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Otitis Externa
Essentials oI Diagnosis
O Otalgia, otorrhea, pruritus, hearing loss, history oI water exposure.
O %ender pinna and canal; canal erythema, edema, and purulent debris.
O ulture Ior reIractory cases.
General onsiderations
Otitis externa is an inflammatory and infectious process oI the EA. Pseudomonas
aeruginosa and Staphylococcus aureus are the most commonly isolated organisms. Less
commonly isolated organisms include Proteus species, Staphylococcus epidermidis,
diphtheroids, and Escherichia coli. Fungal otitis externa is discussed in the next section.
Pathogenesis
In the preinIlammatory stage, the ear is exposed to predisposing Iactors, including heat,
humidity, maceration, the absence oI cerumen, and an alkaline PH. %his can cause edema oI the
stratum corneum and occlusion oI the apopilosebaceous units. In the inIlammatory stage,
bacterial overgrowth ensues, with progressive edema and intensiIied pain. Incomplete resolution
or persistent inIlammation Ior more than 3 months reIers to the chronic inIlammatory stage.

linical Findings
Symptoms oI otitis externa may vary, depending on the stage and extent oI disease. %he clinical
diagnosis is suggested by the presence of otalgia, otorrhea, aural fullness, pruritus,
tenderness to palpation, and varying degrees oI occlusion of the EAC. %he patient may also
present with hearing loss that results Irom occlusion oI the EA by edema and debris. Signs oI
otitis externa include pain on distraction of the pinna, EAC erythema, edema, otorrhea,
crusting, and, in more advanced disease, lymphadenopathy of the periauricular and anterior
cervical lymph nodes. Skin changes oI cellulitis may be present as well. In the chronic stage,
the skin oI the EA may be thickened. A culture may be helpIul Ior inIections that are reIractory
to treatment.
%reatment
%reatment Ior otitis externa involves meticulous atraumatic debridement oI the EA with the
aid oI a microscope. Analgesia can be achieved with nonsteroidal anti-inIlammatory drugs
(NSAIDs), opioids, or topical steroid preparations. AIter cleansing is complete, otic drop
preparations that are antiseptic, acidiIying, or antibiotic (or any combination oI these) should be
used. II the degree oI stenosis oI the canal is severe, a wick may be careIully placed in an eIIort
to deliver the drops to the medial portion oI the canal.
Available antiseptic preparations include acetic and boric acids, ichthammol, phenol,
aluminum acetate, gentian violet, thymol, thimerosal (eg, Merthiolate), cresylate, and
alcohol. Available antibiotic preparations include ofloxacin, ciprofloxacin, colistin, polymyxin
B, neomycin, chloramphenicol, gentamicin, and tobramycin. Polymyxin B and neomycin
preparations are oIten used in combination Ior the treatment oI S aureus and P aeruginosa
inIections. OIloxacin and ciproIloxacin are single-agent antibiotics with an excellent spectrum oI
coverage Ior pathogens encountered in otitis externa. Preparations with steroids help to reduce
edema and otalgia. Systemic antibiotics are indicated Ior inIections that spread beyond the EA.
For chronic otitis externa, a canalplasty may be indicated Ior thickened skin that has caused canal
obstruction. Patients must be instructed to avoid EA manipulation and water exposure iI they
have a history oI recurrent otitis externa.
Otomycosis
Essentials oI Diagnosis
O Pruritus, otalgia, otorrhea, Iullness, hearing loss, no response to topical antibiotics.
O Fungal elements on physical examination.
O Positive KOH prep or Iungal culture.
General onsiderations
Otomycosis is an inIlammatory process oI the external ear canal due to inIection with Iungi and
is responsible Ior more than 9 oI the diagnoses oI otitis externa. In 80 oI cases, the etiologic
agent is spergillus, whereas andida is the next most Irequently isolated Iungus. Other more
rare Iungal pathogens include Phycomycetes, Rhi:opus, Actinomyces, and Penicillium.
Pathogenesis
Otomycosis has similar predisposing Iactors to bacterial otitis externa. Patients with diabetes
mellitus or an immunocompromised state are particularly susceptible to otomycosis.
linical Findings
Patients with otomycosis most Irequently present with pruritus, aural fullness, and otorrhea,
and may also complain of otalgia and hearing loss. %he hearing loss associated with
otomycosis usually results Irom the accumulation oI mycotic debris.
Otoscopy oIten reveals mycelia, establishing the diagnosis. %he EAC may be erythematous and
fungal debris may appear white, gray, or black. Patients have typically been tried on topical
antibacterial agents with no signiIicant response. %he diagnosis can be conIirmed by identiIying
Iungal elements on a KOH preparation or by a positive Iungal culture.
%reatment
%he treatment oI otomycosis includes cleansing and debriding the EAC, acidifying the canal,
and administering antifungal agents. NonspeciIic antiIungal agents include thimerosal (eg,
Merthiolate) and gentian violet. ommonly used speciIic antiIungals include clotrimazole,
Nystatin (otic drops or powder), and ketoconazole. Itraconazole is the only orally
administered antiIungal agent that is eIIective against Aspergillus
Otitis Media: Introduction
%he term otitis media (OM) reIers to an inflammatory process within the middle ear cleIt. Otitis
media can be either acute or chronic. %here is no absolute time period, but, in general, disease
that persists Ior more than 3 months should be considered as chronic.
A subclassiIication oI acute and chronic OM is summarized in %able 491. Otitis media
associated with cholesteatoma is considered separately in hapter 50, holesteatoma. %he
eustachian tube appears to be central to the pathogenesis oI all Iorms oI OM (with the possible
exception oI cholesteatoma). %he normal physiologic Iunctions oI the eustachian tube are to (1)
maintain the gaseous pressure within the middle ear cleIt at a level that approximates
atmospheric pressure; (2) prevent reflux oI the contents oI the nasopharynx into the middle ear;
and (3) clear secretions from the middle ear by both mucociliary transport and a "pump action"
oI the eustachian tube.


%able 491. lassiIication oI Otitis Media.


Acute Otitis Media
Suppurative
Nonsuppurative
Recurrent
Chronic Otitis Media
Suppurative
%ubotympanic
holesteatoma
Nonsuppurative
Otitis media with eIIusion

%he failure of any or all of these normal functions of the eustachian tube can result in OM.
Both anatomic and Iunctional obstruction oI the eustachian tube results in the Iailure oI normal
regulation oI the middle ear pressure. Anatomic obstruction is most commonly caused by
inflammation oI the eustachian tube mucosa or extrinsic compression by tumor or large
adenoids. Functional obstruction usually occurs as a result oI either the Iailure oI the normal
muscular mechanism oI eustachian tube opening, as seen in cleft palate, or insufficient
stiffness oI the cartilaginous portion oI the eustachian tube, oIten seen in infants and young
children. %he more acute angle oI the eustachian tube seen in children, compared with adults,
may also result in the impaired Iunction oI the eustachian tube opening. II the eustachian tube is
abnormally patent or short, its normal protective Iunction against the reIlux oI nasopharyngeal
contents is lost. %hese abnormalities are oIten seen in patients with Down syndrome, which may
account Ior the high rate oI OM in this particular patient population. Normal Iunction oI the
eustachian tube is also dependent on ciliary function; thereIore, any condition that aIIects
mucociliary clearance, such as viral infection, bacterial toxins, or inherited abnormalities of
ciliary structure, can predispose to OM.

Acute Otitis Media
Essentials oI Diagnosis
O Otalgia.
O Pyrexia.
O %hickened, bulging, hyperemic tympanic membrane.
O Hearing loss.
O Otorrhea.
General onsiderations
Acute otitis media (AOM) is one oI the most common inIectious diseases seen in children, with
its peak incidence in the first 2 years of life. Most oI the population will suIIer at least one
episode oI AOM at some point in their childhood. It can occur in suppurative, nonsuppurative,
and recurrent Iorms. In nonsuppurative AOM, inIlammation oI the middle ear cleIt mucosa
occurs either without Iormation oI an eIIusion or with a sterile eIIusion. %his type oI AOM is
oIten seen prior to, or in the resolution stage oI, the acute suppurative OM; however, resolution
may occur beIore Irank suppuration. Recurrent AOM is deIined as 3 episodes oI acute
suppurative OM in a 6-month period, or 4 episodes in a 12-month period, with complete
resolution oI symptoms and signs between the episodes.
%he epidemiology oI AOM and otitis media with eIIusion (OME) overlaps to such an extent that
the risk Iactors apply to both conditions. Both environmental and host Iactors play a role in the
epidemiology oI OM %able 492). Attendance at day-care facilities is one oI the major risk
Iactors Ior OM. hild care results in many children being in close contact, which increases the
exposure to respiratory tract pathogens responsible Ior OM. %he risks associated with child care
attendance are variable and are related to the number oI children in a Iacility, the hours spent in
child care, the child's age at entry, and whether siblings are in child care. Breast-Ieeding appears
to have a protective eIIect against OM, particularly when breast-Ieeding is used exclusively Ior
at least the Iirst 36 months oI liIe. %he protective mechanism of breast-feeding has not been
clearly demonstrated, but is likely to be related to antibacterial and immunologic beneIits
conIerred by breast milk.
%able 492. Factors Relevant to the Epidemiology oI Otitis Media.


Environmental Factors
Day-care attendance
Not being breast-Ied
Exposure to tobacco smoke
Seasonal variation in respiratory inIections
Host Factors
Genetics
ImmunodeIiciency
Birth deIects
leIt palate
Down syndrome

Exposure to cigarette smoke has been implicated in the etiology oI OM. Passive smoking
results in inIlammation oI the mucosa oI the middle ear cleIt as well as impaired mucociliary
clearance, which lead to an increased susceptibility to inIection. %here is a seasonal variation in
the incidence oI OM; it is more common in winter months, which mirrors the incidence oI upper
respiratory tract inIections.
Genetics play an important role in the etiology oI OM. Males have a higher incidence oI OM
than Iemales, a Iact that is true oI most inIections oI inIancy and childhood. %he sibling,
maternal, and paternal histories oI OM are all independently related to a child's risk oI
developing OM. Although OM is largely a uniIorm worldwide condition, some racial variations
in the rates oI OM exist; this condition is more prevalent in Native Americans, Alaskan and
anadian Eskimos, and Australian Aboriginals. %hese genetic variations may be related to
anatomic and physiologic variations in the eustachian tube.
Otitis media is seen almost universally in children with cleft palate. Because the tensor veli
palatini muscle lacks its normal insertion into the soft palate, it is unable to open the
eustachian tube properly on swallowing. A small number oI patients suIIering Irom OM have
an abnormal host deIense owing to various conditions such as immunoglobulin deIiciency,
malignant neoplasms, immunosuppressive therapy, and AIDS.
Pathogenesis
In most cases oI AOM, an antecedent viral upper respiratory tract infection leads to
disruption of eustachian tube function. Inflammation of the middle ear mucosa results in an
eIIusion, which cannot be cleared via the obstructed eustachian tube. %his eIIusion provides a
Iavorable medium Ior proliIeration oI bacterial pathogens, which reach the middle ear via the
eustachian tube, resulting in suppuration.
Although viral inIection is important in the pathogenesis oI AOM, the majority oI patients
develop subsequent bacterial colonization, and thereIore AOM should be considered a
predominantly bacterial inIection. Many studies, using tympanocentesis, have identiIied
Streptococcus pneumoniae (up to 40), Haemophilus influen:ae (2530), and Moraxella
catarrhalis (1020) as the organisms most commonly responsible Ior AOM. Less Irequently
identiIied pathogens include group A streptococci, Staphylococcus aureus, and gram-negative
organisms such as Pseudomonas aeruginosa. In all studies oI the microbiology oI AOM, a
signiIicant number oI cultures prove negative. %his Iinding may occur Ior a variety oI reasons,
including (1) antibiotic therapy beIore tympanocentesis; (2) nonbacterial pathogens (eg, viruses,
chlamydia, and mycoplasma); and (3) pathogens that do not proliIerate in classic culture
conditions (eg, mycobacteria and anaerobic bacteria). Recent studies on bacteriology oI AOM
show that the polymerase chain reaction (PR) methods produce positive results in patients in
whom cultures have been negative by the conventional methods.
%he role oI the adenoids (ie, the pharyngeal tonsils) in the pathogenesis oI AOM and OME
remains unproven. %here are two mechanisms by which the adenoids may inIluence OM: (1)
physical obstruction oI the eustachian tube when the adenoids are enlarged and (2) a reservoir
oI pathogenic bacteria harbored in the adenoid tissue, which predisposes the patient to
repeated episodes of AOM.
Prevention
Strategies Ior the prevention oI AOM include prophylactic antibiotics, vaccines, and surgery.
%he most commonly recommended regimen Ior antibiotic prophylaxis oI recurrent AOM is
once-daily oral amoxicillin at 20/mg/kg/d. Although antibiotic prophylaxis has been
demonstrated to signiIicantly reduce the number oI episodes oI AOM, this eIIect has to be
considered along with the increased incidence oI antibiotic-resistant organisms emerging as a
direct result oI the widespread prescription oI antibiotics.
A pneumococcal vaccine has been introduced Ior use in inIants and children younger than 2
years as well as in children older than 2 years who are at a high risk oI recurrent AOM.
However, until vaccines Ior other bacteria and viruses commonly responsible Ior AOM are
available, the eIIect oI vaccination will be limited. %he prophylactic use oI tympanostomy tubes
(not myringotomy alone) has been demonstrated to reduce the number oI episodes oI AOM and
hence the need Ior antibiotics. Adenoidectomy also has a demonstrable eIIect, though more
modest than that seen with tympanostomy tubes.
linical Findings
nnbnnnSymptoms and Signs
Before the onset of symptoms of AOM, the patient Irequently has symptoms oI an upper
respiratory tract infection. Older children usually complain oI earache, whereas inIants
become irritable and pull at the affected ear. A high fever is oIten present and may be
associated with systemic symptoms of infection, such as anorexia, vomiting, and diarrhea.
Otoscopy classically shows a thickened hyperemic tympanic membrane, which is immobile on
pneumatic otoscopy.
Further progression oI the inIective process may lead to the spontaneous rupture of the
tympanic membrane, resulting in otorrhea. II this occurs, the otalgia and Iever oIten subside.
At this stage, it is oIten not possible// to visualize the tympanic membrane because oI the
discharge in the ear canal.
Special %ests
In most cases oI AOM, no Iurther investigations are necessary since the diagnosis is clinical. II
symptoms are severe, a blood count oIten reveals a leukocytosis, and blood cultures may detect
bacteremia during episodes oI high Iever. A culture oI the ear discharge is helpIul in guiding
antibiotic therapy in patients in whom the Iirst-line treatment is unsuccessIul. II recurrent AOM
occurs along with recurrent inIections in other systems, then an underlying immune deIiciency
(commonly IgA and IgG deIiciency) should be considered and appropriate investigations
requested. iliary motility disorders need to be considered iI recurrent AOM is associated with
recurrent/chronic respiratory or sinus inIections. Radiologic investigation is not recommended
unless complications are suspected.
DiIIerential Diagnosis
In any patient who has otorrhea, particularly iI it is recurrent, a diagnosis oI chronic
suppurative otitis media (CSOM), either tubotympanic or with cholesteatoma, should be
considered. Otitis externa also presents with otalgia and otorrhea and may be the primary
diagnosis, or it may be secondary to the inIected discharge Irom the middle ear.
II otalgia is the primary complaint, then reIerred pain should be considered, particularly when
otoscopy reveals a normal tympanic membrane. %he common sites oI origin oI referred otalgia
are the teeth and temporomandibular joints. In adults, malignant neoplasms oI the pharynx
and larynx may present with otalgia as the only symptom.
In neonates and inIants with a high Iever and systemic upset, the possibility oI meningitis should
be considered.
%reatment
Nonsurgical Measures.,
WatchIul Waiting
%he current practice guidelines advise on an initial watchIul waiting without antibiotic therapy
Ior healthy 2-year-olds or older children with nonsevere illness (mild otalgia and Iever 39
) because AOM symptoms improve in most within 1-3 days. However, guidelines should not
replace clinical judgment. WatchIul waiting is not recommended Ior children 2 years old iI
AOM is certain.
Antibiotic %herapy
II AOM does not settle aIter the watchIul waiting period, then antibiotic therapy should begin.
%he use oI antibiotics is probably beneIicial, but there is a trade-oII between beneIits and side
eIIects. %here is no diIIerence demonstrated in recurrence rates or the development oI
complications among diIIerent antibiotics. Amoxicillin (80 mg/kg/d given in three divided
doses for 10 days) remains the first-line therapy Ior AOM, although with increasing numbers
oI resistant strains oI bacteria, it may be necessary to use more broad-spectrum antibiotics in the
Iuture. In resistant cases, amoxicillin should be given in combination with clavulanate.
Adjunctive %herapy
%he adjunctive therapy Ior AOM should include analgesics and antipyretics. %here is no role
Ior oral decongestants or antihistamines in the treatment oI AOM.
Surgical Measures
A minority oI patients with AOM Iail to respond to medical therapy or develop a complication.
Myringotomy is then indicated to allow the drainage oI pus Irom the middle ear space.
Randomized trials have shown myringotomy to be ineIIective in uncomplicated AOM.
Prognosis
%he vast majority oI uncomplicated episodes oI AOM resolves without any adverse outcome. In
some cases, suppuration resolves, but a sterile middle ear eIIusion persists. II this effusion
persists for more than 3 months, then a diagnosis oI OME should be made. OI patients who
develop a perforation of the tympanic membrane with otorrhea, a small proportion go on to
develop CSOM because oI the Iailure oI the tympanic membrane to heal.

Otitis Media with EIIusion
Essentials oI Diagnosis
O Persistent hearing loss.
O Dull, immobile tympanic membrane.
O "Flat" tympanogram.
General onsiderations
Otitis media with eIIusion is deIined as the persistence of a serous or mucoid middle ear
effusion for 3 months or more. Various terms, such as chronic secretory otitis media, chronic
serous otitis media, and "glue ear," have been used to describe the same condition. It is the most
common cause oI hearing loss in children in the developed world and has peaks in incidence at 2
and 5 years oI age. %he risk Iactors Ior OME are closely interrelated with those associated with
AOM and have already been described in the previous section. In Iact, the Iormation oI a middle
ear effusion Irequently occurs after an episode of AOM, and children with OME are Iar more
likely to suIIer Irom recurrent AOM.
Pathogenesis
Under normal conditions, the middle ear mucosa constantly secretes mucus, which is removed
by mucociliary transport into the nasopharynx via the eustachian tube. As a consequence,
Iactors resulting in an overproduction of mucus, an impaired clearance oI mucus, or both can
result in the Iormation oI a middle ear eIIusion.
Both viral and bacterial inIection can lead to the increased production and viscosity oI
secretions Irom the middle ear mucosa. InIection also leads to inflammatory edema oI the
mucosa, which may obstruct the eustachian tube. %emporary paralysis of cilia by bacterial
exotoxins Iurther impedes the clearance oI an eIIusion. Bacteriologic studies have demonstrated
that the bacteria commonly responsible Ior AOM are cultured Irom about halI oI chronic
eIIusions. %he Iact that not all patients with OME have a history oI inIection suggests that other
mechanisms are involved in the Iormation oI a middle ear eIIusion. Experimental studies have
conIirmed that the failure of eustachian tube opening can result in a middle ear effusion.
Because gas is constantly being absorbed into the microcirculation oI the middle ear mucosa,
a negative pressure develops in the middle ear cleIt iI the eustachian tube is blocked. %his
negative pressure results in the transudation of fluid into the middle ear cleIt. %he Iact that a
middle ear eIIusion can develop as a result oI barotrauma (eg, scuba diving) supports this
theory Ior the pathogenesis oI middle ear eIIusions. Allergy has also been implicated in the
pathogenesis oI OME; however, evidence to support this theory is lacking.
Exposure to passive smoking is also likely to contribute to ciliary dysIunction and hence to
OME. %here is an optimum viscosity oI mucus at which eIIective mucociliary transport occurs.
II the mucus Iormed in a middle ear eIIusion is either too serous or too mucoid, then the cilia
will be unable to clear it eIIiciently. Recently, the concept oI bioIilms in the pathogenesis oI
otitis media has been raised, but the evidence is not conclusive. Biofilms are the structured
community oI bacterial cells adherent to the mucosa and have antibacterial resistance property.
Prevention
Since OME oIten occurs as a direct result of AOM, the measures Ior preventing AOM
previously described should also reduce the incidence oI OME. Avoidance oI risk Iactors (see
%able 492) could also reduce the chance oI a child developing OME, but its eIIectiveness
remains unproven.
linical Findings
Symptoms and Signs
Otitis media with eIIusion may be completely asymptomatic and detected only on routine
audiologic screening. %he most common symptom oI OME is hearing loss. Although older
children may complain oI reduced hearing, in many cases the hearing loss is noticed by parents,
nursery nurses, or teachers. In younger children, the only symptom may be delayed speech
development or behavioral problems. Another common symptom is a "blocked" Ieeling in the
ear, which may cause inIants and young children to pull at their ears. More rarely, symptoms oI
earache, tinnitus, or balance disorder may be present.
Otoscopy classically reveals a dull gray- or yellow-colored tympanic membrane that has
reduced mobility on pneumatic otoscopy. II the tympanic membrane is translucent, an air-
fluid level or small air bubbles within the middle ear eIIusion may be seen.
Special %ests
%ympanometry
%ympanometry is a valuable tool Ior the investigation oI OME. It is easy to use, provides
reproducible results, is inexpensive, and is widely tolerated by patientseven young children.
By measuring the compliance oI the middle ear transIormer mechanism, it provides an objective
assessment oI the status oI the middle ear. %ympanometry produces a peak (ie, maximal
compliance) when the pressure in the external ear canal equals that oI the middle ear. By varying
the pressure in the external ear, the tympanometer is able to provide inIormation on the status oI
the middle ear (%able 493). II there is an eIIusion in the middle ear, then compliance does not
vary with changes in canal pressure, and a Ilat (%ype B) tympanogram is produced. II the air in
the middle ear is at or near atmospheric pressure, then a normal (%ype A) tympanogram is
produced. Negative middle ear pressure results in a %ype tympanogram, with the compliance
peak being at less than 99 daPa (deca Pascal).
%able 493. %ypes oI %ympanogram.


Tympanogram Type Middle Ear Pressure Typical Appearance of Trace
A 99 daPa to 200 daPa

B No compliance peak

400 daPa to 100 daPa



daPa deca Pascal.
Audiometry
Patients who have OME usually have a moderate conductive hearing loss. Audiometry provides
an assessment oI the severity oI hearing loss and is thereIore important in both monitoring the
progress oI the condition and providing inIormation useIul Ior management decisions. For
example, in patients with hearing thresholds oI 20 dB or better, it is unlikely that surgical
intervention is indicated, despite the presence oI OME.
DiIIerential Diagnosis
%here is considerable overlap between AOM and OME, and it may be diIIicult to distinguish
between the two on Iirst presentation unless otalgia and Iever are prominent. Other causes oI
conductive hearing loss in childhood are much less common than OME, and congenital
abnormalities oI the ossicular chain are Irequently associated with abnormalities oI the external
ear or present as part oI a syndrome.
In adults presenting with a unilateral middle ear eIIusion, the possibility oI a nasopharyngeal
carcinoma should be considered.
%reatment
Observation
A large number oI patients with OME require no treatment, particularly iI the hearing
impairment is mild. Spontaneous resolution occurs in a signiIicant proportion oI patients. A
period oI watchIul waiting oI 3 months Irom the onset (iI known) or Irom the diagnosis (iI onset
unknown) beIore considering intervention is thereIore advisable. Ideally, early treatment should
be initiated in patients in whom spontaneous resolution is unlikely. A multicenter randomized
controlled trial identiIied both the season oI attendance (ie, July to December) and a bilateral
hearing impairment oI ~ 30 dB as Iactors that make spontaneous resolution less likely. Early
intervention should be considered iI there is a signiIicant delay in speech and language
development or iI OME is present in an only hearing ear.
Nonsurgical Measures
%he medical treatment oI OME is controversial and there is a wide geographic variability in
practice. AutoinIlation with purpose-built nasal balloon has been shown to be beneIicial,
although compliance is generally poor. Medical treatments include antibiotics, steroids,
decongestants, and antihistamines. %he use oI antibiotics in OME has been shown to be eIIective
in a small proportion oI patients, but the eIIect is likely to be short-lived. %he small chance oI
beneIit Irom antibiotic therapy needs to be considered along with the Iact that a number oI
patients treated with antibiotics develop signiIicant side eIIects, such as gastroenteritis and atopic
reaction. A meta-analysis oI the use oI topical and systemic steroids Ior the treatment oI OME
Iound a short-term improvement in hearing, but no lasting beneIit. Steroids are thereIore not
recommended in the treatment oI OME. %here is no evidence to support the use oI
decongestants, antihistamines, or mucolytics Ior the treatment oI OME.
Surgical Measures
%he surgical options Ior OME are tympanostomy tubes and adenoidectomy. Myringotomy and
aspiration oI middle ear eIIusion without ventilation tube insertion has a short-lived beneIit and
is not recommended.
Insertion oI %ympanostomy %ubes
%he aim oI tympanostomy tube insertion is to allow ventilation oI the middle ear spacehence
to improve hearing thresholds. %he prolonged ventilation oI the middle ear may also allow
resolution oI chronic inIlammation oI the middle ear mucosa. omplications include
myringosclerosis, purulent otorrhea, and residual perIoration aIter extrusion. %here are two main
types oI tympanostomy tubes: short-term tubes (eg, grommets), which remain in the tympanic
membrane Ior an average oI 12 months, and long-term tubes (eg, T-tubes), which can remain
Ior several years. %he high incidence oI residual perIoration Iollowing the use oI long-term
ventilation tubes indicates that they should not be used in uncomplicated cases.
Adenoidectomy
ontroversy still exists over the role oI adenoidectomy in the treatment oI OME. %he rationale
Ior adenoidectomy is that it relieves nasal obstruction, improves eustachian tube Iunction, and
eliminates a potential reservoir oI bacteria. Evidence does suggest that adenoidectomy is
eIIective in reducing the morbidity oI OME. However, because oI the potential risks associated
with adenoidectomy (primarily hemorrhage and, rarely, velopharyngeal insuIIiciency), many
surgeons use tympanostomy tubes alone as a Iirst-line treatment and consider adenoidectomy
when repeated tympanostomy tube insertion is required Ior recurrent OME.
Prognosis
%here is a sharp decline in the prevalence oI OME in children over 7 years oI age, which reIlects
improved eustachian tube Iunction and maturation oI the immune system.


hronic Suppurative Otitis Media (%ubotympanic)
Essentials oI Diagnosis
O hronic or recurrent otorrhea or both.
O Hearing loss.
O %ympanic membrane perIoration.
General onsiderations
hronic suppurative otitis media is deIined as a persistent or intermittent infected discharge
through a nonintact tympanic membrane (ie, perIoration or tympanostomy tube). hronic
perIoration oI the tympanic membrane can occur without suppuration and is oIten reIerred to as
"inactive" SOM.
hronic suppurative otitis media is particularly prevalent in developing countries and is more
common in lower socioeconomic groups in the developed world. Many oI the epidemiologic
Iactors discussed in the section on AOM equally apply to the development oI SOM.
Pathogenesis
%here are a number oI mechanisms by which a persistent tympanic membrane perforation
may develop. In most cases, SOM occurs as a consequence oI an episode oI AOM with
perforation, with subsequent failure of the perforation to heal. %here is also an association
between OME and chronic perIoration. %he continued presence of a middle ear effusion leads,
in some cases, to degeneration of the fibrous layer of the tympanic membrane. %his
weakness oI the tympanic membrane both predisposes to perforation and reduces the
likelihood oI spontaneous healing. Although most tympanic membranes heal spontaneously aIter
the extrusion oI ventilation tubes, a small percentage do not. %raumatic perIorations, particularly
iI large, may fail to heal.
%here are two main mechanisms by which a chronic perforation can lead to continuous or
repeated middle ear infections: (1) Bacteria can contaminate the middle ear cleIt directly Irom
the external ear because the protective physical barrier oI the tympanic membrane is lost. (2) %he
intact tympanic membrane normally results in a middle ear "gas cushion," which helps to prevent
the reIlux oI nasopharyngeal secretions into the middle ear via the eustachian tube. %he loss oI
this protective mechanism results in the increased exposure oI the middle ear to pathogenic
bacteria Irom the nasopharynx.
%he most commonly isolated bacteria responsible Ior SOM are P aeruginosa, S aureus, and the
Proteus species.
linical Findings
Symptoms and Signs
%ypically, a patient with SOM presents with a history oI otorrhea, which may be either
intermittent or continuous, and hearing loss. %he discharge is usually mucopurulent, although
chronic infection of the middle ear may lead to polyp or granulation tissue Iormation, which
can result in bloodstained otorrhea. Pain is not a usual Ieature oI SOM and its presence
should alert the physician to the possibility oI a more invasive pathology.
Inspection may reveal scars Irom previous surgery Ior chronic ear disease. %o properly visualize
the tympanic membrane, it is necessary to suction the discharge Irom the external auditory canal
with an operating microscope. %he middle ear mucosa, seen through the perIoration, is
edematous, sometimes to the point oI polyp Iormation. II the perIoration is oI suIIicient size, it
may be possible to identiIy the presence oI ossicular discontinuity due to necrosis of the long
process of the incus.
Special %ests
A swab oI the discharge should be sent Ior culture and sensitivity, preIerably beIore beginning
antimicrobial therapy. An audiologic evaluation is necessary, because the majority oI patients
have an associated conductive hearing loss.
Since the diagnosis oI SOM can be made clinically, radiologic investigation is not usually
indicated. omputed tomographic (%) scans are useIul in demonstrating bony anatomy and are
essential iI an intracranial extension oI the inIection is suspected. However, % scanning is poor
in diIIerentiating between the soIt tissue opacity caused by SOM and cholesteatoma.
DiIIerential Diagnosis
%he primary diIIerential diagnosis is the presence oI a cholesteatoma. Both pathologies present
with a very similar clinical course, and the presence oI severe inIlammation or granulation tissue
can cause diIIiculty with the diagnosis. Reexamination aIter a course oI medical treatment
usually provides an accurate diagnosis.
II granulations are severe and unresponsive to antimicrobial therapy, then chronic granulomatous
conditions such as Wegener granulomatosis, mycobacterial inIection, histiocytosis X, and
sarcoidosis should be considered. Biopsy oI the granulation or polyp in these circumstances is
recommended.
Pain is not usually a prominent Ieature oI SOM, and its presence should raise the possibility oI
necrotizing otitis externa (particularly in the immunocompromised, eg, AIDS patients or elderly
diabetics) or a malignant neoplasm oI the eternal canal or middle ear.
%reatment
%he treatment goals oI uncomplicated SOM are to eliminate inIection, prevent Iurther
inIection, and restore normal Iunctioning to the middle ear. Both medical and surgical
interventions play a role in achieving these aims (%able 494).
%able 494. %reatment Summary Ior Otitis Media.


Acute Otitis Media (AOM) Otitis Media with
Effusion
Chronic Suppurative
Otitis Media
WatchIul
waiting
Up to 72 hours with
analgesia/antipyretics iI
nonsevere and patient ~ 2 years
old
For 3 months Irom
onset or diagnosis
NI
Medical
therapy
Antibiotics (amoxicillin) NI Aural toilet and topical
antibiotics (quinolones)
Surgical
intervention
Myringotomy Ior reIractory
AOM
V% insertion iI
unresolved aIter 3
months
%ympanoplasty
ortical mastoidectomy in
nonresponding mastoiditis
Adenoidectomy on
second V% insertion
%ympanomastoid
surgery iI reIractory to
medical therapy


NI, not indicated; V%, ventilation tube.
Nonsurgical Measures
Aural %oilet
Aural toilet is important Ior the successIul treatment oI SOM, particularly when topical
medication is used. learing the discharge Irom the external auditory canal allows the topical
agent to reach the middle ear in an adequate concentration.
%opical Antibiotics
Although topical antibiotics are more eIIective than systemic antibiotics in the treatment oI
SOM, many contain aminoglycosides, which are potentially ototoxic. Ototoxicity has been
demonstrated in animal models, and the use oI gentamicin Ior vestibular ablation in Meniere
disease is well documented. However, sensorineural hearing loss as a result oI the use oI topical
aminoglycosides in SOM is rarely reported. %his circumstance is probably due to a
combination oI the relatively low concentration oI aminoglycoside reaching the middle ear and
edema oI the middle ear mucosa, which prevents the direct absorption oI the drug through the
round window. Despite the risk oI ototoxicity, topical aminoglycosides are widely prescribed by
otolaryngologists Ior the treatment oI SOM because the beneIits oI eIIective treatment
outweigh the risks. %he recent availability oI topical oIloxacin preparations may prove to be as
eIIective as topical aminoglycosides without the ototoxic potential.
Systemic Antibiotics
Systemic antibiotics tend to have a poor penetration oI the middle ear and are thereIore less
eIIective than topical antibiotics. Because P aeruginosa is the primary pathogen responsible Ior
SOM, the choice oI oral systemic antibiotics is limited. Both ciproIloxacin and oIloxacin have
good antipseudomonal activity. UnIortunately, these quinolone antibiotics are not recommended
in children owing to the possibility oI causing arthropathies. %his circumstance limits the choice
oI systemic antibiotics in children to broad-spectrum penicillins, such as piperacillin and
cephalosporins, which must be administered parenterally.
Surgical Measures
Some cases oI SOM resolve with medical treatment, and iI the patient is asymptomatic, then no
Iurther intervention is required. However, iI otorrhea recurs or persists despite medical treatment
or iI the patient Ieels handicapped by a residual conductive hearing loss, surgical therapy should
be considered.
%ympanoplasty
Ideally, surgery should be carried out when the inIection has been adequately treated and the
middle ear mucosa is healthy, since the chance oI a successIul outcome is increased. In this
situation, a tympanoplasty, with repair oI the tympanic membrane and ossicular chain (iI
required), is recommended.
%ympanomastoid Surgery
In cases that are reIractory to medical treatment, it is necessary to perIorm tympanomastoid
surgery (tympanoplasty combined with a cortical mastoidectomy). %he aims oI this procedure
are to aerate the middle ear and mastoid, remove chronically inIlamed tissue, repair the tympanic
deIect, and reconstruct the ossicular chain. %he achievement oI all oI these goals oIten requires
more than one procedure.