RIANTIKA NUR UTAMI

LI LBM 1 THT
 Bagaimana anatomi dari sistem pendengaran?
 Bagaimana histologi sistem pendengaran?
 Bagimana fisiologi dari sistem pendengaran?
 Mengapa pada psien didapat tidak bisa mendengar dan keluar
cairan bening
 Enapa ditemukan nyer telinga kanan, anak tidak mau makan dan
minum, dan apa hubungan dengan mengorek-ngorek telinga?
 Apa etiologi pada scenario?
 Apa hasil interpretasi dar pmeriksaan?
 Apa interpretasi pmeriksaan otoskopi?
 Apa DD dan diagnosis dari scenario dan manifestasi klinis dr
masing masig DD?
 Apa patofisiologi dan patogenesiss dari scenario?
 Pemeriksaaan penunjang apa yag perlu dilakukan?
 Apa terapi yang diberikan pada kasus tersebut
HISTO LOGI
Meatus acusticus eksterna
FISIO LOGI
Mengorek-ngorek telinga

kalor

luka
Dolor (nyeri) Nyeri tekan tragus

inflamasi
Rubor (merah) Hiperemis CAE

infeksi Ganggu penghantaran

Tumor (udem)
suara

eksudat ↑ serumen

Membran timpani sulit

Keluar cairan dinilai Kurang dapat mendengar
bening
Pathophysiology
 OE is a superficial infection of the skin in the EAC. It may be classified as follows:
 Acute diffuse OE – This is the most common form of OE, typically seen in swimmers; it is
characterized by rapid onset (generally within 48 hours) and symptoms of EAC inflammation
(eg, otalgia, itching, or fullness, with or without hearing loss or jaw pain) as well as tenderness
of the tragus or pinna or diffuse ear edema or erythema or both, with or without otorrhea,
regional lymphadenitis, tympanic membrane erythema, or cellulitis of the pinna [9]
 Acute localized OE – This condition, also known as furunculosis, is associated with infection of
a hair follicle
 Chronic OE – This is the same as acute diffuse OE but is of longer duration (>6 weeks)
 Eczematous (eczematoid) OE – This encompasses various dermatologic conditions (eg, atopic
dermatitis, psoriasis, systemic lupus erythematosus, and eczema) that may infect the EAC and
cause OE
 Necrotizing (malignant) OE – This is an infection that extends into the deeper tissues adjacent
to the EAC; it primarily occurs in adult patients who are immunocompromised (eg, as a result
of diabetes mellitus or AIDS) and is rarely described in children; it may result in cases of
cellulitis and osteomyelitis (see Cellulitis, Osteomyelitis, and Chronic Osteomyelitis Imaging)
 Otomycosis - Infection of the ear canal secondary to fungus species such
as Candida or Aspergillus
The processes involved in the development of OE
can be divided into the following four categories:

 Obstruction (eg, cerumen buildup, surfer’s exostosis,

or a narrow or tortuous canal), resulting in water
retention
 Absence of cerumen, which may occur as a result of
repeated water exposure or overcleaning the ear
canal
 Trauma
 Alteration of the pH of the ear canal
 If moisture is trapped in the EAC, it may cause maceration of the skin and
provide a good breeding ground for bacteria. This may occur after
swimming (especially in contaminated water) or bathing—hence the
common lay term “swimmer’s ear.” It may also occur in hot humid weather.
Obstruction of the EAC by excessive cerumen, debris, surfer’s exostosis, or
a narrow and tortuous canal may also lead to infection by means of
moisture retention.
 Trauma to the EAC allows invasion of bacteria into the damaged skin. This
often occurs after attempts at cleaning the ear with a cotton swab, paper
clip, or any other utensil that can fit into the ear.
 Once infection is established, an inflammatory response occurs with skin
edema. Exudate and pus often appear in the EAC as well. If severe, the
infection may spread and cause a cellulitis of the face or neck.
 Necrotizing (malignant) OE is a rare complication that occurs in patients
who are immunocompromised or in those who have received radiotherapy
to the skull base. In this condition, bacteria invade the deeper underlying
structures of the soft tissues and cause osteomyelitis of the temporal bone.
This is a life-threatening disorder with an overall mortality that historically
has approached 50%.
Infeksi dapat terjadi sebagai akibat faktor-
faktor predisposisi tertentu sebagai berikut:

 1. Perubahan pH kulit kanalis yang biasanya asam

menjadi basa.

 2. Perubahan lingkungan terutama gabungan

pcningkatan suhu dan kelembaban.

 3. Suatu trauma ringan seringkali karena bereuang

atau membenihkan telinga secara berlebihan.
ETIO LOGI
ETIOLOGY
 OE is most often caused by a bacterial pathogen; other varieties
include fungal OE (otomycosis) and eczematoid (psoriatic) OE. [12] In
one study, 91% of cases of OE were caused by bacteria. [7] Others
have found that as many as 40% of cases of OE have no primary
identifiable microorganism as a causative agent. The most common
causative bacteria are Pseudomonas species (38% of all cases), [12]
Staphylococcus species, and anaerobes and gram-negative organisms.

 Fungal OE may result from overtreatment with topical antibiotics or

may arise de novo from moisture trapped in the EAC. It is caused by
Aspergillus 80-90% of the time; Candida and other organisms have
also been isolated. This condition is characterized by long, white,
filamentous hyphae growing from the skin surface. Besides otorrhea,
erythema and edema of the EAC are common. In severe cases, soft
tissue stenosis may be present. Extension of the infection may
manifest as cellulitic skin changes involving the concha of the auricle
and the tragus.
 Eczematoid (psoriatic) OE is associated with the
following conditions:
 Eczema
 Seborrhea
 Neurodermatitis
 Contact dermatitis from earrings or hearing aid use
 Purulent otitis media with perforation of the tympanic
membrane and drainage; this may mimic OE to an extent,
but it is usually painless and does not cause any swelling
of the ear canal
 Sensitivity to topical medications
 Chronic OE is a fairly common condition that is
sometimes the result of incomplete treatment of acute
OE. [13] More often, however, chronic OE is caused by
overmanipulation of the ear canal as a consequence of
cleaning and scratching. Such overmanipulation results in a
low-grade inflammatory response that causes further
itching of the skin. Eventually, the skin thickens, and canal
stenosis may occur.

 Necrotizing OE occurs in patients who are

immunocompromised and represents a true osteomyelitis
of the temporal bone.
Risk factors for OE include the following:
 Previous episodes of OE
 Swimming, diving, or participating in aquatic activities
 Use of earplugs or probing of the EAC (possibly
secondary to trauma to the EAC)
 Hot, humid weather
 Use of a hearing aid
 Coexistence of eczema, allergic rhinitis, or asthma
 Comorbidities such as diabetes mellitus, AIDS, leukopenia,
or malnutrition
 Signs and symptoms
 The key physical finding of OE is pain upon palpation of the tragus (anterior to ear canal) or
application of traction to the pinna (the hallmark of OE). Patients may also have the following
signs and symptoms:
 Otalgia - Ranges from mild to severe, typically progressing over 1-2 days
 Hearing loss
 Ear fullness or pressure
 Erythema, edema, and narrowing of the EAC
 Tinnitus
 Fever (occasionally)
 Itching (especially in fungal OE or chronic OE)
 Severe deep pain - Immunocompromised patients may have necrotizing (malignant) OE
 Discharge - Initially, clear; quickly becomes purulent and foul-smelling
 Cellulitis of the face or neck or lymphadenopathy of the ipsilateral neck (occasionally)
 Bilateral symptoms (rare)
 History of exposure to or activities in water (frequently) (eg, swimming, surfing, kayaking)
 History of preceding ear trauma (usually) (eg, forceful ear cleaning, use of cotton swabs, or
water in the ear canal)
ANAMNESIS
 History
 Patients with otitis externa (OE) may complain of the following:
 Otalgia, ranging from mild to severe, typically progressing over 1-2 days
 Hearing loss
 Ear fullness or pressure
 Tinnitus
 Fever (occasionally)
 Itching (especially in fungal OE or chronic OE)
 Severe deep pain – If this is experienced by a patient who is immunocompromised
or diabetic, be alerted to the possibility of necrotizing (malignant) OE
 Discharge – Initially, the discharge may be clear and odorless, but it quickly becomes
purulent and foul-smelling
 Bilateral symptoms (rare)
 Frequently, a history of exposure to or activities in water (eg, swimming, surfing, and
kayaking)
 Usually, a history of preceding ear trauma (eg, forceful ear cleaning, use of cotton
swabs, or water in the ear canal)
Px Fisik
 The key physical finding of OE is pain upon palpation of the tragus (anterior to ear canal) or
application of traction to the pinna (the hallmark of OE). Examination reveals erythema,
edema, and narrowing of the external auditory canal (EAC), and a purulent or serous
discharge may be noted (see the image below). Conductive hearing loss may be evident.
Cellulitis of the face or neck or lymphadenopathy of the ipsilateral neck occurs in some
patients.
 The tympanic membrane may be difficult to visualize and may be mildly inflamed, but it should
be normally mobile on insufflation. Eczema of the pinna may be present. By definition, cranial
nerve (CN) involvement (ie, of CNs VII and IX-XII) is not associated with simple OE.
 Fungal OE results in severe itching but typically causes less pain than bacterial OE does. A
thick discharge that may be white or gray is often present. Whereas pseudomonal infection
produces purulent otorrhea that may be green or yellow, Aspergillus otomycosis looks like a
fine white mat topped by black spheres. Upon close examination, the discharge may contain
visible fungal elements (eg, spores or hyphae) or have a fuzzy appearance.
 The sine qua non of necrotizing OE is pain that is out of proportion to the clinical findings.
Upon close examination, granulation tissue may be present in the ear canal.
 In severe cases, the infection may spread to the surrounding soft tissues, including the parotid
gland. Bony extension may also occur into the mastoid bone, temporomandibular joint, and
base of the skull, in which case cranial nerves VII (facial), IX (glossopharyngeal), X (vagus), XI
(accessory), or XII (hypoglossal) may be affected.
penunjang
 Diagnosis
 The patient’s history and physical examination, including otoscopy, usually provide sufficient information for
the clinician to make the diagnosis of OE. Note that a patient who is diabetic or immunocompromised with
severe pain in the ear should have necrotizing OE excluded by an otolaryngologist.
 Laboratory testing
 Typically, laboratory studies are not needed, but they may be helpful if the patient is immunocompromised, if
the usual treatment measures are ineffective, or if a fungal cause is suspected. Tests may include the
following:
 Gram stain and culture of any discharge from the auditory canal
 Blood glucose level
 Urine dipstick
 Imaging studies
 Imaging studies are not required for most cases of OE. However, radiologic investigation may be helpful if an
invasive infection such as necrotizing (malignant) OE is suspected or if the diagnosis of mastoiditis is being
considered.
 Imaging modalities may include the following:
 High-resolution computed tomography (CT) - Preferred; better depicts bony erosion [5]
 Radionucleotide bone scanning
 Gallium scanning
 Magnetic resonance imaging (MRI) - Not used as often as the other modalities; may be considered
secondarily or if soft-tissue extension is the predominant concern [6]
 Px penunjang gangguan pendengaran  test rinne, weber,
swabach
 Audiometri  apa aja?
 DD gangguan pendengaran
 Telinga luar  otitis eksterna, serumen
 Telinga tengah
 Telinga dalam SNHL
 Prinsip-prinsip penatalaksanaan yang dapat diterapkan
pada semua tipe "otitis eksterna" antara
 lain:
 1. Mernbersihkan liang telinga dengan pengisap atau kapas
dengan berhati-hati.
 2. Penilaian terhadap sekret, edema dinding kanalis, dan
membrana timpani bilamana mungkin;
 keputusan apakah akan menggunakan sumbu untuk
mengoleskan obat.
 3. Pemiliban pengobatan lokal.
 Complications of OE are rare and may include the following:
 Necrotizing OE (the most significant complication)
 Mastoiditis
 Chondritis of the auricle (from spread of acute OE to the pinna,
particularly in patients with newly pierced ears)
 Bony erosion of the base of the skull (skull base osteomyelitis [15] )
 Central nervous system (CNS) infection
 Cellulitis or lymphadenitis
 Diabetic ketoacidosis is often present in diabetics with this condition.
 Herpes zoster may initially present with symptoms similar to those of OE,
and vesicular eruption may occur 1-2 days after the initial symptoms.
Ramsay Hunt syndrome is a rare complication of herpes zoster and
presents with peripheral unilateral facial palsy. Patients should be counseled
on this possible presentation and advised to seek medical care if it occurs.
 Radang
telinga
tengah

3. OME
2. OMK
OMA (akut) (Otitis media
(kronik)
dg Efusi)
 Kausa :
◘ ISPA (sebagian besar)
◘ Cairan masuk ke rongga telinga :
-tersedak
-muntah
-bayi
-minum sambil tiduran
-tekanan negatif relatif dr rongga t.tengah
-menyelam.
◘ melalui gendang telinga perforasi
 Perjalanan Penyakit:

 Stadium 1: Salphingitis ( rdg. Tuba Eustachii)

- telinga terasa tersumbat (oklusio
tuba)
- gembrebeg (tinitus low frequency)
- ‹ dengar (tipe CHL)
- otofoni (mendengar suara sendiri)
- otoskopi → MT normal

 Stadium 2 : Pre supuratif ( rdg mukoperios t.tengah)

- gejala stadium 1 bertambah hebat
- panas/otalgia +
- MT merah (vaskularisasi jelas)
- manubrium malei ke perifer
OMA (otitis media akuta)
 Stadium 3 : Supurasi / pustulasi → Std. perforasi
- gejala stadium 1 lbh hebat lagi
- anak-anak : sering rewel / kejang !!
- MT bullging (otalgia) → ada ttk. Iskemik
(bercak kuning) → nekrosis !! → dpt
terjadi
perforasi. → stadium 4 ?
ok. Trombophlebitis dari
vena
- gejala mereda
- keluar discharge purulen
- MT merah membara
OMA (otitis media akut)

 Stadium 4: Resolusi

● MT utuh : - gejala mereda

- sakit/panas hilang
- berlanjut menjadi OME

● MT perforasi : - dpt menutup kembali → sikatrik

tanpa stratum fibrosum
- menjadi OMK (otitis media kronik)
PROGNOSIS OMA :
 Sembuh setelah std. Resolusi.
- sembuh spontan tanpa perforasi
- sembuh dg perforasi→ bila menutup → sikatrik
- sembuh setelah parasentesis

 TIDAK sembuh.
- tanpa perforasi → OME → sekret kental → Glue ear

- dg. perforasi → OMK

→ bila sembuh dan tetap perforasi
→ Dry ear
Tx. OMA: therapi kausanya !
>> ISPA →Strep.β Hemolitikus
group A
 1. Parasentesis pd stadium 2,3
Alasan : cegah perforasi spontan
cegah komplikasi
penyembuhan primer
dpt mengobati lokal
mengurangi rs. Sakit
drainase
 2. AB
 3. Simptomatik : analgetik/antipiretik
dekongestan,mukolitik
 OTITIS MEDIA KRONIK (OMK)

Deff: Radang mukoperios c.timpani ditandai

dg tanda radang kronik

Permasalahan :
1. m.timpani → permanent perforasi
syndrome/pps
2. mukosa → persistent mucosal disease/pmd
3. tulang → cholesteatoma

Klasifikasi : ● Tipe Tubotimpanal (1,2)

● Tipe Aticoanthral (3)
Cholesteatoma :

Merupakan tumor → jar. dalam mati dr. disquamasi

epitel gepeng

Klasifikasi : 1. kongenital
2. aquisita → primer
→ sekunder
ad.1. Kongenital:
- asal :sel embrional
- lokasi : os petrosus
- dx. → obst. tuba (-) otitis media (-)
→ m. timpani (+)
→ N.VII → perot
DX. Banding Cholesteatoma

Tanda2 Kongenital Aquisita Aquisita

primer sekunder
obstr. tuba - ++ +/-
riwayat OM - +/- +
m. Timpani utuh retraksi perforasi sentral
perforasi atik marginal

lokasi os.petrosus epitimpani meso/hipotimpani

asal sel embrional retraksi sel metaplasia teori
invaginasi imigrasi teori
teori
OTITIS MEDIA dg EFUSI (OME)
 Deff : rdg mukoperiost t.tengah yg ditandai adanya
cairan dan m.timpani utuh

 Nama khusus tergantung dr. efusinya !!

 Causa OME → obstruksi tuba kronis
 Patogenesis OME:
- obstr. tuba kronis → pertukaran gas di C.timpani tetap
→ O2 diresorbsi , CO2 dikeluarkan
- CT → O2 ↓, CO2 ↑
- kapiler → PO2 ↓, PCO2 tetap
→ permeab. kapiler ↑→ keluar di darah/serum
→ udem CT → efusi OME/serous ( PASIF)
 Bila b’langsung terus :
→ merangsang sel2 mukosa epitel
→ terbentuk sel sekretorik, sel goblet → zat
mukous
OME (AKTIF)
 Diagnosis :
- Anamnesis → otofoni, tinitus, diplakusis,
- Pemeriksaan otoskopi → MT (N,retraksi,bulging)
- pemeriksaan tuba→ oclusi tuba +
- pemeriksaan pendengaran → garpu tala , audiometri
 Therapi : Tergantung Komplikasi (MT,CT )
 - keluarkan cairan
- medikamentosa
- cari causanya → causa oclusio tuba kronis
KOMPLIKASI OMK
mastoiditis Akut : hemorhagik –
koalesen

Kronik
anthritis sub periosteal abses Subcutan abses
Abses Bezold
Maurette abses
Gelle abses
perisinus abses thromboplebitis :
( phlebitis) abses
otak,retrobulber,sepsis

Meningitis subdural abses

difuse
labirintitis sirkumskripta
laten
Cholesteatoma
petrositis facial palsy