PEMICU 4

Kelompok 16
BAGAIKAN DITERJANG OMBAK
BESAR
 Kelompok 16
Tutor : dr. Mira Amaliah Sp.THT-KL
1. Fransisca Selvia (Ketua)
2. Rio Alexsandro (Sekertaris)
3. Chelsea Phinata (Penulis)
4. Wilson Wiradijaya
5. Inge Angelyca
6. Ivonne Sonia P.
7. William
8. Raynaldo
9. Fandi Apriyan
10.Dias Azizah Putri
11.Deshinta C.N Ritung
12.Chelcya C. Dewi
13.Peter Gunardi
 Pemicu 4
Seorang perempuan berusia 38 tahun datang ke IGD RS dengan keluhan pusing berputar hebat
disertai rasa mual. Pasien merasa dirinya seperti diombang-ambing diatas kapal kecil di tengah
ombak yang besar, sehingga untuk berdiri pun dia harus bertumpu.
Pada mulanya, dia merasakan telinga kanannya tertutup dan berdengung hebat ketika bangun
tidur tadi pagi, kira-kira 5 jam yang lalu. Dia lalu pergi ke dokter praktik di dekat rumah dan diberi
obat. Tetapi, sebelum meminum obat keluarganya memutuskan untuk membawanya ke IGD RS
Pasien mengatakan keluhan pusing berputar disertai mual dan muntah pernah dialaminya ketika
berpergian dengan mobil keluar kota dan bisa diatasinya dengan minum obat anti mabuk. Tapi
keadaan yang seperti ini, baru kali ini dialaminya.
Selain itu, selama 3 bulan terakhir, pasien juga mengalami telinga kiri berdengung , mimisan, dan
hidung yang semakin buntu. Sebulan terakhir dia menemukan ada benjolan dileher samping kiri.
Dia sudah beberapa kali berobat ke dokter untuk keluhannya ini, tetapi belum membaik
Dokter juga menanyakan riwayat penyakit yang pernah dideritanya dan pasien pernah menderita
cacar ular tapi tidak tau untuk penyakit yang lain.
Dokter kemudian melakukan pemeriksaan tanda-tanda vital, pemeriksaan telinga, hidung meliputi
rhinoskopi anterior dan rhinoskopi posterior, dan orofaring. Dokter juga melakukan pemeriksaan
kelenjar getah bening leher kanan dan kiri.
Setelah pemeriksaan selesai, dokter memutuskan untuk merawat inap pasien tersebut dan
menganjurkan untuk melakukan pemeriksaan penunjang termasuk pemeriksaan pendengaran.
Apakah yang saudara pelajari dari kasus tersebut:?
 Unfamilliar terms
Cacar ular = Herpes Zooster
 Problem
1. Apa penyebab keluhan pusing dan mual?
2. Apa hubungan telinga kanan terasa tertutup dan berdengung hebat dengan
keluhan (ketika bangun tidur)?
3. Mengapa keluh9.an yang sekarang bisa timbul tanpa berpergian?
4. Apa hubungan keluhan dengan riwayat mabuk perjalanan?
5. Apa yang menyebabkan telinga kiri berdengung, mimisan, dan hidung buntu?
6. Apa penyebab benjolan di leher kiri? Dan apa hubunggan dengan keluhan
mual-muntah?
7. Mengapa walaupun sudah berobat beberapa kali, benjolan tidak membaik?
8. Apa hubungan antara timbulnya benjolan di leher kiri dengan mimisan, telinga
berdengung, dan hidung tersumbat?
9. Apa hubungan cacar ular dengan keluhan pusing mual?
10.Mengapa perlu dilakukan pemeriksaan KGB?
11.Mengapa perlu diperiksa tanda vital?
12.Pemeriksaan penunjang apa yang perlu dilakukan?
13.Mengapa pasien perlu dirawat di RS?
 Brainstorming
1. Kemungkinan gangguan keseimbangan (vestibulum,
n.vestibularis terlalu sensitif), otak, mata, proprioseptif
2. Infeksi virus, perubahan tekanan darah (aliran darah ke
telinga dalam berkurang)
3. - Adanya perbedaan persepsi yang disampaikan ke sistem
vestibulum.
- Karena ada gangguan keseimbangan, infeksi virus,
perubahan tekanan darah
4. Mungkin ada (Gangguan fisiologis dalam telinga)
5. - Infeksi virus, bakteri, masa hidung buntu ada
perbedaan tekanan (tuba eustachius dan cavum tympani)
Telinga kiri berdengung
- Tekanan darah meningkat Mimisan
6. Benjolan : Pembesaran KGB Kemungkinan masa di
nasofaring (Kemungkinan tidak ada hubungan dengan mual-
muntah)
7. Mungkin : Keganasan
8. Benjolan primer tersembunyi yang terlihat metastasis
9. Infeksi cacar ular dorman di sel ganglion vestibularis
( benjolan di leher)
10. Untuk mengetahui : etiologi, metastase, dan derajat
keparahan.
11. - TD : memengaruhin keseimbangan
- Suhu : Demam (mungkin infeksi nadi, napas)
12. Pemeriksaan radiologi, lab, biopsi (KGB, tergantung
pemeriksaan radiologi)
13. Termasuk kegawatdaruratan THT
 Mind Map

Anatomi

Gangguan
Keseimbang Fisiologi
an
Gangguan
Telinga
Dalam
(Pendengar
an dan
Keseimbang
an)
Gangguan
Keganasan
Pendengara
THT
n

KGD
 Learning Objective
1. Anatomi telinga dalam
2. Fisiologi pendengaran dan keseimbangan
3. Gangguan pendengaran ( Tuli,
Timpanosklerosis, Presbiakusis, Trauma
akustik akut)
4. Gangguan Keseimbangan ( Vertigo perifer,
BPPV, Labirinitis, Meniere, Mabuk
Perjalanan, Neuritis Vestibularis)
5. Keganasan THT ( Karsinoma nasofaring,
Laring, Angiofibroma Juveille)
Menjelaskan anatomi dan fisiologi (pendengaran-
keseimbangan)

LO 1-2
 Pendengaran
Persepsi energi suara oleh saraf
Identifikasi suara (apa)
Lokalisasinya (di mana)

Gelombang suara: getaran udara yang

merambat
Molekul udara tekanan (pemadatan)
Molekul udara tekanan (peregangan)
 Frekuensi nada (Hz)
Intesitas kekuatan suara (dB) N:
10-100 dB
Overtone (frekuensi tambahan)
warna suara
234
Telinga luar
Lokalisasi suara (mengumpulkan
gelombang suara pinna):
Gelombang suara mencapai telinga
yang lebih dekat (waktu pola lepas
muatan neuron)
Suara menjadi kurang intens ketika
mencapai telinga yang lebih jauh
 VCN: low frequency
DCN: high frequency
Spherical cells (AVCN): primary-like sound
(primary input)
Stellate/multipolar cells (DCN or PVCN): pattern
of sound, intensity
Octopus cells (PVCN): signals motor nuclei
startle response, loud or unexpected sounds
Superior olivary complex (binaural comparisons):
Lateral: discontinous and low frequency
Medial: intensity
 Inferior colliculus (what a sound is):
Recognizing patterns in sound
Controlling middle ear muscles
Motor nuclei turning the head to
sound source
Superior colliculus: visual and
auditory maps
Medial geniculate nuclei: thalamus
awareness modified by learning
Keseimbangan
 Keseimbangan
Struktur sensorik lain membantu
mempertahankan keseimbangan
Keseimbangan merupakan kerjasama
dari mata, otot, dan alat
keseimbangan.
Mata menyampaikan pesan apakah
kita berdiri tegak atau miring.
Otot menyampaikan pesan mengenai
posisi badan dan anggota badan.
 Keseimbangan
Fungsi Sistem Vestibular adalah
Keseimbangan
Mempertahankan kepala pada posisi tegak
Menyesuaikan pergerakan mata untuk
mengkompensasi gerakan kepala

Sistem vestibular mengontrol langsung

pergerakan bola mata untuk mengkompensasi
pergerakan kepala yang tiba-tiba (Refleks
Vestibulo-ocular), mempertahankan gambaran
pada retina untuk tetap.
Stimulasi pada sistem vestibular belum dapat
dijelaskan dengan pasti, terdiri dari :
Stimulasi pada verstibular sacs nausea
Stimulasi pada kanalis semisirkularis rasa pusing
(dizziness) dan pergerakan mata yang ritmik
 Keseimbangan
Refleks Sistem Vestibular
1. Vestibulo-Ocular Reflex
Mempertahankan keseimbangan pergerakan bola mata
selama pergerakan rotasi kepala.

2. Ototith-Ocular Reflex
Mempertahankan keseimbangan pergerakan bola mata
selama pergerakan linear kepala.

3. Vestibulo-Colic Reflex
Mempertahankan keseimbangan kepala dan bahu.

4. Vestibulo-Spinal Reflex
Mempertahankan keseimbangan otot ekstremitas bawah.
Mengirim informasi mengenai gravitasi dan pergerakan linear
ke otot tubuh.
 Aliran Kelenjar Getah Bening
(Kepala-Leher)
Lymph node groups
Submental nodes
submandibular nodes
upper deep cervical nodes
middle deep cervical nodes
lower deep cervical nodes
posterior triangle nodes
paralaryngeal nodes
Paratracheal nodes
parotid nodes
suboccipital nodes
 Submental Group
These nodes are situated in the
midline, inferior to the mandible and
between the anterior bellies of the
digastric muscles
They drain the anterior floor of the
mouth
 Submandibular Group
These nodes are divided into six groups
Preglandular
Prevascular
Retrovascular
retroglandular
intraglandular
deep nodes
These nodes can best be described as those related to
the submandibular gland and those related to the facial
vessels
Cancers of the floor of mouth, tongue and buccal cavity
metastasize much more commonly to the perivascular
nodes, which should be cleared in a neck dissection
 Jugular Chain
80% of lymph nodes in the neck are
closely associated with the internal jugular
vein.
The lymphatic channels are found within
the loose areolar tissue that exists around
the internal jugular vein and within the
carotid sheath. The nodes occur anterior
posterior and lateral to the vein.
 The most superior segment of the vein extends from the
skull base to the level of the carotid bifurcation which
Surgical anatomy of the neck coincides with the level at
which the greater cornu of the hyoid bone crosses the
internal jugular vein. At the most superior extent of the
vein, it runs deep to the digastric muscle Nodes found
here are referred to as the jugulodigastric nodes.
Jugulodigastric nodes are the first echelon node for the
drainage of the posterior faucial region, especially the
palatine tonsil between the upper and middle jugular nodes
lie the junctional nodes. They represent a lymphatic
anastamosis of the submandibular nodes, the
retropharyngeal nodes and the jugular chain of nodes.
 The middle jugular nodes are found between the
carotid bifurcation and the level at which the
omohyoid tendon crosses the internal jugular vein.
They are first echelon nodes for the larynx
midhypopharynx and upper thyroid gland
The lower jugular nodes are those between the tendon
of omohyoid and down to the thoracic inlet. They are
sometimes referred to as the prescalene group of
nodes. They form an important confluence between
the mediastinal node group, the axillary group and the
neck. This communication can be a reason why neck
nodes may ppear secondary to disease outside the
neck
 Posterior Nodes
The posterior triangle contains lymph
nodes that are arranged into two groups:
those that are found along the accessory
nerve
The nodes along the accessory are the first
echelon for the nasopharynx and second echelon
for the areas drained by the anterior neck nodes
are related to the thyrocervical vessels
those related to the thyrocervical vessels
 Lymph Node Levels
The most widely accepted system for describing the lymph
nodes in the neck originates from the Memorial Sloan Kettering
Hospital, New York and was adopted by the American Academy
of Otolaryngology Head and Neck Surgery (AAOHNS) in 1991. It
is a system designed by surgeons and radiologists rather than
anatomists, and divides the neck into six levels, of which I to V
are paired in the lateral neck, and level VI describes midline
neck nodes from hyoid to sternal notch
The system has been further classified by the Head and Neck
Cancer Committee of the American Academy of
Otolaryngology Head and Neck Surgery to include subzones,
which will also be described. The reason for this added
complexity was to more accurately differentiate node groups
that drain different but contiguous structures
 Lymph Node Levels
Level This level refers to the submental and submandibular nodes and
I drains the lip, oral cavity and tongue
Subzone la refers to the submental nodes
Subzone la drains anterior floor of mouth, lower lip and ventral
tongue
Subzone Ib to the submandibular nodes
subzone Ib drains other sub sites in the oral cavity
Level This forms the upper jugular group of nodes and drains the
II oropharynx, larynx, hypopharynx and parotid.
The course of the spinal accessory nerve divides this level into two
subzones
Level IIa lies anteroinferior to the spinal accessory nerve
lIb lies posterosuperior to the spinal accessory nerve
The lIb subzone is also known as the submuscular recess.It is a
clinically useful anatomical differentiation because positive level Iia
disease mandates lIb dissection, however elective dissection for
laryngeal and hypopharyngeal malignancy can exclude level lIb
Level This refers to the middle jugular nodes and drains
III the larynx and pharynx. Level III is not further
subdivided by the new nomenclature because, despite
being the largest of the jugular levels, there is little variation
Level IV Level IV refers to the lower jugular group of nodes.
This is a small area, which again drains the larynx and
hypopharynx.
Attempts have been made to subdivide
this area but have not been successfulowing to its small size
Level V This is the posterior triangle group of nodes and drains the other
lymphatic regions in the neck.
It has been divided into sub zones.
The Va lies superior to the inferior belly of the omohyoid muscle
The Va area contains the chain of nodes along the accessory
nerve, which drain the nasopharynx
the Vb level is inferior to the omohyoid muscle
The Vb level contains nodes related to the thyrocervical trunk
which drains the thyroid glan
Level VI This is the anterior or central group of nodes. This includes the
paratracheal, peri thyroidal and Delphian nodes
Level This corresponds to the superior mediastinal tissues. It is not
VII recognized by most American texts.
Gangguan Pendengaran

LO 3
Age-related sensorineural
hearing impairment
 Definition
Bilateral
Exclude hearing loss caused by
primary factor
Loss of high frequency

Scott-Brown's
 Pathology
Outer
Cerumen increase, Reduced ephitelial
migration, Increased hair growth,
Potensial collapse of ear cannal,
enlargement of pinna
Middle
Tympanic membrane, Artrict changes and
ossification, Degeneration middle ear
muscles, Calcification of cartilaginous
Scott-Brown's
 Inner
Loss of hair cell at the basal end of
organ corti, Degeneration cochlear
nerve, Vascular or metabolic involves
athropy of the cochlear, Mechanical
or cochlear conductive, Cochlear
duct are not evident (organels
involve), Mixed.

Scott-Brown's
 Symptom
Associated with the common high
frequency loss patern
Poor auditory discrimination
Flat audiogram

Scott-Brown's
 Genetics
1. Monozygotic Vs Dizygotic twins
For younger men
2. Family based Parent-Child-Sibbling
3. Ahl Gene Mitochondria mutations

Scott-Brown's
 Environtmental Factors
Noise exposure
Ciggarete smoking
Alcohol use
Systolic blood pressure
Blood hyperviscosity

Scott-Brown's
Diagnosis and Management
No agreed age
Best on 20
Hearing loss occurred from 40-60
years old
>50 can diagnosis, <50 alternative
diagnosis
Clear diagnosis / Nonsydromic?

Scott-Brown's
1. Nangkep tapi ga baik
2. Tau ada suara tapi ga nangkep
3. Keliatan orang Cuma berbisik
4. Disertai tinnitus

Scott-Brown's
 Investigations
Various audiometric
Magnetic Resonance Scan

Scott-Brown's
 Diagnosis
Over age 60, normal examinations
finding, symetrical
Family history

Scott-Brown's
 Management
Unspecific: psycological, practical
Hearing aids

Scott-Brown's
Ototoxicity

Scott-Brown's
 Introductions
Ireversible: Aminoglycosides,
Chemotherapeutic
Reversible : Diuretic, etc

Scott-Brown's
Aminoglicoside

Scott-Brown's
 AethioPathology
Etiology: Bacteria, Sepsis, Tb, Cystic
fibrosis, dialysis
Pathology: Sensory neuroephitelium,
outer hair cell,Type 1, Crista Ampuli
Secondary degenaration of
auditory nerve

Scott-Brown's
 Pathophysiology
Binding to Phosphatidylionositol
biphosphate binding iron
Generates Hidroxyl Radicals
Apopotosis
Blockage of polyamine

Scott-Brown's
 Predisposition
Nucleotide 1555A to G substitution
on the mithochondrial 12S rRNA
Using Loop diuretics

Scott-Brown's
 Relative
1. Netilmycin lebih baik
2. Gentamycin untuk Menniere
3. Aminoglicoside risk
4. Gentamycin 10% hearing loss

Scott-Brown's
 Sign and Symptom
Permanent, bilateraly, symetrical
Sign : High frequency loss
Px: Monitoring

Scott-Brown's
 Risk Factor
1. Genetic
2. Renal Liver Failure
3. Sepsis
4. Metabolic Reserves and Nutritional
Status
5. Gestation 18-20 weeks

Scott-Brown's
 Other
Cisplatin : Carcinoma; Bilateral,
progresive, high frequency; Auditory
nerve damage, Vestibuli better
Loop Diuretics: Reversible;
Associated ataxia
Salicylates: RA
Quinine : Malaria
Erythromycin

Scott-Brown's
 Management and monitoring

1. Recognize
2. Monitor (ottoacoustic,audiometry,
ultrahigh frequency, reasesment)

Scott-Brown's
 Treatment
1. Cochlea
2. Vestibuli
3. Genetics
4. Infant

Scott-Brown's
Pemeriksaan
Noice Induced Hearing
Loss
Trauma Akustik Akut
 Definisi
Berkurangnya ketajaman
pendengaran yang berhubungan
dengan adanya paparan suara
sebelumnya.
Bisa bertahan hanya beberapa jam-
hari (TTS)
Bisa juga permanen (PTS)
Trauma akustik : suatu keadaan
dimana seseorang terpapar suara
yang sangat keras, sehingga
 Patologi
Mekanisme metabolik
Glutamat berlebih
Aliran darah di koklea berkurang
Mekanisme struktur
Depolimerisasi filamen aktin dari stereosilia
Pembengkakan stria vaskularis, ujung saraf
afren dan sel penyokong
Apoptosis & Nekrosis
Pada saat terpapar suara yang sangat keras,
dapat dilihat adanya perubahan apoptosis
pada OHC. Terutama kondensasi nukleus dan
penyusutan sel.
 Gejala
Suara yang didengar tidak jelas, bukan
masalah volume. (mis. Susah
berkomunikasi melalui telepon).
Keluhan bisa disertai tinnitus &
hiperakusis
Lebih sering pada pria usia pertengahan.
Bisa juga pada yang lebih muda, tapi
keluhannya lebih ke tinnitus
Sebelumnya ada riwayat mendengar
suara yang keras.
 Diagnosis
Tidak ada pemeriksaan spesifik.
Pemeriksaan fisik telinga,
pendengaran
Diagnosa ditegakkan berdasarkan
gambaran klinis pasien.
 Management
Non spesifik
KIE (belajar bahasa bibir, face to face
conversation)
konseling
Spesifik
Hearing aid
Tinnitus training therapy
 Pencegahan
Sejak diagnosa ditegakkan maka harus
dilakukan pencegahan agar tidak
menimbulkan kerusakan yang lebih
parah :
Hindari sumber suara yang keras
Earplug atau earmuffs
 Prognosis
Kurang baik karena irreversible
Sebaiknya dicegah dengan
menggunakan pelindung telinga
TIMPANOSKLEROSIS
 TYMPANOSCLEROSIS
Tympanosclerosis refers to hyaline deposits of
acellular material visible as white plaques in the
tmpanic membrane and as white nodular deposits
in the submucosal layers of the middle ear on
otoscopy.
The end result of a healing process, in which
collagen in fibrous tissue hyalisizes, loses its
structure and becomes fused into a homogenous
mass.
Calcification and ossification may occurred
Locations: Tympanic membrane, middle ear
mucosam epitympanum, ossicular ligaments and
muscle tendons
 Theories of pathogenesis:
Local immmunologic hypersensitivity
Increased oxygen concentration in the middle ear with exposure to
oxygen radicals
Local inflammatory activity

COM healing. Free of active suppuration

If occurred in tympanic membrane, usually has little consequence

to middle ear transmission. Unless there is a large plaque that
extends from the annulus to the manuburium, fixing the latter.
Surrounding the ossicles in the epytympanum and the stapes
superstructure or footplate in the oval window, causes varying
degrees of immobility of the ossicular chain.
 Otosclerosis
localized hereditary disorder affecting
endochondral bone of the otic capsule that
is characterized by disordered resorption
and deposition of bone
Clinical otosclerosis
lesion that involves stapes bone &
stapediovestibular joint conductive hearing
impairment
Cochlear otosclerosis
occurrence of pure sensorineural hearing
impairment due to otosclerosis in an ear without any
conductive component to hearing impairment
 Epidemiology
 Etiology
Genetic predisposition
Females 2x >, defects in expression of the COL1A1
gene, type 1 osteogenesis imperfecta
Measles
Measles RNA has been found in archival & fresh
footplate specimen with otosclerosis, anti-measles
antibody >>
Autoimmune disease
Antibodies to type II collagen
Biochemistry
As a result of
 Histopathology
Bone of otic capsule is unique very little remodelling &
contains small region of immature cartilaginous tissue
(globuli interossei)
Otosclerotic lesions
Areas of bone resorption, new bone formation, vascular
proliferation, connective tissue stroma (fibroblasts & histiocytes)
Absence of acute inflammatory cells / PMN
Blue mantle areas of the otic capsule that stain more basophilic
Enlargement of perivascular spaces followed by deposition of
immature bone
Remodelling continues production of more mature bone
Proliferation of blood vessels

Active (spongiotic) areas of > cellularity, vascularity (schwartzes

sign), & bone resorption & formation
Inactive (sclerotic) focus consisting mineral bone
Distribution of the lesion anterior of oval window, round window
niche, stapes footplate, posterior of oval window; walls of internal
auditory canal, around vestibular & cochlear aqueducts, semicircular
canal, malleus & incus
 Pathology of conductive hearing impairment
Expansion of the focus anterior to oval window
fibrous fixation of footplate (conductive impairment
30-40 dB)
Diffuse bony ankylosis involving the entire
circumference of the annular ligament
conductive loss > 40dB
Bone remodelling cytokines & angiogenic factors
deposition of connective tissue & >> vascularity
fibrovascular proliferative
Otosclerotic bone can invade the round window
niche
 Pathology of sensorineural hearing
impairment
Sensory & neural elements of cochlea & stria
vascularis are intact
The focus reaches the endosteum of the cochlea
atrophy of spiral ligament with impairment of
fibrocytes & replacement by an amorphous
eosinophilic substance (hyalinization)
Cytokines released by remodelling bone reached
the ligament disrupt fluid & ion homeostasis
within the cochlea sensorineural hearing
impairment
 Diagnosis
Otoscopy
Flamingo flush/schwartzs sign (vascularity on tympanic
membrane of an active otosclerosis) rare
Can also occur when the membrane is abnormal (chronic otitis
media)
Gold standard surgery
bone around the oval window may be whiter than normal
After surgical removal bony atic wall thicker than normal
Histological diagnosis
Pure tone audiometry
Air-bone gap & Carhart notch
Radiology
High resolution CT
 Management
Fluoridation of drinking water
Oral fluorides
Conventional hearing aids
Effective method of managing conductive hearing
impairment
Bone-anchored hearing aids
Surgery
Stapedectomy & mobilization of the stapes
Fenestration procedures
Mobilization of the stapes revisited along with stapedectomy
with prostheses in the later half of 20 th century
 Idiopathic Sudden Sensorineural
Hearing Loss
Defined as demonstrating a
threshold change for the worse of at
least 30 dB in at least three
contiguous audiometric frequencies
ISSNHL is almost always unilateral
The peak ages are 30 to 60 years
 Tinnitus is usually present
Vertigo is frequent, either spontaneous or as
isolated positional vertigo
65% of patients recover completely with or
without treatment, most within 2 weeks
Low-frequency losses have a better
prognosis than high-frequency losses
This is true off all types of rapidly
progressive or fluctuating sensorineural
hearing loss (SNHL), not just ISSNHL
 Examination
Audiogram (including the Stenger
test to detect functional hearing loss)
OAE test, sometimes present
MRI or ABR : to rule out a tumor
Gangguan Keseimbangan

LO 4
VERTIGO
 VERTIGO PERIFER
Vertigo perifer (peripheral vertigo) disebabkan oleh
disfungsi struktur perifer hingga ke batang otak (brain
stem). Beberapa kondisi yang dapat menyebabkan vertigo
perifer antara lain:
1.Benign paroxysmal positional vertigo
2.Drug-induced vertigo(vertigo yang disebabkan oleh
obat)
3.Labyrinthitis
4.Mnire's disease
5.Vestibular neuritis
Penatalaksanaan : antihistamin, antikolinergik, antiemetik,
danbenzodiazepines.
 Vertigo Sentral
Vertigo sentral (central vertigo) melibatkan proses
penyakit yang memengaruhi batang otak (brain
stem) ataucerebellum. Beberapa penyakit yang
dapat menyebabkan vertigo sentral antara lain:
1.Acoustic schwannomasataumeningiomas
2.Cerebellar pontine angle tumors
3.Cerebellar infarction
4.Cerebellar hemorrhage
5.Vertebrobasilar insufficiency
Penatalaksanaan : rujuk ke dokter spesialis saraf
(neurologist) dan dokter ahli bedah saraf
(neurosurgeon) jika diperlukan
MENIERES DISEASE
 Menieres disease
Definition: Disorder characterized by
spontaneous attacks of vertigo, associated
fluctuating sensorinerual hearing loss,
tinnitus, & aural fullness

Etiology:
Idiopathic
Endolymphatic Hydrops
Periodic rupture of membranous labyrinth
Inner ear or temporal bone disease
 Clinical manifestations
Reccurrent attacks of spontaneous
vertigo, nause, vomitng
Low-frequency hearing loss, tinnitus,
aural fullness
 Phase of the attacks
Irrritative phase
Horizontal/horizontal-torsional nystagmus, beats
towards the affected ear (last < 1 hour)
Paretic phase
Nystagmus beats away from the affected ear
(several hours 1 or 2 days)
Recovery phase
Nystagmus beats towards the affected ear again
(last like the 2nd phase)
 Later stage of the disease drop
attacks
Patient simply drop to the ground without
warning fracture & serious injury
 Diagnosis
>2 spontaneous vertigo
Hearing loss documented by pure tone
audiogram on at least one occasion
Tinnitus / aural fullness

DD
Vestibular neuritis
Migrainous vertigo
Autoimmune inner ear disease
 Management
< production of endolymph
Strict sodium restriction (urinary sodium <50mmol/day)
Diuretics
Surgery
Endolymphatic sac surgery
Vestibular neurectomy
Labyrinthectomy
Hearing << hearing aids by cochlear implantation
Systemic aminoglycosides (streptomycin & gentamycin)

Complications
Continue to have vertigo attacks
BPPV (Benign Paroxysmal Position Vertigo)
Bppv

Benign paroxysmal position vertigo

gangguan keseimbangan perifer yang
sering dijumpai.

BPPV merupakan penyebab umum

vertigo perifer.
CIRI-CIRI
- Perasaan kuat dari vertigo berputar
yang dipicu ketika pasien melakukan
perubahan posisi atau bergeser
terutama posisi kepala (posisi tidur ke
bangun, extending the neck,
membungkuk, mencoba meraih
mengambil objek dari rak atau
tempat yang tinggi, mengganti
bohlam lampu)
-vertigo muncul 8 detik setelah
berubah posisi
- terjadi nystagmus yang dipicu oleh
perubahan posisi kepala
- self limiting (lasting for a few weeks /
months)
- BPPV dapat berlangsung dalam waktu
yang lama dan dapat mempengaruhi
kehidupan sehari-hari pasien, dapat
menganggu bahkan dapat
menyebabkan kelumpuhan.
- BPPV memiliki periode remisi spontan
Etiologi
Etiologi disebabkan oleh :
1. cupulolitiasis
2. canalolitiasis
Canalolitiasis
terlepasnya otoconia (calcium carbonat kristal)
yang berasal dari makula dari utriculus

dapat mengapung bebas di endolymp

otoconia yang lepas terapung bebas berpindah

berputar mempengaruhi cupula (di cupula dari
ampula di posterior canalis semisirkularis)
Canalithiasis umumnya di bagian posterior
duktus semisirkularis.
Cupulolitiasis
Otoconia yang lepas dan menempel pada
cupula epithelium sensori atas dari canal
semisircularis posterior ( deposit otoconia ini
terlihat sebagai granular amorf halus seperti
basofilik mempunyai berat spesifik yang
berbeda dari cupula yang dapat
mempengaruhi sensitivitas dari end organ
sebagai respon perubahan tekanan gravitasi
sehingga memicu efek gravitasi langsung)
Cupulolithiasis umumnya terjadi di lateral
(horizontal) duktus semisirkularis
 Canal utama yang terkena biasanya
bagian posterior canalis
semisirkularis pada 80-90% kasus,
setelah itu horizontal canalis
semisirkularis pada sekitar 10%
kasus, dan anterior canalis
semisirkularis pada sekitar 2% kasus.
BPPV dapat mengenai lebih dari 1
canalis semisirkularis secara
bersamaan.
- BPPV yang berulang dapat
disebabkan oleh trauma kepala.
- BPPV tidak harus selalu disebabkan
karena trauma kepala yang berat.
- BPPV dapat disebabkan fraktur
dasar tengkorak.
- BPPV dapat disebabkan oleh injury
pada otolith organ disebabkan oleh
neuritis.
- BPPV dapat terjadi setelah infeksi
Diagnosis banding
-Vestibular neuritis
-Labirinitis
-Penyakit Meniere
Test diagnosis BPPV
-Test Dix-Hallpike Maneuver
Tidak dilakukan pemeriksaan ini pada
acute middle ear disease,
cholesteatoma.
Management
1.Reposition the otolith particles out
of the semicircular ducts or cupula
2. penambahan medical,
pharmacologicalmdan surgical bila
pasien gagal berulangkali mencoba
reposisi canal.
Canalith repositioning
maneuvers
Epley maneuvers
-Untuk posterior canal dan anterior canal
Canalith repositioning for
horizontal canal BPPV
Lempert 360 roll.
Untuk horizontal
Pharmacologic therapy
- low dose valium and antiemetics
seperti phenothiazines (phenergan or
compazine)
- cupulolithiasis, chronic
disequilibrium : long acting vestibular
suppressants seperti clonazepam
(klonopin)
NEURITIS VESTIBULARIS
 Definisi
neuritis vestibular gangguan atau
hilangnya Input vestibular aferen
total atau subtotal dari satu labirin
secara tiba-tiba, spontan, dan
terisolasi
 Etiologi
Infeksi virus pada nervus vestibular,
misalnya infeksi laten HSV tipe 1
pada ganglion vestibular superior
dan inferior
Ganglion vestibular superior : lebih
panjang dan sempit dibandingkan
dengan ganglion vestibular inferior
gangguan pada neuritis vestibular
lebih banyak pada ganglion
vestibular superior
 Manifestasi Klinis
Acute Spontaneous Vertigo
mengikuti onset, peningkatan intensitas vertigo dalam kurun waktu
jam, dan biasanya diperburuk oleh gerakan kepala, sementara itu
diminimalkan dengan menjaga kepala tetap dan mata ditutup
Mual
Muntah
Ketidakseimbangan postural
pada mencoba untuk berdiri atau berjalan, pasien merasa goyah dan
mungkin akan mengarah ke sisi labirin yang terkena
Nystagmus horisontal-torsi spontan (fase akut)
karena nystagmus ditekan oleh fiksasi visual, mungkin tidak
terdeteksi pada pemeriksaan neurologis standar untuk
menghilangkan fiksasi visual dapat menggunakan oftalmoskop atau
lensa pembesar frenzel mungkin diperlukan untuk mendeteksi
nystagmus dalam kasus ini
 Diagnosis
Meskipun neuritis vestibular adalah diagnosis klinis,
beberapa investigasi dapat membantu dalam menilai
pasien selama fase akut penyakit :
Subjective Visual Horizontal (SVH) test : investigasi yang
paling berguna pada kasus dugaan neuritis vestibular
Electronystagmography untuk mengidentifikasi karakteristik
hipofungsi vestibular unilateral pada neuritis vestibular
Tes kalori juga berkontribusi sedikit dalam tahap akut
penyakit. Tes kalori lebih berguna untuk mendemonstrasikan
paresis kanal sekitar 3-4 hari setelah onset
CT-Scan
MRI dari saluran pendengaran internal selama fase akut
neuritis vestibular dapat menunjukkan peningkatan saraf
vestibular superior di ganglion Scarpa
 DD
infark cerebellar
infark labirin
Penyakit Meniere (pada serangan
pertama)
vertigo migren dan vertigo akut yang
terkait dengan multiple sclerosis
 Tatalaksana
Terapi suportif juga harus diberikan selama fase akut neuritis
vestibular beberapa obat dapat digunakan untuk mual
termasuk phenothiazine : prochlorperazine (Compazine),
and promethazine (Phenergan), antidopaminergic
metoclorpamide (Reglan), dan 5-HT receptor antagonist
odansentron (Zofran)
Kortikosteroid dan antiviral (Methylprednisolone, Valcyclovir,
atau kombinasi Methylprednisolone+Valcyclovir)
Methylprednisolone : 100 mg selama 3 hari pertama kemudian di
tapering 20 mg setiap 3 hari selama 22 hari
Valcyclovir : 1000 mg 3x sehari selama 1 minggu
Pada fase subakut direkomendasikan untuk vestibular
rehabilitation exercise
MOTION SICKNESS
 Dapat timbul tiba-tiba pada orang-
orang yang bepergian dengan
kendaraan, mis. Mobil, pesawat,
terutama kapal/perahu
Rasa mual
Keringat dingin
Pusing
Muntah
 PATOFISIOLOGI
Pergerakan di artikan oleh otak melalui 3 jalur yang
berbeda dari sistem saraf yang menerima sinyal dari:
Telinga dalam (sensing motion, acceleration, and
gravity),
Mata (penglihatan)
Jaringan terdalam dari permukaan tubuh
(proprioceptors)

Ketika tubuh sengaja melakukan gerakan, cthnya ketika

sedang berjalan, input dari ketiga jalur tadi akan
dikoordinasi oleh otak.
Tapi ketika terjadi gerakan yang tidak disengaja, seperti
saat di dalam kendaraan, maka otak tidak melakukan
koordinasi. Terjadi konflik antara jalur-jalur tersebut
sehingga menimbulkan apa yang disebut motion
sickness
 TERAPI
Antihistamin : Antagonis reseptor H1
Diphenhydramine
Dimenhydrinate
ES utama: sedasi
 PENCEGAHAN

Hindari makan dan minum berlebihan (terutama makanan

berat, pedas / berlemak)
Hindari memakan makanan yang berbau tajam.
Pilih tempat duduk yang sebisa mungkin menghasilkan sedikit
pergerakan.
Jangan duduk menghadap arah yang berlawanan dengan laju
kendaraan
Jika di mobil, duduklah di depan kalau bisa
Jangan membaca selama perjalanan
Terkadang memusatkan pandangan ke satu titik dapat
membantu meringankan mual
Jika memungkinkan, aliran udara segar sangat membantu
mencegah mabuk kendaraan
Jangan berdekatan dengan orang yang sedang mabuk
kendaraan
Dapat meminum obat yang mencegah mabuk kendaraan
sebelum melakukan perjalanan
LABIRINITIS
 Bacterial Labyrinthitis
Develop through dissemination of
infection from middle ear space
(associated with otitis media or result
of bacterial spread through bony
fistula in cholesteatoma and chronic
otitis media)
May also develop as a result of the
spread of bacteria from subarachnoid
space into the perilymphatic fluid
 Clinical Picture
Acute/ subacute hearing loss
Vertigo
Malaise
Fever
Upper respiratory infection
Signs of acute otitis media / suppurative otitis
media
Bacterial invasion inflammation and tissue
destruction with fibro-osseus reaction
auditory and vestibular functional loss
 Histopathology
Bacterial labyrinthitis :
Serous / toxic labyrinthitis
Suppurative otogenic labyrinthitis
Suppurative meningogenic labyrinthitis
 Serous Labyrinthitis
Irritation of the labyrinth caused by
invasion of bacterial toxins (from
acute/ chronic otitis media,
perilyimphatic fistula or meningitis)
vertigo and sensorineural hearing
loss
Less severe form ear function
generally restored
Severe cases partial / complete
loss of hearing or vestibular function
 Acute Suppurative Otogenic
Labyrinthitis
Caused by bacterial invasion into the inner ear
resulting vertigo and hearing loss
A complication of chronic tympanomastoiditis,
leading to progressive osteolytic destruction of
the body labyrinth with invasion of granular tissue
Leads to an accumulation of polymorphonuclear
leukocytes local precipitate formed in the
perylimph endolymph endolymphatic
hydrops
Followed by necrosis of the membranous labyrinth
(with spread to meninges)
 Suppurative Meningogenic
Labyrinthitis
Spread of bacteria from the
subarachnoid space into the
labyrinth
Usually via cochlear aqueduct
 Common Microorganism
-haemolitic streptococci
Pneumococci
Staphylococci
Haemophilus influenzae
Proteus vulgaris
Pseudomonas aeruginosa
 Viral Labyrinthitis
Clinical picture:
Associated with acute disturbance of auditory and
vestibular function with vertigo and nystagmus
lasting three to five days
It has been known that many acute conditions
affecting the auditory and vestibular functions
are associated with influenza viruses and
respiratory infections together
Viral labyrinthitis affecting one or both ears,
sometimes through viraemia or direct spread
via subarachnoid space infection
 Clinical Picture
Cytomegalovirus
Cochleosaccular degeneration
Endolymphatic hydrops
Fibrosis
Fibro-osseous proliferation
Mumps
Deafness
Vertigo
 Clinical Picture
Herpes zoster
Deep burning pain (ear region)
Vesicular eruptions (external ear canal,
concha)
Hearing loss
Vertigo
Facial paresis
Otosyphilis
Degeneration of inner ear structure
Hearing loss
KEGANASAN

LO 5
KARSINOMA NASOFARING
NASOPHARYNGEAL CARCINOMA
Common among ethnic Chinese in and around
the Guangdong province of China, certain
regions of Southeast Asia, northern Africa, and
among Inuit (Eskimo) population in Alaska.
Risk factors:
EBV infections
High consumptions of salted fish and other
preserved food (especially during childhood)
Tobacco smoking
Genetic predesposition
 Etiologi:
Genetic (HLA systems)
Epstein Barr Virus
Environmental carcinogen
Pathophysiology
Unclear. Genetic and role of EBV.
Environmental carcinogen enhance the
entrance of the EBV genome into the
nasopharyngeal epithelium.
 Histological Staging
Classification T1 Only nasopharyngeal
Type I Squamos cell T2 Cavitas nasal, oropharyngeal
carcinoma T3 sinus paranasal
(keratinizing): T4 N.cranial, orbital, infratemporal
Well differentiated
Moderately differentiated
N1 Unilateral <6cm, beneath fossa supraclavicula
Poorly differentiated
N2 Bilateral<6cm, beneath fossa supraclavicula
Type II Nonkeratinizing
N3 bilateral >6cm, spread to fossa supraclavicula
carcinoma
TypeIII Undifferentiated
M0 NO metastasis
carcinoma
M1 metastasis
 Clinical Features
Early tumor may cause no symptoms
Commonest complaints:
Upper neck swelling, mostly unilateral
Nasal symptoms: blood-stained nasal discharge, nasal
obstruction, post-nasal drip, frank epistaxis
Aural symptoms: deafness, tinnitus, and otalgia
Neurological complaints: headache or cranial nerve
symptoms (V and VI)

Horners syndrome
Trismus
Ophtalmoplegia
 Examinations
Full head and neck examinations
Serology: IgA anti VCA for EBV
FNAB (type and staging)
CT Scan and MRI
Therapy: megavoltage external radiotherapy
Complications: Xerostoma, oropharyngeal
mucositis, taste bud disturbance, and alopecia
Differential diagnose: nose polyp, amelanotic
melanoma
 Nasal cavities & paranasal sinus
Etiology
malignancy
Carcinogenic compounds
Hard woods in the furniture industry
Exposure to nickel
Smoking
Chromium, polycyclic hydrocarbons
Alfatoksin
Mustard gas & thorotrast
Radiation
Viral & genetic

Lymphatic drainage
Anteroinferior part of nasal cavity facial, parotid,
submandibular nodes
Remainder of the nose posterior pathway runs anterior
the eustachian tube retropharyngeal nodes
upper deep cervical chain
 Patern of tumor spread
Local invasion
 Regional spread
Most common nodes submandibular &
jugulodigastric nodes

Distant metastase
Adenocarcinomas 18%
Squamous cell carcinoma 10%
bones, brain, liver, lung, skin poor
prognosis
 Staging
 Surgical pathology
Squamous cell carcinoma
Polypoid appearance
Adenocarcinoma
Adenoid cystic carcinoma
Olfactory neuroblastoma
Arises from the basal cells within the olfactory
neuroepithelium
Sinonasal undifferentiated carcinoma
Melanoma
Polypoid mass to an area of ulceration
Haemangiopericytomas
 Presentation
Maxillary sinus carcinoma
Facial pain with/-out progressive anesthesia of
the cheek by infiltration of the infraorbital nerve
Erosion of the medial wall epistaxis
Obstruction of the nasolacrimal duct epiphora
Destruction of the posterior wall & spread into
pterygopalatine & infratemporal fossa trismus,
maxillary & mandibular trigeminal nerve deficits
Inferior wall loosening of the premolar & molar
dentition
Superior wall proptosis & diplopia
Breaks into anterolateral wall visible
swelling/distortion of the cheek
 Ethmoid sinus carcinomas
Unilateral nasal obstruction & epitaxes
Epiphora, orbital swelling, proptosis & diplopia

Frontal sinus tumours

Orbital symptoms

Sphenoid sinus tumours

Invade the cavernous sinus infiltrate the contained
cranial nerves diplopia & facial pain

Nasal cavity tumours

Unilateral stuffiness & blockage
Sinus outflow obstruction tendency to bleed or spot nasal
secretion
 Clinical evaluation
Endoscopy, imaging (CT & MRI), biopsy

Management
General pre-/postoperative radiotherapy &
chemotherapy
Surgery for maxillary tumors
Maxillectomy (partial, total, extended)
Other surgical procedures
Anterior craniofacial resection
Lateral craniofacial resection
Orbital exenteration
 Prognosis
 Juvenile angiofibroma
uncommon, benign & extremely vascular tumour
that arises in the tissues within the sphenopalatine
foramen; locally invasive
The tumour extends into the nasopharynx, paranasal sinuses,
pterygopalatine & infratemporal fossa
Larger tumours can involve orbit & cavernous sinus

Pathology
Well defined, lobulated, covered by nasopharyngeal mucosa
Consists of proliferating, irregular vascular channels within a
fibrous stroma
Tumour blood vessels lack smooth muscle & elastic fibers
sustained bleeding
 Etiology
Androgen receptors are present in vascular
& stromal elements of the tumours (75%)
Vascular endothelial growth factors has
been found localized on both endothelial &
stromal cells
Overexpression of insulin like growth factor
II
Mutations of adenomatous polyposis coli
(APC) gene
 Presentation
Reccurrent severe epitaxes + nasal obstruction
Early symptoms swelling of cheek, trismus, hearing
loss secondary to eustachian tube obstruction,
anosmia, nasal intonation
Invasion of the orbit proptosis, diplopia, visual loss,
facial pain, headache
Anterior rhinoscopy
Abudant mucopurulent secretions in the nasal cavity
obscure the tumour from vision
The soft palate often displaced inferiorly by the bulk of
tumour (pink reddish mas that fills the nasopharynx)
 Assessment
Plain lateral skull radiographic
Anterior bowing of the posterior wall of the
maxillary sinus
CT & MRI

Stagging system (Fisch)

 Treatment
Preoperative embolization
Some tumours acquire blood supply from other
vessles like internal carotid artery
Preoperative chemotherapy
Flutamide (nonsteroidal androgen receptor
blocker)
Surgical resection
Endoscopic endonasal techniques
Open approaches
Radiotherapy
KARSINOMA LARING
 Laryngeal Carcinoma
Most Common head and neck cancer
in worldwide
Increasing in development country
Benign vs Malignant
 Benign Laryngeal
Carcinoma
Most Common : Papilloma / RRP (Recurrent
Respiratory Papillomatosis)
In Young Adult (18-39 years old) with
hoarseness or following biopsy of an
incidentally discovered laryngeal 'polyp
It is more commonly seen at the junction of
the respiratory epithelium with the
squamous epithelium, generally at the glottis
Caused by the human papilloma virus (HPV)
subtype 6c-f and 11
 Surgical management aims to debulk tumours,
originally by microforceps, but in recent decades
with lasers.
Unfortunately, the growths recur regularly,
requiring repeat operations.
Papilloma recurrence can occur up to 30 years
after remission.
Adjunct medical treatments, aimed at containing
the virus and growth of tumours, include indole-3-
carbinol or its dimer diindolylmethane, interferon,
podophyllum, cidofivir or photodynamic therapy.
 Malignant Laryngeal
Carcinoma
Laryngeal cancer is the eleventh most
common cancer in men worldwide
Squamous cell carcinoma is by far the most
common type of tumour, comprising 90
percent or more of all laryngeal
malignancies in large series.
Microscopically, it is characterized by the
presence of 'prickle' cells and keratin
whorls.
Marker : cytokeratin
 Risk Factor
Alcohol is thought to promote
carcinogenesis through acetaldehyde
exposure, malnutrition and
desiccation of mucosa.
Tobacco acts via polycyclic aromatic
hydrocarbons, like benzopyrene,
whose products bind directly to DNA
and RNA.
 Diagnose :
MRI / CT Scan
PET Scan
Biopsy
Endoscopy
Treatment :
Chemotherapy
Endoscopic Resection
Laryngectomy
 Post-Laryngectomy
Rehabilitation
Stroma Filter X Candida
Psychososial support
Follow Up
For the first years monthly
Second years two Monthly
Third-Fifth years 3-5 Monthly
ANGIOFIBROMA JUVENILE
 Juvenille Angiofibroma
Is an uncommon, benign and extremely
vascular tumour that arises in the tissues within
the sphlenopalatine foramen. Rarely, it is found
at other sites nasal cavity and paranasal
sinuses.
Almost exclusively in adolencent males. Also
being found in children, the elderly, young, and
even pregnant women.
As it grows, the tumour extends into the
nasopharynx, paranasal sinuses,
pterygopalatine and infratemporal fossa. Larger
tumour can involve the orbit and cavernous
sinus.
 Pathogenesis
Juvenille Angiofibromas present as well-defined,
lobulated tumours that are covered by
nasopharyngeal mucosa.
The tumour consist of proliferating, irregular
vascular channels within a fibrous stroma. Tumour
blood vessels typically lack smooth muscle and
elastic fibres, this feature contributing to its
reputation for sustained bleeding.
Recent immunocytochemical techniques have
been used to show that androgen receptors are
present in both the vascular and stromal
elements
A much smaller proportion of tumours also have
 Pathogenesis
The angiogenic growth factor (vascular
endothelial growth factor VEGF) has been found
localized on both endothelial and stromal cells,
perhaps indicating that both cell types play a role
in tumour development.
Overexpression of insulin-like growth factor II
(IGFII) has also been found in a large number of
juvenille angiofibromas. It is thought that
overexpression of IGFII might be associated with
a tendency to reccurence and poorer prognosis.
Also beend reported to develop 25 times more
frequently in patients with familial adenomatous
polyposis, a condition that is associated with
mutation of the adenomatous polyposis coli (APC)
 Etiology
Androgen receptors are present in
vascular & stromal elements of the
tumours (75%)
Vascular endothelial growth factors
Overexpression of insulin like growth
factor II
Mutations of adenomatous polyposis
coli (APC) gene
 Tanda & gejala
Epitaksis berat rekuren dan obstruksi nasal
Gejala awal: bengkak pada pipi, trismus,
gangguan pendengaran sekunder karena
obstruksi tuba eustachius, anosmia, nasal
intonation
invasi ke orbita: proptosis, diplopia, visual loss,
facial pain, headache
rinoskopi anterior sekret mukopurulen
berlebih di kavitas nasal menyembukan tumor
Pink reddish mass di nasofaring
 Pemeriksaan
Plain lateral skull radiographic
Anterior bowing of the posterior wall of
the maxillary sinus
CT & MRI
Stagging system (Fisch)
 Presentation
Recurrent severe epistaxes accompanied by
progressive nasal obstructionclassical
symptoms.
There is a delay of at least six or seven months
between the onset of symptoms and
presentation. By that time, it is usual for the
youth to have other signs symptomps of tumour
growth and extension (include swelling of the
cheek, trismus, hearing-loss secondary to
Eustachian tube obstruction, anosmia, and a
nasal intonation or plummy quality to the voice)
 Presentation
More extensive tumour growth with invasion of the
orbit and cavernous sinus, may cause proptosis,
diplopia, visual loss, facial pain, headache
Anterior rhinoscopy is likely to confirm the
presence of abundant mucopurulent secretions in
the nasal cavity that usually obscure the tumour
from vision, though a few patients have tumour
prolapsing from the anterior nares.
The soft palate is often displaced inferiorly by the
bulk of the tumour which can be seen clearly as a
pink or reddish mass that fills the nasopharynx
 Assesment
In the past plain lateral skull radiograpic
Nowdays, the diagnosis is based on the CT and MRI
appearances that are sometimes confirmed by
angiography.
A trans-nasal biopsy is not necessary and can provoke
brisk haemorrhage.
The exact extent or stage of the tumour can only be
determined by a combination of CT and MRI and this is
vital when planning the surgical resection.
Several staging systems have been proposed but that of
Fisch is the most robust and practical. It defines clearly
which tumours can be resected by endonasal techniques
and those that would be better tackled by more open or
infratemporal fossa/neurosurgical approaches.
 Assesment
The radkowski staging system
appeals to those involved with the
management of smaller tumours as
there are more subdivisions but in
reality, this adds little to its utily.
Diagnostic angiography is
undertaken to evaluate the source of
blood supply and as a prelude to
selective embolization
 Fisch staging system of juvenille
angiofibromas

Type Details
1 Tumour limited to the nasopharyngeal cavity; bone
destruction negligible or limited to the sphlenopalatine
foramen
2 Tumour invading the pterygopalatine fossa or the maxilary,
ethmoid or sphenoid sinus with bone destruction.
3 Tumour invading the infratemporal fossa or orbital region:
(a) Without intracranial involvement
(b)With intracranial extradural (parasellar) involvement
4 Intracranial intradural tumour
(a) Without infiltration of the cavernous sinus, pituary fossa
or optic chiasm
(b)With infiltration of the cavernous sinus, pituary fossa or
optic chiasm
 Radkowski classification of juvenille
angiofibromas
Stage Details
Ia Limited to the nose and nasopharyngeal area
Ib Extension into one or more sinuses
IIa Minimal extension into pterygopalatine fossa
IIb Occupation of the pterygopalatine fossa without orbital
erosion
IIc Infratemporal fossa extension without cheek or
pterygoid plate involvement
IIIa Erosion of the skull base (middle cranial fossa or
pterygoids)
IIIb Erosion of the skull base with intracranial extension with
or without cavernous sinus involvement
 Tatalaksana
Embolisasi preoperatif
Flutamide (nonsteroidal androgen receptor
blocker)
Kemoterapi preoperatif
Bbrp tumor mendapatkan suplai darah dari
pembuluh lain seperti arteri carotid interna
Reseksi bedah
Endoscopic endonasal techniques
Open approaches
Radiotherapy
 Surgical resection-techniques and
approaches
Most small tumours were resected either through a transpalatal
approach, lateral rhinotomy or mid-facial degloving approach.
Open approaches can be used for tumours of all stages and
certainly were the only option before the application of endonasal
endoscopic techniques became more wide-spread.
Nowdays, stage Fisch 1, 2 and some type 3 tumours are suitable
for endoscopic resection using one or two surgeon techniques.
There is much to be gained by endonasal endoscopic techniques,
e.g reduced intraoperative blood loss, fewer postoperative
complications and a reduced length of hospital stay.
Furthermore, the tumours resected by endoscopic techniques
tend to be relatively small.
Fisch type 3 tumours suitable for endoscopic resection have
limited medial invasion of the infratemporal fossa
 Surgical resection-techniques and
approaches
Endoscopic endonasal techniques
Preoperative embolization is usually undertaken, not-
withstanding its doubtful benefit.
Induction of anaesthesia nose is prepared with a
vasocontrictor (4% cocaine or epinephrine
1:10.000)the anterior end of the middle turbinate is
resected at the outset of the procedure an anterior
ethmoidectomy together with removal of the medial
wall of the maxillary sinus then remove to achieve
complete lateral exposure of the tumour dissection
then continues into the sphenoid until its rostrum is
reached following which the tumour can be peeled
inferiorly.
 Surgical resection-techniques and
approaches
Open approaches
Using the exposure afforded by this
approach, the anterior, medial, lateral and
posterior walls of the maxillary antrum
can be removed. This produces a very
large cavity that is confluent with the
nasal cavity and post-nasal space and
control of its blood supply. Extensions into
the inferior part of the orbit and
infratemporal fossa can also be removed
 Surgical resection-techniques and
approaches
Radiotherapy
All series report that regression of
angiofibromas after radiotherapy is
very slow indeed, often taking two to
three years before radiological
stabilization is achieved. In other
words, reduction in the size of
tumour take place, but residual
tumour remains.
 Complication
Recurrence is by far the most common complication
encountered.
The one single factor that seems to correlate with
recurrence is the age if the patient at the time of
presentation. The younger the patient the more likely that
future recurrence will develop.
From a surgical stand point, most recurrences develop as a
consequence of invasion of the basispenoid. A more
meticulous exploration of this area at the time of primary
surgery has been reported to have a dramatic effect on the
rate of recurrent disease. Radiological monitoring is
necessary for all these patients.
Disease-free status five years after primary surgery
probably represent cure. The same cannot be said for those
who have experience recurrent disease.
 Other complication surgically induced infraorbital
nerve sensory deficits are recognized as a potential
complication of mid-facial degloving, as is nasal
vestibular stenosis.
With more extensive resections, ocular problems may
be experienced.
Late complication also develop following radiotherapy
and are relatively common. Growth retardation,
panhypopituitarism, tomporal lobe necrosis, cataracts,
radiation keratopathy, together with skin, thyroid and
nasopharyngeal malignancies were the most common
probles encountered in the first 10-15 years after
treatment.
For these patients, lifetime monitoring and assesment
is necessary.
Serial interval MRI should become a standard of care
for these patient
Stagging system
 References
Sherwood, human physiology
Scott Browns otorhinolaryngology,
7th edition
Ballengers
 KESIMPULAN
Ka: Meniere
KI : Karsinoma Nasofaring
 SARAN
Meniere: tatalaksana meniere seperti
pembatasan asupan sodium,
penggunaan diuretik untuk vertigo.
Kalo masih berkelanjutan tindakan
bedah.
Karsinoma: lakukan FNAB untuk
tentukan tipe dan grading