LAPORAN KASUS

MASTOIDITIS KRONIK

Disusun Oleh:
Edwin Halim 07120110101

Pembimbing:
Dr. Pulo R.S. Banjarnahor, Sp. THT

KEPANITERAAN KLINIK DEPARTEMEN TELINGA HIDUNG

TENGGOROK
FAKULTAS KEDOKTERAN UNIVERSITAS PELITA HARAPAN
 Daftar Isi
Laporan Kasus .................................................................................................................. 43
Identitas Pasien ..........................................................................................................................43
Anamnesis ....................................................................................................................................43
Keluhan Utama ....................................................................................................................................... 43
Keluhan Tambahan................................................................................................................................ 43
Riwayat Perjalanan Penyakit .............................................................................................................. 43
Riwayat Penyakit Dahulu .................................................................................................................... 65
Riwayat Penyakit Keluarga ................................................................................................................ 65
Riwayat Sosial dan Kebiasaan ........................................................................................................... 65
Riwayat Alergi ........................................................................................................................................ 65
FIFE............................................................................................................................................................ 65
Pemeriksaan Fisik .....................................................................................................................76
Pemeriksaan Penunjang.................................................................................................... 1211
Pemeriksaan Radiologi ...................................................................................................... 1312
Diagnosis Banding ............................................................................................................... 1413
Resume .................................................................................................................................... 1413
Daftar Masalah ...................................................................................................................... 1413
Pengkajian Masalah ............................................................................................................ 1413
Prognosis ................................................................................................................................ 1514
Tinjauan Pustaka ........................................................................................................ 1817
Mastoiditis .............................................................................................................................. 1817
Background ......................................................................................................................................... 1817
Etiology ................................................................................................................................................ 1918
Epidemiology ..................................................................................................................................... 2019
Prognosis ............................................................................................................................................. 2120
History ..................................................................................................................................... 2322
Physical Examination ...................................................................................................................... 2423
Diagnostic Considerations ............................................................................................................. 2423
Differential Diagnoses..................................................................................................................... 2524
Imaging Studies ................................................................................................................................. 2625
Approach Considerations.................................................................................................. 2726
Medication Summary .......................................................................................................... 2928
Pharmacologic Therapy..................................................................................................... 3029
Myringotomy/Tympanocentesis and Tympanostomy Tube Placement .......... 3029
Mastoidectomy...................................................................................................................... 3130
Preoperative details .......................................................................................................................... 3130
Intraoperative details........................................................................................................................ 3231
Complications associated with mastoidectomy ....................................................................... 3736
DAFTAR PUSTAKA ............................................................................................................... 3938
Laporan Kasus .............................................................................................................3
Identitas Pasien .................................................................................................................... 3
Anamnesis ............................................................................................................................ 3

2
 Keluhan Utama .................................................................................................................. 3
Keluhan Tambahan ............................................................................................................ 3
Riwayat Perjalanan Penyakit ............................................................................................. 3
Riwayat Penyakit Dahulu .................................................................................................. 5
Riwayat Penyakit Keluarga ............................................................................................... 5
Riwayat Sosial dan Kebiasaan........................................................................................... 5
Riwayat Alergi .................................................................................................................. 5
Pemeriksaan Fisik ............................................................................................................... 5
Pemeriksaan Penunjang ..................................................................................................... 8
Resume ............................................................................................................................... 10
Daftar Masalah .................................................................................................................. 10
Pengkajian Masalah .......................................................................................................... 10
Prognosis ............................................................................................................................ 11
Tinjauan Pustaka ....................................................................................................... 13
Mastoiditis .......................................................................................................................... 13
Background ..................................................................................................................... 13
Etiology ........................................................................................................................... 14
Epidemiology .................................................................................................................. 15
Prognosis ......................................................................................................................... 16
History ................................................................................................................................ 18
Physical Examination ...................................................................................................... 19
Diagnostic Considerations ............................................................................................... 19
Differential Diagnoses ..................................................................................................... 20
Imaging Studies ............................................................................................................... 21
Approach Considerations ................................................................................................. 22
Medication Summary ........................................................................................................ 24
Pharmacologic Therapy .................................................................................................... 25
Myringotomy/Tympanocentesis and Tympanostomy Tube Placement ....................... 25
Mastoidectomy ................................................................................................................... 26
Preoperative details ......................................................................................................... 26
Intraoperative details ....................................................................................................... 27
Complications associated with mastoidectomy ............................................................... 31

3
 Laporan Kasus

Identitas Pasien
Nama : Bp. FY
Umur :21 tahun
Jenis kelamin : Pria
Agama : Kristen
Pekerjaan : Mahasiswa
Alamat :-
Status : Belum menikah

Anamnesis
Anamnesis dilakukan secara autoanamnesis tanggal 66 Februari 2015. Pasien
masuk IGD tanggal 3 Februari 2015.

Keluhan Utama

Terdapat sekret telinga berbau disertai darah 2 hari SMRS.

Keluhan Tambahan

Sakit kepala, demam dan vertigo 2 minggu yang lalu, disusul pilek 1 minggu
yang lalu.

Riwayat Perjalanan Penyakit

Pasien datang dengan keluhan keluar sekret berbau disertai darah dr telinga 2
hari yang lalu. Ia mengatakan sekret tersebut sudah lama keluar secara periodik (>5
tahun yang lalu), namun baru beberapa hari ini mulai mengeluarkan darah. Dimulai

4
maupun berakhirnya sekresi dari sekret tersebut tidak dirasa dicetuskan oleh apapun.
Pasien juga mengaku tidak ada yang memperingan ataupun memperburuk sekresi
sekretnya.Saat ia datang, terlihatfistul pre-auriretro-aurikuler A.S. dengan sekret
purulen yang bau. Di ruang gawat darurat, pasien mengatakan bahwa ia mual dan
muntah setiap kali makan sejak 3 hari SMRS.

Sebelum ia masuk kerumah sakit, pasien mengaku sudah mengalami demam,

sakit kepala, dan vertigo selama 2 minggu SMRS, yang kemudian disusul pilek 1
minggu SMRS. Pasien mengatakan bahwa ia tidak mengukur suhu demamnya. Sakit
kepala pasien dirasakan diseluruh kepala dengan karakteristik berdenyut. Pasien
mengakatan tidak Pasien mengakui bahwa karakteristik sakit kepala dan vertigo 2
minggu SMRS sama dengan yang ia alami sekarang, namun dengan tingkat
keparahan yang lebih hebat.

Pasien mengaku ia merasa otalgia dg skala 3-4/10 disertai pendengaran yang

berkurang. Nyeri tidak membaik atau memburuk dengan apapun, tidak menyebar ke
mandibula, dan bersifat konstan. Penurunan pendengaran pasien sudah kronis (>5
tahun), namun diakui terasa memburuk secara sangat signifikan belakangan ini.
Sebelum kejadian ini, penurunan pendengaran pasien dirasa tidak terlalu mengganggu
hidup sehari hari pasien.

Sebelum masuk RSUS, pasien telah berobat ke klinik terkait permasalahan ini,
namun obat yang diberikan hanya memberi sedikit perbaikan, yang kemudian disusul
dengan perburukan kondisi pasien. Pasien tidak mengingat dan tidak membawa resep
obat yang dikonsumsi.

Pada saat auto-anamnesa tanggal 66 Februari, pasien mengalami otalgia yang

bertambah hebat dengan skala 8/10, disertai vertigo. Saat ini pasien tidak dapat
membedakan lagi antara otalgia yang ia alami dengan sakit kepala. Pasien mengakui
tidak mengalami demam selama dirawat dirumah sakit, namun mual dan muntah terus
berlanjut tanpa perubahan dari awal masuk RS. Pasien mengatakan bahwa ia sulit
makan karena seringkali muntah setelah makan. BAK pasien lancar, namun BAB
agak sulit. Pasien tidak mengalami penglihatan ganda, sesak nafas, nyeri dada,
ataupun gangguan fungsi motorik.

5
 Pasien mengatakan bahwa fistula pre-auriretro-aurikuler yang ia alami sudah
ada sejak >5 tahun yg lalu dan telah lama mengalami otorea yang rekurren, baik dari
fistula maupun dari liang telinga, namun ia tidak dapat mengatakan dengan persis
kapan ia mulai mengalami otorea.

Riwayat Penyakit Dahulu

Pasien menyangkal memiliki riwayat konsumsi obat-obatan jangka panjang,

dan tidak pernah mengkonsumsi obat-obatan periodik (Tuberkulosis).Tidak ada
riwayat penyakit jantung, ginjal, diabetes maupun stroke. Pasien mengaku pernah
mengalami beberapa episode vertigo sebelumnya. Vertigo tersebut dikatakan tidak
memiliki pola tertentu, membaik bila pasien diam saja selama beberapa menit, dan
diiringi oleh otorea dari liang telinga maupun fistula.

Riwayat Penyakit Keluarga

Tidak ada keluarga pasien yang mengidap diabetes mellitus. Tidak ada riwayat
penyakit jantung, ginjal, maupun keganasan.

Riwayat Sosial dan Kebiasaan

Pasien menyangkal memiliki riwayat merokok ataupun minum alkohol. Pasien

tinggal di kos-kosan/asrama.

Riwayat Alergi

Pasien mengakui memiliki alergi terhadap ikan asin.

FIFE

Feeling : Pasien merasa sangat terganggu dengan penyakitnya

Idea : Pasien mengira ini penyakit telinga yang kumat
Fear : Pasien takut kuliahnya tertunda lebih lama lagi
Expectation : Pasien ingin secepatnya keluar dari rumah sakit

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Pemeriksaan Fisik
Status Generalis
Kesadaran: Kompos Mentis
(Pada tgl 3 Feb) :

TD: 135/90

Nadi: 94x/ menit

Pernapasan: 20x/ menit

Suhu: 37.1oC

Kepala: Bentuk tulang kranii normal, tidak ditemukan

benjolan ataupun daerah nyeri tekan.

Mata: Konjungtiva tidak diperiksa, sclera ikterik -/-

Tidak ditemukan drooping eyelid(Parese N. VII)

Tidak ditemukan displacement superior maupun

inferior dari bola mata

Tidak ditemukan proptosis (Inflamasi Peri-orbita)

Telinga: Serumen + / ?

Jaringan granulasi pada A.S., serumen pada A.D.

Tragus dan auricle kanan intak,pada aurikel kiri nyeri

tekan (+)disertai proptosis daun telinga dan
ditemukan fistula pada bagian belakang fossa
triangulariscrus superior (antihelix).

Hidung: Bentuk normal, tidak ada deviasi septum, tidak ada

luka. Pada saat pemeriksaan tidak ditemukan adanya
sekret.

Mulut: Tidak tampak kering, tidak tampak cyanosis, tonsil

tidak diperiksa, tidak ada deviasi bibir.

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 Leher: Tidak tampak luka, tidak tampak pembesaran
kelenjar getah bening.

Thoraks: Inspeksi: Bentuk dada normal dengan

pergerakan simetris.

Palpasi: -

Perkusi: -

Auskultasi: -

Abdomen: Inspeksi: Bentuk abdomen normal dan

simetris, tidak tampak lesi.

Auskultasi: Bising usus normal.

Perkusi: -

Palpasi: -

Ekstremitas: Atas: Refleks Hoffman-Traumer negatif.

Bentuk normal, tidak tampak
deformitas dan edema, akral hangat,
capillary refill tidak diperiksa.

Bawah: Normal, tidak tampak deformitas

maupun edema, akral hangat. Kernig
sign positif, kaku kuduk positif,
babinski negatif, dan brudzinski sign
negatif. Refleks babinski tidak
diperiksa.

Status Lokalis

Telinga

Inspeksi:

Aurikula Aurikula
Sinistra Dextra

8
 Pinna Deformitas Proptosis -

Meatus Ukuran Tidak ada Tidak ada

pembesaran pembesaran

Kulit Eritem/ Edema pada - Formatted: Right: 0.02"

jaringan bagian temporal,

fibrotik/ luka/ terdapat fistul
edem pre-auriretro-
aurikuler
dibelakang fossa
triangularisCrus
Superior (anti-
helix)

Discharge + -

Berbau seperti
keju busuk

Otoskop

Meatus Nyeri tekan Liang telinga

akustikus tragus (+) tertutup
eksterna serumen
Liang telinga
tertutup jaringan
granulasi

Reflek cahaya - -

Membran Warna - -
timpani
Edem - -
(Tidak dapat
Bentuk - -
divisualisasi)

Palpasi: Nyeri tekan -/+

9
 Tes Pendengaran
o Whispered voice test: Tidak dilakukan
o Tes Garpu Tala dengan 512 Hz
Rinne : Tidak dilakukan
Webber : Tidak dilakukan
Swabbach: Tidak dilakukan

Hidung

Inspeksi

-Bentuk hidung : Simetris, tidak tampak deformitas pada

piramida nasi esksterna

-Hematom :-

Rinoskopi Anterior

-Kavum nasi anterior : tidak tampak perdarahan ataupun sekret

-Konka inferior : Eutrofi / Eutrofi

-Konka media : tidak terlihat

-Septum nasi : Deviasi ke kiri

-Polip : -/-

-Benda asing : -/-

-Edem : -/-

Palpasi
-Nyeri tekan os nasal : -/-
-Krepitasi : -/-

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Tenggorokan

Inspeksi
-Bibir kering, tidak ada luka
-Mukosa baik, gingivitis (-), gigi lengkap, lubang (-)
-Pallatum mole dan pallatum durum baik, cleft (-), abnormal arch
(-), telangiectasia (-).
-Lidah baik, atrofi (-)
-Tonsil T1/T1, simetris, hiperemis (-)
-Uvula tidak deviasi
-Faring tidak hiperemis

Wajah

Inspeksi
-Edem pada regio temporalis sinistra
-Eritem (sulit terlihat)

Palpasi
-Nyeri tekan regio temporalis (-/+)

Leher

Inspeksi
-M. Sternocleidomastoid dan M. Trapezius kiri dan kanan simetris
-Trakea tampak di garis tengah
-Tidak tampak luka/ massa

Palpasi

-Trakea teraba pada garis tengah

-Tidak teraba pembesaran kelenjar getah bening kedua sisi leher

-Kelenjar tiroid tidak terfiksasi dan tidak membesar

11
Pemeriksaan Penunjang

Tanggal 3 Februari 2015

Jenis Pemeriksaan Hasil Nilai Rujukan

Hemoglobin 16.61 12 16g/dL

Hematokrit 49.53 37 47%

Eritrosit 6.56 4.3 6.0juta/uL

Leukosit 8.06 4.800 10.800/uL

Hitung Jenis :

Basofil 1 01%

Eosinofil 5 13%

Batang 3 26%

Segmen 68 50 70 %

Limfosit 17 20 40 %

Monosit 6 28%

Trombosit 272 150.000 400.000/uL

ESR 3 0 15 mm/hour

MCV 75.5 80 100 fL

MCH 25.3 26 34 pg

MCHC 33.5 32 36 g/dL

SGOT <35 U/L

SGPT <40 U/L

Albumin 3.5 5.0 g/dL

Ureum 20-50 mg/dL

Kreatinin 0.5-1.5 mg/dL

Asam urat 2.4 5.7 mg/dL

Natrium (Na) 143 135 147 mmol/L

Kalium (K) 3.7 3,7 5,2 mEq/L

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Klorida (Cl) 105 95 105 mmol/L

HbA1c 5.7 6.4%

Gula Darah Sewaktu

Pemeriksaan Radiologi

Hasil Pemeriksaan CT Mastoid (Non-kontras, potongan Axial + Koronal):

Kesan:

Mastoiditis kiri
Sinusitis Etmoidalis dan Maksilaris Bilateral
Deviasi Septum nasi ke kiri

13
Diagnosis Banding
Mastoidits Kronik dengan penyebaran intrakranial
Otitis Media Suppuratif Kronik dengan kolesteatoma

Resume
Pasien datang dengan keluhan sekret dan darah yang keluar dari telinga kiri 2
hari SMRS yang disertai sakit kepala, vertigo, dan mual muntah. Sekret dan darah
keluar secara periodik dan bersifat hilang-timbul pada periode-periode tersebut.Pasien
mengaku memiliki fistul pre-auriretro-aurikuler telinga kiri selama >5 tahun yang
lalu, namun baru berobat 2 minggu yang laluSMRS ke klinik karena mengalami pilek
dan demam yangmencetuskan gejala serupa dengan sekarang, namun lebih ringan,
yang kemudian disusul pilek 1 minggu SMRS. Pasien memiliki gangguan
pendengaran pada telinga kiri selama kurang lebih sama dengan munculnya fistul pre-
auriretro-aurikuler (>5 tahun lalu), namun beberapa hari terakhir terjadi perburukan
pendengaran yang signifikan, disertai dg otalgia yang bertambah hebat. Pada
pemeriksaan fisik ditemukan proptosis daun telinga, fistula pre-auriretro-aurikuler
dibelakang fossa triangulariscrus superior (antihelix), dan sekret berbau seperti keju
busuk dari liang telinga yang terisi jaringan granulasi maupun dari saluran fistul.
Pemeriksaan lab menunjukkan hemoglobin yang meningkat, dengan MCV dan MCH
yang sedikit menurun. Imaging CT mastoid menunjukkan adanya mastoiditis pada air
cells mastoid sinistra.

Daftar Masalah
Mastoiditis Sinistra dengan Fistula pre-auriretro-aurikuler
Cephalgia

Pengkajian Masalah
1. Mastoiditis Sinistra dengan fistula pre-auriretro-aurikuler
a. Klinis:

14
 i. Terdapat fistul pada kepala pasien, diseberang fossa
triangulariscrus superior (antihelix) aurikel sinistra
b. Rencana diagnosis:
i. CT-scan Mastoid
c. Penatalaksanaan:
i. Persiapan bedah mastoid
ii. Bilas liang telinga dengan H2O2 sembari menunggu jadwal
bedah untuk mengurangi sekret dan nyeri telinga
iii. Pemberian antibiotik untuk menahan/melokalisir infeksi
terlebih dahulu sebelum operasi
2. Cephalgia D.D. meningitispenyebaran reaksi inflamasi kedalam ruang
intrakranial
a. Klinis:
i. Terdapat sakit kepala yang disertai mual dan muntah.
b. Pemeriksaan fisik:
i. Kernig sign serta kaku kuduk yang positif, namun brudszinski
sign dan hoffman-traumer negatif.
c. Pemeriksaan Lab:
i. CBC tidak menunjukkan adanya tanda infeksi
d. Penatalaksanaan:
i. Pemberian obat anti-emetik dan analgesia sembari menunggu
jadwal operasi mastoidektomi

Prognosis
Ad vitam: bonam
Ad functionam: dubia ad bonam
Ad sanationam: bonam

15
04/02/2015 07/02/2015 13/02/2015

S: sakit kepala, otalgia dan S: muntah (-), mual (-), sakit S: A.S. mengeluarkan darah.
mual, muntah 3x/hari kepala (-), otalgia (-) Pusing (-), Sakit Kepala (-),
mual & muntah (-), otalgia (-).
Intake per oral hampir selalu Intake pasien rendah, sulit
dibarengi muntah makan. Pasien meminta pulang
secepatnya
O: CM O: CM
O: CM
Telinga: Telinga:
Telinga:
A.S. : Sekret (+), jaringan A.S. : Sekret (+), jaringan
granulasi (+), nyeri tekan granulasi (+), nyeri tekan A.S. : Sekret (+), sekret
tragus (+), proptosis daun tragus (-), proptosis daun berdarah (+), jaringan
telinga (+), bengkak sekitar telinga (+), bengkak sekitar granulasi (+), nyeri tekan
daun telinga sinistra, hearing daun telinga sinistra masih tragus (-), proptosis daun
loss (+) ada. telinga (+), bengkak (-).

A.D. : Serumen (+), otalgia (-), A.D. : tidak diperiksa A.D. : tidak diperiksa
nyeri tekan tragus (-),
proptosis daun telinga (-) Kaku kuduk & Kernig sign (-) A: Operasi belum
memungkinkan 3 hari
Kaku kuduk & Kernig sign (+) A: CT scan mastoiditis A.S. kedepan; pasien dijadwal
disertai sinusitis ethmoidalis kontrol tgl 20 Feb mendatang
Hoffman traumer & dan maksilaris bilateral.
Brudzinski (-) Septum nasi deviasi ke kiri. P: Persiapan pasien untuk
rawat jalan
A: Mastoiditis kronik A.S. P: Booking OT dan jadwal
dengan fistul retro-aurikuler mastoidektomi Th/
dan jaringan granulasi susp.
kolesteatoma Th/ Levofloxacin 1x500 mg

Cephalgia susp. meningitis IVFD NaCl 0.9% Tarivid 2x gtt II A.S.

P:CT Mastoid Aminofluid 1000 cc/24 jam Lapifed 3x1 tab

Th/ Tarivid 2x gtt II A.S. Acetylcystein 3x1

IVFD NaCl 0.9% H2O2 3% 2x gtt II A.S. Sucralfat 3x1

Metronidazole 3x500 IV Domperidon 3x10 mg Flamicort 3x200 mg

Tarivid 2x gtt II A.S Ceftriaxone 2x2 gr IV Paracetamol 3x500 mg (p.r.n)

Ketorolac 3x30 mg

Mional 3x50 mg

Ondansetron 2x8 mg IV

Omeprazole 2x20 mg
17
 Tinjauan Pustaka
Mastoiditis
Background
A purist's definition of mastoiditis includes all inflammatory processes of the mastoid air cells
of the temporal bone. As the mastoid is contiguous to and an extension of the middle ear cleft,
virtually every child or adult with acute otitis media (AOM) or chronic middle ear
inflammatory disease has mastoiditis. In most cases, the symptomatology of the middle ear
predominates (eg, fever, pain, conductive hearing loss), and the disease within the mastoid is
not considered a separate entity (see the image below).

Mastoiditis with subperiosteal abscess. Note the loss of the skin crease and the pointed abscess.

Acute mastoiditis is associated with AOM. In some patients, the infection spreads beyond the
mucosa of the middle ear cleft, and they develop osteitis within the mastoid air-cell system or
periosteitis of the mastoid process, either directly by bone erosion through the cortex or
indirectly via the emissary vein of the mastoid. These patients have acute surgical mastoiditis
(ASM), an intratemporal complication of otitis media.

Chronic mastoiditis is most commonly associated with chronic suppurative otitis media and
particularly with cholesteatoma formation. Cholesteatomas are benign aggregates of
squamous epithelium that can grow and alter normal structure and function of surrounding
soft tissue and bone. This destructive process is accelerated in the presence of active infection
by the secretion of osteolytic enzymes by the epithelial tissue.

Progression of mastoiditis
Mastoiditis progresses in the following 5 stages and may be arrested at any point (see
Presentation and Workup):

18
 Hyperemia of the mucosal lining of the mastoid air cells
Transudation and exudation of fluid and/or pus within the cells
Necrosis of bone by loss of vascularity of the septa
Cell wall loss with coalescence into abscess cavities
Extension of the inflammatory process to contiguous areas

Patient education

Warn patients and their families of possible cosmetic deformity following mastoid surgery.

Etiology
As with most infectious processes, consider host and microbial factors when evaluating
surgical mastoiditis. Host factors include mucosal immunology, temporal bone anatomy, and
systemic immunity. Microbial factors include protective coating, antimicrobial resistance, and
ability to penetrate local tissue or vessels (ie, invasive strains). As the clearance of the
mastoid is dependent upon a patent antrum, resolution is unlikely unless this anatomical
isthmus opens by control of mucosal swelling, which otherwise creates a reservoir for
infection.

Host factors

Most children presenting with acute surgical mastoiditis (ASM) are younger than age 2 years
and have little history of otitis media. This is an age at which the immune system is relatively
immature, particularly with regard to its ability to respond to challenges from polysaccharide
antigens.

Host anatomical factors may have a role. The mastoid develops from a narrow outpouching of
the posterior epitympanum (ie, the aditus ad antrum). Pneumatization occurs shortly after
birth, once the middle ear becomes aerated, and this process is complete by age 10 years.
Mastoid air cells are created by invasion of epithelium-lined sacs between spicules of new
bone and by degeneration and redifferentiation of existing bone marrow spaces.

Other areas of the temporal bone pneumatize similarly, including the petrous apex and the
zygomatic root. The antrum, as with the mastoid air cells, is lined with respiratory epithelium
that swells when infection is present. Blockage of the antrum by inflamed mucosa entraps
infection within the air cells by inhibiting drainage and precluding reaeration from the
middle-ear side.

Persistent acute infection within the mastoid cavity may lead to a rarifying osteitis, which
destroys the bony trabeculae that form the mastoid cells (hence the term coalescent
mastoiditis). Essentially, coalescent mastoiditis is an empyema of the temporal bone that,
unless its progress is arrested, drains either through the natural antrum to give spontaneous
resolution or creates further complication by draining unnaturally to the mastoid surface,
petrous apex, or intracranial spaces. Other temporal bone structures or nearby structures, such
as the facial nerve, labyrinth, and venous sinuses, may become involved.

19
Microbial factors
Reported pathogens in mastoiditis include the following:

Streptococcus pneumoniae Most frequently isolated pathogen in acute mastoiditis,

prevalence of approximately 25%
Group A beta-hemolytic streptococci
Staphylococcus aureus
Streptococcus pyogenes
Moraxella catarrhalis
Haemophilus influenzae
Pseudomonas aeruginosa
Mycobacterium species
Aspergillus fumigatus and other fungi
Nocardia asteroides - Case report[1]

Because acute otitis media (AOM) is the antecedent disease, the most common etiologic
agent causing surgical mastoiditis is Streptococcus pneumoniae, followed by Haemophilus
influenzae and group A Streptococcus pyogenes (GAS). Each of these bacteria has invasive
forms and is recovered most often from children presenting with ASM. More than half of the
Streptococcus pneumoniae recovered are of serotype 19, followed by serotypes 23 and 3.

The literature and the authors' experience indicate that a high frequency of multidrug-resistant
Streptococcus pneumoniae (MDRSP) is now associated with ASM, and this may alter
selection of antimicrobials (40-50% penicillin resistant, approximately 25% ceftriaxone
resistant). Treatment of AOM with antimicrobials in the previous month increases the
frequency of MDRSP.[2]

Gram-negative organisms and Staphylococcus aureus are recovered more frequently from
patients with chronic mastoiditis.

Half of children admitted with acute mastoiditis have no previous history of recurrent AOM.
In those children, Streptococcus pneumoniae has been the leading pathogen, while
Pseudomonas aeruginosa has been more prevalent in children with recurrent AOM.

Epidemiology
Incidence of surgical mastoiditis from acute otitis media is reported as 0.004% in the United
States.[3] Some fear that untreated otitis media increases the risk of acute mastoiditis and is the
cause of higher incidences in developing countries and very young children.[4, 5]

The Inuit population has a high predilection for middle-ear disease and, as a likely
consequence, mastoiditis.

Rates of antibiotic treatment for otitis in the Netherlands, Norway, and Denmark were 31%,
67%, and 76%, respectively. The incidence of mastoiditis was approximately 4 cases per
100,000 children per year over 5 years.

20
Acute mastoiditis is a disease of the very young. Most patients present when younger than age
2 years, with a median age of 12 months. However, it can occur in persons of any age.

A retrospective review of pediatric patients in Colorado found that despite an initial drop in
the incidence of acute mastoiditis in children under age 2 years following the introduction of
heptavalent pneumococcal conjugate vaccine (PCV7), the incidence rose again to pre-PCV7
levels within a few years. The study, by Halgrimson et al, examined pediatric inpatient data
from 1999-2008 for documented cases of acute mastoiditis or patients who had undergone
mastoidectomy.[6]

The investigators found that the annual incidence of acute mastoiditis in children under age 2
years dropped from 11.0 per 100,000 population in 2001, a year after PCV7 was introduced,
to 4.5 per 100,000 population in 2003. By 2008, however, the incidence had again risen, to
12.0 per 100,000 population. An increase in the prevalence of S pneumoniae isolates
nonsusceptible to penicillin also occurred in Colorado, from 0% between 1999 and 2004 to
38% between 2005 and 2008. Halgrimson and colleagues suggested that the presence of non-
PCV7 pneumococcal serotypes and a rise in pneumococcal antibiotic resistance may have
caused the incidence of acute mastoiditis to increase.[6]

Another study, however, found that the introduction of pneumococcal conjugate vaccines
may have led to a national reduction in pediatric mastoiditis rates. The study, by Marom et al,
looked at insurance claims from a nationwide managed health care plan to analyze health care
visits associated with otitis media in children aged 6 years or younger. The investigators
found that between 2008 and 2011, mastoiditis rates decreased from 61 per 100,000 child-
years to 37 per 100,000 child-years.[7]

Prognosis
Expect patients with acute surgical mastoiditis (ASM) to recover completely provided that the
facial nerve, vestibule, and intracranial structures are not involved. Cosmetic deformity of the
operated ear can usually be prevented with judicious placement of the incision and the
development of flaps to pull the ears posteriorly when replaced.

Conductive hearing loss should resolve provided that the ossicular chain remains intact.
Conduct testing after otorrhea has ended and the ear has healed.

Extension of the infectious process of mastoiditis can include the following:

Posterior extension to the sigmoid sinus (causing thrombosis)

Posterior extension to the occipital bone to create an osteomyelitis of calvaria or a
Citelli abscess
Superior extension to the posterior cranial fossa, subdural space, and meninges
Anterior extension to the zygomatic root
Lateral extension to form a subperiosteal abscess
Inferior extension to form a Bezold abscess
Medial extension to the petrous apex
Intratemporal involvement of the facial nerve and/or labyrinth

21
Complications
Complications of mastoiditis include the following:

Hearing loss
Facial nerve palsy
Cranial nerve involvement
Osteomyelitis
Petrositis
Labyrinthitis
Gradenigo syndrome - Otitis media, retro-orbital pain, and abducens palsy
Intracranial extension - Meningitis, cerebral abscess, epidural abscess, subdural
empyema
Sigmoid sinus thrombosis
Abscess formation - Citelli abscess (extension to occipital bone, calvaria),
subperiosteal abscess (abscess between the periosteum and mastoid bone, resulting in
the typical appearance of a protruding ear; see the image below), and Bezold's
abscess (abscess of soft tissues that track along the sternomastoid sheath; Bezold
abscesses are very rare complications and are usually found only in adults with a
well-pneumatized mastoid tip)

Mastoiditis with subperiosteal abscess. Note the loss of the skin crease and the pointed abscess.

Meningitis and facial nerve paralysis are possible in mastoiditis. Approximately 7% of

patients may develop intracranial complications related to acute mastoiditis. These
complications can include sigmoid sinus thrombosis, epidural abscess, and meningitis.
Persistent otalgia or otorrhea with associated neurologic symptoms in a patient taking oral
antibiotics are ominous signs that suggest a complication.

Otogenic meningitis is the most common intracranial complication of neglected otitis media.
In the Western world, such complications seldom occur in children and adolescents and are
extremely rare in adults. The current use of antibiotics and of more sophisticated surgery has
greatly diminished the incidence of otogenic meningitis; however, this has resulted in
physicians having less experience with diagnosis and treatment of this complication.
Emergency surgical treatment is mandatory.

22
In a study done by Luntz et al of 223 consecutive cases of acute mastoiditis, 16 patients
presented with complications, including cerebellar abscess, perisinus empyema, subdural
abscess or empyema, extradural abscess, cavernous sinus thrombosis, lateral sinus
thrombosis, bacterial meningitis, labyrinthitis, petrositis, and facial nerve palsy. [8]

History
Most patients (>80%) have no history of recurrent otitis media. Persistent otorrhea
beyond 3 weeks is the most consistent sign that a process involving the mastoid has
evolved.

The patients fever may be high and unrelenting in acute mastoiditis, but this may be
related to the associated acute otitis media (AOM). Persistence of fever, particularly
when the patient is receiving adequate and appropriate antimicrobial agents, is
common in acute surgical mastoiditis (ASM).

Pain is localized deep in or behind the ear and is typically worse at night. Persistence
of pain is a warning sign of mastoid disease. This may be difficult to evaluate in very
young patients. Hearing loss is common with all processes that involve the middle ear
cleft.

For infants, be attentive to any nonspecific history consistent with infection, such as
poor feeding, fever, irritability, or diarrhea.

In a study by Oestreicher-Kedem et al, the mean interval from onset of illness to

mastoiditis was found to be 4.5 days.[9] Ear cultures most often grew S pneumoniae
and P aeruginosa (23.7% each). Complications occurred in 15.8% of cases. The only
factor differentiating children with and without complications was the white blood
cell count (high in children with complications).

The findings in this study indicate that acute mastoiditis is not only a complication of
prolonged infection of the middle ear but also may present as an acute infection of the
mastoid bone that can progress within 48 hours. The complication rate remains high,
and antibiotic treatment at the onset of symptoms does not prevent complications. A
high white blood cell count on admission may serve as a predictive factor for
complicated cases.

In a study by Niv et al of 113 patients with acute mastoiditis (128 episodes) treated
between 1990 and 2002, the authors concluded that (1) a significant increase in the
incidence of acute mastoiditis in infants had been recorded, although the reason for
the trend was uncertain; (2) in most infants with acute mastoiditis, the disease arose
after the infant's initial AOM episode, and most of the infants had not received prior
antibiotic therapy; (3) infants showed more severe clinical signs and symptoms of
acute mastoiditis than did older patients; (4) S pneumonia was the most common
pathogen isolated in middle ear fluid cultures, but there was a greater involvement of
S pyogenes in the cases of acute mastoiditis than had been reported for AOM.[10]

23
Physical Examination
Acute mastoiditis is a serious bacterial infection of the temporal bone and is the most
common complication of otitis media. Frequent symptoms include mastoid area
erythema, proptosis of the auricle, and fever.[11]

Tenderness and inflammation over the mastoid process is the most consistent sign of
acute surgical mastoiditis (ASM). Periosteal thickening requires comparison to the
other side, and some lateral displacement of the auricle may be present. Subperiosteal
abscess displaces the auricle laterally and obliterates the postauricular skin crease. If
the crease remains, the process is lateral to the periosteum.

Although the diagnosis of acute surgical mastoiditis can often be made on a clinical
basis alone, computed tomography (CT) scanning may be performed for confirmation
of the diagnosis, evaluation of potential complications, and surgical planning. Also
keep in mind that it is possible to have mastoiditis with no history of otitis media,
normal external anatomy, no tenderness, and no external signs of infection.

Otitis media is revealed on otoscopy, often with 1 of the following additional features:

Sagging of the posterosuperior canal wall (possibly a sign of ASM, although not as
reliable in infants)
Nipplelike protrusion of the central tympanic membrane, usually oozing pus
Findings consistent with a complication of extension beyond the mastoid process and
its covering periosteum or another intratemporal complication, such as facial palsy

In adults, the most common symptoms of mastoiditis are otalgia, otorrhea, and
hearing loss, and the physical signs of mastoiditis (ie, swelling, erythema, tenderness
of the retroauricular region) are usually present. Localization and enlargement of the
pathological process within the middle ear spaces can be determined based on CT
scan findings.

Diagnostic Considerations
A high index of suspicion, judicious use of diagnostic modalities, and close follow-up
care are recommended to make a diagnosis in a timely manner

Conditions to consider in the differential diagnosis of mastoiditis include the

following:

Basilar Skull Fracture

Cellulitis
Cysts
Deep Neck Infections
Lymphadenopathy
Parotitis
Stroke
Trauma
Tumors
Histiocytoses

24
 Sarcoidosis
External otitis
Mastoid trauma
Suppuration of postauricular lymph node
Furuncle of meatus of the ear
Suppuration of the postauricular (mastoid) lymph node - This node collects drainage
from the scalp and becomes inflamed with infections involving this region

Catscratch disease and atypical mycobacteria tend to have poor response to

antimicrobials and a high frequency of nodal abscess formation. Differentiation from
acute surgical mastoiditis (ASM) is relatively easy with preservation of the skin
crease and presence of a normal middle ear.

Lateral sinus thrombosis causes mastoid air sinus abnormalities; this is due to venous
congestion as a consequence of this condition.

Differential Diagnoses
Bell Palsy
Otitis Externa
Otitis Media

Approach Considerations

Despite the use of antibiotics, acute mastoiditis still remains a threat for patients with
acute otitis media (AOM), especially for children younger than age 5 years. Great
care is required on the part of clinicians to make an early diagnosis in order to
promote adequate treatment and to prevent complications.[11]

Material for culture and sensitivity should be obtained from the ear (via
tympanocentesis or myringotomy), blood, any abscess, and mastoid tissue (if it
becomes available). Obtain and evaluate spinal fluid if any suggestion exists of
intracranial extension of the process.

Complete blood count

A complete blood count (CBC) and sedimentation rate are obtained for baseline
studies used to evaluate the efficacy of therapy. A high white blood cell count on
admission may serve as a predictive factor for complicated cases.

Audiometry

In the light of the prevailing medicolegal climate, an audiometric evaluation must be

obtained. Audiometry is seldom appropriate or useful for children with ASM, but it
must be performed after convalescence from the acute phase and with children who
have chronic mastoiditis. In the at-risk population (children < 2 y), thresholds for air
and bone conduction under headphones are only rarely obtained.

25
Tympanocentesis/myringotomy

Tympanocentesis is a puncture of the tympanic membrane for aspiration of middle ear

fluid. The tympanic membrane typically heals within several days. Send fluid for
cultures, Gram stain, and acid-fast stain. It is often possible in an acute infection to
convert a tympanocentesis into a myringotomy without undue discomfort by
widening the needle hole with alligator forceps.

Myringotomy is a small incision of the tympanum to express fluid from the middle
ear in chronic or recurrent otitis media; it often relieves discomfort associated with
pressure from acute otitis media (AOM). Tympanostomy tube insertion is also
performed in most cases to allow for continued drainage and so that administered
therapeutic otic drops reach the middle ear.

Imaging Studies
CT scanning

CT scanning of the temporal bone is the standard for evaluation of mastoiditis, with
published sensitivities ranging from 87-100%. Some argue that all suspected cases of
mastoiditis warrant CT scan evaluation.[12]

The following findings are used to differentiate acute otitis media (AOM)/acute
mastoiditis without osteitis, acute surgical mastoiditis (ASM), and chronic
mastoiditis:

Opacification of the mastoid air cells and middle ear by inflammatory swelling of
mucosa and by collection of fluid
Loss of sharpness or visibility of mastoid cell walls due to demineralization, atrophy,
or necrosis of bony septa
Haziness or distortion of the mastoid outline, possibly with visible defects of the
tegmen or mastoid cortex
Enhancement of areas of abscess formation
Elevation of the periosteum of the mastoid process or posterior cranial fossa
Osteoblastic activity in chronic mastoiditis

It is this authors belief that in the presence of clear clinical indications of acute
surgical mastoiditis, CT scanning may be omitted prior to surgical intervention,
avoiding unnecessary radiation exposure as recommended by the US National
Institutes of Health.[13]

MRI

Magnetic resonance imaging (MRI) is not typically the radiographic study of choice;
however, it is helpful in showing inflammatory processes and differentiating certain
tumors. Do not use MRI as a method of evaluating the mastoid, although it is the
standard for evaluation of contiguous soft tissue, particularly the intracranial
structures. However, MRI is the preferred imaging modality for the potential
complications of ASM (ie, abscess formation, sinus thrombosis).

26
Plain radiography

In areas of the world where CT scanning is not immediately available, plain

radiographs of the mastoids demonstrate clouding of the air cells with bone
destruction in ASM. In the vast majority of cases, radiographs suffice to establish the
diagnosis but lack the sensitivity to differentiate the stages of the disease and fail to
show the petrous apex in any great detail.

Approach Considerations
Surgical therapy confined to the ear includes myringotomy/tympanocentesis,
tympanostomy tube placement, and mastoidectomy. In the preantimicrobial era,
mastoidectomy was performed in as many as 20% of patients with acute otitis media
(AOM). By 1948, this figure had dropped to less than 3%, and it is presently thought
to be performed in fewer than 5 cases per 100,000 persons with AOM. (See the
images below.)

Extent of cortical mastoidectomy in a well-pneumatized mastoid.

Cortical mastoidectomy in a densely sclerosed mastoid.

Indications for the simple mastoid operation include cases of acute suppurative otitis
media that fail to respond to appropriate antibiotic therapy and progress to coalescent

27
mastoiditis. Incidence of mastoiditis and, thus, mastoidectomy should decline further
with the availability and administration of conjugated pneumococcal vaccine.

When considering surgery, the risks of exposure to general anesthesia must be

weighed against the risk of complications and progression of the infection.
Contraindications to surgery include a low hemoglobin concentration and general
systemic illness that must be controlled (eg, diabetes, hypertension, poor cardiac
condition, bleeding disorders with prolonged bleeding and clotting time).

Acute mastoiditis without osteitis or periosteitis

This is the only mastoid condition treated purely with medical management. Standard
antibiotic therapy is administered for AOM, and resolution is anticipated within 2
weeks.

If complications occur (pain and fever persist beyond 48 h or tenderness increases),

obtain cultures via the middle ear, commence new antimicrobial therapy, and obtain
imaging of the mastoid. Consider mastoidectomy if symptoms persist or if the new
antibiotics fail.

Acute mastoiditis with osteitis

This is a surgically treated disease, although coverage with appropriate antibiotics is mandatory.
Mastoidectomy with insertion of a tympanostomy tube is required to remove areas of coalescence
within the temporal bone.

This author uses single-, high-dose systemic steroids preoperatively or intraoperatively to control
swelling, nausea, and inflammation without negatively impacting the childs immunological response.

Antibiotic selection should provide good intracranial penetration and MDRSP coverage. With the high
frequency of invasive resistant strains in mastoiditis, initial therapy of intravenous vancomycin and
ceftriaxone is most appropriate until results of the culture and sensitivity studies are available.

Postoperatively, antibiotic/steroid drops are used to keep the tube patent and to reduce middle ear
swelling.

Patients with spread of empyema beyond the mastoid require drainage of the abscess and
mastoidectomy. Intracranial spread requires a combined neurosurgical and otolaryngological approach.

Acute mastoiditis with periosteitis

Postauricular swelling and erythema without subperiosteal abscess or mastoid osteitis

can be treated more conservatively, using parenteral antibiotics, high-dose steroids,
and tympanostomy tube insertion. Vancomycin and ceftriaxone are recommended
until cultures become available. Again, systemic steroids slow the inflammation and
promote drainage.

If substantial resolution of pain, fever, and erythema does not occur within 36-48
hours after institution of therapy, mastoidectomy is warranted.

28
Transfer

If transfer is required, it invariably relates to the availability of subspecialists, most

notably pediatric otolaryngologists or otologists, pediatric neurosurgeons, or pediatric
critical care specialists. Available radiographs should be copied and should
accompany the patient, along with any available laboratory data. Instruct patients to
take nothing by mouth until the receiving subspecialists evaluate their conditions.

When transfer is not possible, occasional operators (particularly in children) should be

aware that it is more important to establish wide communication between mastoid
cavity and middle ear than to open all the air cells of the mastoid. Almost always,
opening the antrum and leaving an external drain will suffice.

Consultations

Early consultation with an otolaryngologist is appropriate and necessary if the

pediatrician is not comfortable performing tympanocentesis. If cultures indicate the
presence of resistant or unusual microbes, consultation with appropriate infectious-
disease specialists may be required. Consultation with a neurosurgeon is appropriate
if evidence of intracranial extension with abscess formation exists.

Monitoring

Monitor the patient's temperature; it usually falls dramatically within the first 24
hours, after which the patient can be allowed up. After obtaining cultures (either by
tympanocentesis or during tympanostomy tube placement, with or without
mastoidectomy), continue initial antibiotic selection until cultures are reported. If the
patient becomes afebrile and if swelling decreases at 48-72 hours, oral medication
may be selected based on culture reports.

Children who have had a mastoidectomy are released from the hospital after the
discharge from the surgically implanted drain abates. The drain is normally removed
48-72 hours postoperatively.

Antibiotic/steroid drops are continued until the otorrhea ceases and the tympanostomy
tube is noted to be open with healing or healed mucosa behind.

Medication Summary
The principal medications used in the treatment of mastoiditis are antibiotics. Other
medications include analgesics, antipyretics, and topical antibiotic-steroid
combinations.

If open mastoid surgery is not undertaken, use of single, high-dose intravenous (IV)
steroids is warranted to decrease mucosal swelling and promote natural drainage
through the aditus ad antrum into the middle ear.

29
A study done by Roddy et al showed that in the post-pneumococcal vaccine era,
ceftriaxone nonsusceptibility was seen in 30% of post-pneumococcal conjugate
vaccine S pneumoniae isolates, compared with 7% of pre-pneumococcal conjugate
vaccine isolates.[14] We can conclude that ceftriaxone alone is insufficient for empiric
antimicrobial therapy in the post-pneumococcal conjugate vaccine era.

Pharmacologic Therapy
Antibiotics are the principal medications used in acute surgical mastoiditis (ASM).
Culture results and the sensitivity of the organism ultimately govern selection of
medications. Until microbiology information is available, the following principles
guide the selection: (1) the antimicrobial must be appropriate to cover the invasive
strains of bacteria most common for AOM, (2) the selected antibiotic should cross the
blood-brain barrier, and (3) the selected therapeutic spectrum should include
consideration of MDRSP organisms that are prevalent in the individuals community.
Specific microbiologic diagnoses should be treated with appropriate antibiotics.

If open mastoid surgery is not undertaken, use of single, high-dose, intravenous

steroids is warranted to decrease mucosal swelling and to promote natural drainage
through the aditus ad antrum into the middle ear.

Other medications used include analgesics, antipyretics, and topical antibiotic/steroid

combinations. After placement of a tympanostomy tube, with or without
mastoidectomy, a pH-balanced solution or suspension of an antibiotic and steroid is
useful to decrease mucosal swelling and to deliver topical antibiotics to the middle ear
and mastoid. Continue the drops until otorrhea ceases and the view through the tube
shows healing mucosa without swelling or obstruction. Multiple combinations are
available, the best being those thin enough to rub through the tube into the middle ear.

Myringotomy/Tympanocentesis and Tympanostomy

Tube Placement
Myringotomy/tympanocentesis is primarily used to obtain specimens and to relieve
discomfort from acute otitis media (AOM). These openings usually heal within a few
days.

A tympanostomy tube allows for drainage of entrapped pus and aeration of the middle
ear and mastoid. It may sometimes allow topical antimicrobials to enter the middle
ear space. Because it is used as a drain, a tympanostomy tube is usually placed during
mastoidectomy.

A tube maintains the opening in the tympanic membrane and provides access to the
middle ear and mastoid for antibiotic/steroid drops and for drainage without concern
for patency of the Eustachian tube. Ear drops containing only antibiotics are less
effective than those containing a steroid to control swelling.

30
Mastoidectomy
Mastoidectomy is surgical removal of infected mastoid air cells. This procedure
involves opening the mastoid air cells by making a postauricular incision and entering
the mastoid by removing the mastoid cortex using a drill. Often, children will have
thinned out cortex with pus coming through the residual bone and the mastoid can be
entered easily and safely using a mastoid curette rather than a drill. Any subperiosteal
abscess is opened during this time. Upon entering the mastoid, the surgeon most often
encounters granulation tissue and swollen polypoid mucosa that block the aditus ad
antrum. Most of the diseased air cells are opened, and access to the middle ear is
gained by removing the blockage at the antrum. After irrigating the ear, a drain is
inserted through the wound, where it is left for at least 2 days.

With a simple (or closed) mastoidectomy, the surgeon either makes an incision behind
the ear to access the mastoid region or removes the infected air cells by approaching
through the ear. Radical mastoidectomy, involves removal of the tympanic
membrane, most middle ear structures, and closing the eustachian tube opening.
Modified radical mastoidectomy preserves the ossicles and tympanic membrane
remnants.

Mastoidectomy is indicated in cases of advanced disease, such as mastoid osteitis,

intracranial extension, abscess formation, when cholesteatoma is involved, or if little
improvement occurs after 24-48 hours of intravenous antibiotics.

Preoperative details

Preoperative preparation entails shaving the area behind the involved side (in the
postaural area) a width of 3 fingers to avoid wound contamination. (See the images
below.)

Preoperative preparation of the patient.

31
Draping the surgical area.

Injection of the area with 2% Xylocaine and 1:100,000 adrenaline to reduce bleeding.

Marking the incision site.

Intraoperative details

A postaural incision is placed a few millimeters from the postaural sulcus. In infants,
the incision is placed higher and more horizontally because the mastoid process is not
developed and the facial nerve is more superficial. (See the image below.)

32
Placement of the incision, a few mm behind the postauricular sulcus.

The incision is deepened through the periosteum to the bone. At this stage, a
subperiosteal abscess will discharge pus. Care must be taken in the upper half of the
incision. The lower border of the temporalis muscle should be identified and
conserved. If incising it to obtain adequate exposure is necessary, the vessels running
at its lower border are first ligated or diathermied. (See the image below.)

Deepening the incision down to the bone.

The periosteum is lifted from the underlying bone with periosteal elevators to expose
the spine of Henle, the Macewen triangle, and the posterior bony margin of the
meatus. In older children and adults, the tendon of the sternomastoid muscle has a
wide attachment to the superficial aspect of the mastoid process; the fibers are scraped
off with a periosteal elevator. (See the image below.)

33
Elevation of the periosteum to expose the mastoid cortex to the mastoid tip.

The periosteum is elevated forward as far as the lateral end of the posterior bony
meatal wall, backward for a few millimeters, and upward (simultaneously pushing up
the temporalis muscle) to the level of the upper attachment of the pinna. A Mollison
self-retaining hemostatic mastoid retractor is inserted to hold the soft tissues away
from the underlying exposed bone.

The surgeon should use known visible landmarks to find the deeper landmarks.
Drilling is commenced posterior to the posterior canal wall in a vertical direction. A
triangle-shaped excavation is created, with the superior limit bounded by the
extension of the linea temporalis (which becomes the floor of the middle fossa as one
drills deeper), the posterior margin bounded by the sigmoid sinus, and the anterior
margin bounded by the thinned wall of the posterior external ear canal.

Mastoid drilling in progress with simultaneous saline irrigation.

Creation of the initial groove and the vertical line.

The mastoid cortex is now removed over the Macewen triangle (which is a rough
guide to the position of the underlying mastoid antrum) using a drill fitted with a large
cutting burr (5-6 mm). In adults, the antrum is encountered at a depth of 15-17 mm. If
there is a deviation in the direction of drilling, the approach to the antrum can be
seriously misaligned.

An ideal method to gauge the antrum is to insert an angled cell seeker beyond the
posterosuperior bony meatal wall (which will be the site of the antrum) and then to
drill toward it.

34
The antrum is usually apparent when opened by the drill. It can be confirmed by
gentle anterior probing with a Dundas-Grant probe, which will slip into the aditus.
Exercise care to avoid dislodging the short process of the incus. Simultaneously, the
size of the aditus should be judged. If it is very small, it may be enlarged slightly with
a fine bone curette to ensure adequate drainage of the middle ear.

The antral exposure is enlarged, opening adjacent cells until the lateral semicircular
canal (the important landmark at this stage) can be identified. The position of middle
and posterior fossa dura and the sigmoid sinus plate must be judged from the lateral
oblique radiograph of the mastoid. Next, all cells in all directions are opened by
drilling gently through their separating trabecula. Clearing all cells from the sinodural
angle is particularly important. The smooth plate of bone covering the middle fossa
dura above and lateral sinus posteriorly is recognized easily. (See the images below.)

Exposure of the antrum and exenteration of the mastoid air cells.

Curetting the aditus to enlarge it.

35
Further exposure.

If the region is filled with necrotic mucosa, it may be safer to scoop out the material
with a curette, always sweeping from the vertical position of the facial nerve as it
descends just below the back of the lateral semicircular canal. Cells along the vertical
portion of the facial nerve are best removed under microscope visualization with a
diamond burr.

In a well-pneumatized skull, cells may extend anteriorly into the root of the zygoma
and posteriorly into the occipital bone. These must also be followed as far as
practicable. Consequent to mastoid clearance, a cavity is created with the antrum at
the deepest point. The cavity is bounded above by the bony tegmen separating the
region from the dura of the middle cranial fossa, behind by the bony plate over the
sigmoid sinus, and in front by the posterior meatal wall and the aditus ad antrum.

In front of the bulge of the sigmoid sinus plate, cell removal uncovers the bone of the
Trautman triangular space, protecting the dura of the posterior canal fossa and leading
to the solid angle where the dense bone of the otic capsule protects the posterior
semicircular canal. Anteriorly and much more superficially, cells should be opened as
far as they extend into the root of the zygoma. Inferiorly, cell pursuit leads to the bone
covering the digastric muscle as it passes forward, deep to the inferior part of the
facial nerve at the stylomastoid foramen.

When cortical mastoidectomy is performed for proved suppurativemastoiditis, the

bone over the sigmoid sinus should be sufficiently removed to allow insertion of a
fine needle into that vessel to confirm that no thrombophlebitis exists within.

Closure of the wound is with interrupted sutures, and most otologists leave a soft
drain in the lower part of the cavity for 1-2 days. A firm pressure dressing controls the
bleeding. (See the image below.)

36
Healed postaural scar.

Although facial nerve monitoring is a useful adjunct, nothing substitutes for

experience and attention to detail when preserving the facial nerve. Experienced
otologists are unlikely to injure the ossicular chain during mastoid surgery.

Care must be taken to avoid damage to the ossicular chain. Persistent conductive
hearing loss caused by tympanosclerotic plaques formed from residual bone dust can
be avoided with copious irrigation at the end of the surgery.

Complications associated with mastoidectomy

Although mastoidectomy is a common surgical procedure in otology, postoperative

complications of various degrees of severity may occur. Such complications include
the following:

Injury to the facial nerve

Dislocation of the incus
Penetration of the middle or posterior fossa
Rupture of the sigmoid sinus
Labyrinthine transgression and destruction

Persistent deafness may be due to incus dislocation or removal. The ear dries, and the
tympanic membrane heals; however, conductive deafness persists. Impedance
audiometry indicates disruption of the ossicular chain. Anterior tympanotomy and
reconstruction of the ossicular chain may be performed.

Persistent deafness may also be caused by persistent infection due to residual cells.
Infection should resolve with proper medical treatment and good drainage. If
infection persists, reopening of the mastoid and exenteration of the remaining cells is
required.

If complete facial nerve paralysis is present immediately postoperatively, the facial

nerve has been damaged intraoperatively. The mastoid must be reopened, and the
vertical part of the nerve must be explored and, if necessary, grafted.

37
Meatal stenosis may ensue if the bony meatal wall has been taken down and if the
skin has been dissected off the bony wall. Meatal stenosis requires excision of the
stenosed area and firm packing of the canal until reepithelization occurs.

Complications reported have included brain abscess 1 week after mastoidectomy in a

child and, in another child, seizures 5 days after the initial mastoidectomy and a
subdural empyema that was drained during the revision surgery. Large bone defects
with exposed middle cranial fossa dura were found during revision surgery in both
patients, and Proteus vulgaris and methicillin-resistant S aureus were isolated from
the mastoid and abscess cavities in these children.

A small epidural collection was diagnosed 2 days after initial mastoid surgery and
was managed with intravenous antibiotics only.

In another reported case, sigmoid sinus thrombosis developed the day after
mastoidectomy was performed for nonresponsive acute mastoiditis. This child
received both intravenous antibiotics and anticoagulants. Timely revision surgery,
combinations of third- or fourth-generation cephalosporins with vancomycin or
metronidazole, and the addition of anticoagulants in cases of sinus thrombosis can
lead to full recovery.

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