) The pathogenesis is probably multi factorial1, but eustachian tube hypofunction, leading to inadequate middle ear aeration, may be the immediate cause. Glue ear often follows acute otitis media or a viral upper respiratory infection. Its prevalence is highest at about two years of age6, hence factors related to immaturity probably

contribute to eustachian tube hypofunction. Some studies have shown an increased incidence of glue ear in association with parental smoking.1 Diagnosis Symptoms include deafness (often presenting as speech delay or poor speech), pain or discomfort (which may cause sleep loss), irritability, bad behaviour and, in 20% of patients, imbalance - so deafness is not the only symptom which may require relief. In some cases, otitis media with effusion is asymptomatic. The appearance of the tympanic membrane may be little different from normal, but any departure from the normal should arouse suspicion of glue ear. Usually the tympanic membrane becomes retracted, opaque and discoloured. Blood vessels (often running radially) may be visible on the surface of the membrane and its mobility is usually reduced (hence the general practitioner may find a pneumatic otoscope useful). Alternatively, a fluid meniscus or bubbles in fluid may be visible through the tympanic membrane. Audiometry is usually diagnostic in co-operative patients. Treatment i. Conservative Most cases resolve spontaneously in 3 months. Therefore, if otitis media with effusion is asymptomatic or if mild deafness is the only significant symptom, it is reasonable to wait until the condition has been present for 3 months before surgical intervention. Meanwhile, social management should be undertaken. This can include changing the child's position in the classrooom, advising extra caution on the roads and encouraging the parents to stop smoking. Auto-inflation of the middle ear is not helpful, apart from the 'Otovent' device which is reported to improve the resolution rate significantly in the short term.1 However, it is not yet known if the device reduces the need for surgical treatment. ii. Drugs During the observation period, medical treatment can be used. A course of antibiotics of 10-30 days' duration is probably somewhat efficacious1 if they have not already been tried. Steroids, with or without antibiotics, have been studied with conflicting results, mostly favouring steroids by a small margin. The potential benefits may be outweighed by the risks and the incidence of relapse.

Antihistamines, nasal decongestants, mucolytic agents and non-steroidal antiinflammatory drugs are not beneficial.1Successful treatment of allergic or infective rhinitis (or sinusitis) may cure otitis media with effusion. iii. Surgery If after 3 months there is no resolution, the insertion of ventilation tubes immediately restores the hearing and relieves other symptoms by aerating the middle ear. However, one must be flexible and treat the patient, not just the disease. Earlier insertion may be indicated in some circumstances including severe pain, worrying tympanic membrane changes, unsteadiness, irritability and communication problems. Conversely, surgery can be delayed if there are minimal or no symptoms or if there is evidence of improvement. Ventilation tubes are beneficial while they function, but afterwards, if maturation has not relieved the underlying causes of eustachian tube hypofunction, there may be a recurrence which requires ventilation tubes to be reinserted. Adenoidectomy is the other surgical treatment frequently used for glue ear, but there is no agreement about its efficacy. It is a bigger operation than ventilation tube insertion and the results may not be as beneficial. I only perform adenoidectomy (usually combined with ventilation tubes) in patients with repeated recurrences of otitis media with effusion or when there is evidence of significant adenoid hypertrophy. Tonsillectomy can also confer benefit in glue ear if enlarged tonsils cause respiratory obstruction or if acute otitis media occurs in association with recurrent tonsilitis. In such cases, indications for tonsilectomy in its own right will be present. Complications It is not known if deafness due to glue ear has a long-term effect on speech and education. There is evidence that children become 'otitis prone' during the first 3 years of life and that educational damage may be greatest during this time.7 Very persistent effusions may be associated with middle ear complications e.g. adhesive otitis media, tympanic membrane atrophy. Chronic suppurative otitis media Chronic suppurative otitis media is usually characterised by a chronic perforation of the tympanic membrane which may be moist (suggesting inflammatory activity) or dry (suggesting inactivity). It may or may not be accompanied by cholesteatoma.

Cholesteatoma is a destructive, serious condition consisting of a collection of keratinising epithelium in the middle ear or mastoid usually associated with a perforation which is most frequently in the attic or postero-superior portion of the tympanic membrane. Unless discharge (which may be foul-smelling) obscures vision, there is often white matter visible in the perforation and usually an incomplete margin of tympanic membrane remnant surrounding the perforation. Chronic suppurative otitis media usually requires surgery. Referral to an ear, nose and throat surgeon is appropriate, especially if cholesteatoma is suspected. References

1. T he NSW Health Department Working Party. Guidelines on the management of paediatric middle ear disease. Med J Aust 1993;159(Suppl):1S-8S. 2. D el Beccaro MA, Mendelman PM, Inglis AF, Richardson MA, Duncan NO, Clausen C, et al. Bacteriology of acute otitis media: a new perspective. J Pediatr 1992;120:81-4. 3. B urke P, Bain J, Robinson D, Dunleavey J. Acute red ear in children: controlled trial of non-antibiotic treatment in general practice. Br Med J 1991;303:558-62. 4. S olley GO. Testing for drug allergy. Aust Prescr 1994;17:62-5. 5. P aradise JL, Bluestone CD, Rogers KD, Taylor FH, Colborn DK, Bachman RZ, et al. Efficacy of adenoidectomy for recurrent otitis media in children previously treated with tympanostomy-tube placement. Results of parallel randomized and non-randomized trials. JAMA 1990;263:2066-73. 6. Z ielltuis GA, Rach GH, van den Bosch A, van den Broek P. The prevalence of otitis media with effusion: a critical review of the literature. Clin Otolaryngol 1990;15:283-8. 7. T eele DW, Klein JO, Chase C, Menyuk P, Rosner BA. Otitis media in infancy and intellectual ability, school achievement, speech and language at age 7 years. Greater Boston Otitis Media Study Group. J Infect Dis 1990;162:685-94.

Self-test questions
The following statements are either true or false (click here for the answers) 1. Asymptomatic otitis media with effusion can cause hearing impairment and requires urgent surgical intervention. 2. A 3-month course of antibiotics may benefit a child with severe attacks of recurrent otitis media occurring every 2-3 weeks.

Content created: October - 1994

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