CONGENITAL MALFORMATIONS

The external and middle ears grow throughout puberty, but the inner ear reaches adult size and shape by midfetal development. Although the pinna, ear canal, and tympanic membrane continue to grow after birth,
congenital abnormalities of these structures develop during the first half of gestation. Malformed external and middle ears may be associated with serious renal anomalies, mandibulofacial dysostosis, hemifacial
microsomia, and other craniofacial malformations.
Pathogenesis
Auricular hillocks(pinna) arise during the sixth week of embryogenesis
Inner two thirds of the EAC are not formed until the 26th week
Untoward events throughout this period could give rise to structural anomalies of the external ear

MICROTIA

Patients typically present at birth with obvious auricular malformations.

GRADE I
- ear exhibits mild deformity
- typically with a slightly dysmorphic helix and
antihelix includes lowset ears, lop ears, cupped ears,
and mildly constricted ears
- Lop ear: characterized by inferiorly angled
positioning of the auricular cartilage
- Cup ear: protrudes with a deep conchal bowl

GRADE II
- all pinna structures are
present, but tissue deficiency
and significant deformity exist

GRADE III
- aka classic microtia or peanut ear
- has few or no recognizable landmarks of the
auricle
- ear lobule usually present and anteriorly
positioned

ANOTIA
When there is a complete
absenCe of the ear and
canal

Treatment
Classically, microtia has been treated by a 4-stage auricular reconstruction. Patients undergo observation until the age of 5 to allow for growth of rib cartilage, which is harvested
for reconstruction, and the development of the contralateral ear

PROTRUDING EARS

an increase in distance from the helical rim to the mastoid

thought to be due to a lack of the antihelical fold and prominence of the conchal bowl
most frequently bilateral

Pathogenesis
result of malformation of cartilage during primitive ear development in intrauterine life.
- The deformity can be corrected any time after 6 years. Correction by otoplasty. The skin is not removed, but the shape of the cartilage is altered. The surgery does not
affect hearing.

ATRESIA AND STENOSIS OF EXTERNAL

AUDITORY CANAL

CONGENITAL MIDDLE-EAR
MALFORMATIONS
CONGENITAL CHOLESTEATOMA

Treatment:
- otoplasty is the mainstay of treatment for protruding ears
- involves changing the shape of the ear cartilage so that the ear is brought closer to the side of the head
often seen in association with malformations of the pinna and the structures of the middle ear
EAC cholesteatoma can develop in the face of severe of EAC stenosis
typical pattern of hearing loss in affected ears is a conductive hearing loss of 5070 dB
subject patient to CT scan to assess for ossicular, facial nerve, and otic capsule abnormalities as well as for the degree of temporal bone pneumatization, and to identify a
cholesteatoma medial to a canal stenosis
Treatment:
Reconstructive ear canal and middle-ear surgery for atresia usually is considered for children older than 5 yr of age who have bilateral deformities resulting in a significant CHL
most malformations involve the ossicles, with the INCUS MOST COMMONLY AFFECTED
other less-common abnormalities of the middle ear include persistent stapedial artery, high-riding jugular bulb, and abnormalities of the shape and volume of the aerated
portion of the middle ear and mastoid
Lesions occurring classically in the anterosuperior quadrant of the mesotympanum (27-67%)
typically present as small pearls adjacent to the long process of the malleus
presence of a discrete, round white lesion seen in the anterosuperior quadrant of an otherwise normal tympanic membrane is suggestive
clinically silent for years but may eventually present with a combination of tinnitus, vertigo, 3040 dB CHL or SNHL
aggressive disease as it is associated with progressive growth with progressive erosion of the ossicles
Treatment: early surgical removal via extended tympanotomy and close monitoring will help prevent permanent damage to the middle and inner ear

PREAURICULAR SINUS/CYST

EXTERNAL EAR DISORDERS

failure of fusion of the auricular hillocks on the dorsum of the 1st branchial arch
remnant of 1st branchial cleft
Present at birth
Not inflamed, unless plug inside is removed
Example: Sometime ear becomes itchy and they milk it and plug is removed; dirty water/sweat will come in and it becomes infected and later
becomes a cyst

Complications:
- Recurrent Infection - because water can easily enter and form cyst

PERICONDRITIS

Diagnosis and Treatment

- Sometimes auricular sinus forms a tract that goes inside the auricle, trace by injecting die at the pit
- Remove everything, excise pit and close
Infection of the tissue that covers the cartilage
Cause:
o
o
o
Symptoms:
o
o
o
o
o

RELAPSING POLYCHONDRITIS
Polychondritis
WHOLE EAR AFFECTED
responsive to antibiotics
Tx: Give corticosteroids

Perichondritis
whole ear affected
responsive to antibiotics

Infection, trauma secondary to ear piercing, insect bite

Trauma (accidental or iatrogenic, laceration or contusion), - ear piercing, especially when done through the cartilage.
Most commonly isolated organism is P. Aeruginosa and S. Aureus

Swelling of the whole pina

Accumulation of blood, excise and drain blood
If not drained will be infected and will have pus
Early perichondritis and cellulitis are both characterized by skin that is red, edematous, and tender.
Perichondritis fails to respond to adequate antimicrobial therapy, consider a noninfectious inflammatory etiology (relapsing polychondritis).

Treatment:
o systemic, often parenteral, antibiotics
o surgery to drain an abscess or remove nonviable skin or cartilage
o Removal of all ear jewelry is mandatory in the presence of infection.
Auricle is painful, erythematous and Edematous
(+) SPARING OF LOBULE
Should be considered in patients who failed to respond to antibiotics
Tx : Oral corticosteroid
severe, episodic, and progressive inflammatory condition involving cartilaginous structures, predominantly those of the ears, nose, and
laryngotracheobronchial tree
Other affected structures may include the eyes, cardiovascular system, peripheral joints, skin, middle and inner ear, and central nervous system

IMPACTED CERUMEN

Cerumen is the product of both sebaceous and apocrine glands, which are
located in the cartilaginous portion of the external auditory canal. It is
known to have protective qualities. It acts as vehicle for the removal of
epithelial debris and contaminants away from the tympanic membrane. It
provides lubrication and prevents dessication of the epidermis with its
associated fissuring.
Types of Cerumen:
WET

DOMINANT

Caucasians
- >80% probability of having wet,
sticky, honey-colored ear wax that
may darken on exposure to
elements.

DRY

Mongoloid races and American

Indian - dry, scaly, rice band
phenotype is more frequent

Blacks :even greater predisposition

o prone to impaction and
hereditary
o Visit ENT twice a year for
removal of cerumen
o Some grows inside inner 3rd of
ear canal and can't be reached
by cotton buds
*Neither variant has a clear association with inflammatory conditions
involving the external canal. Studies have shown that both wet and dry
cerumen have quite similar bactericidal effect. It is the fatty acids,
lysozyme, and immunoglbulin components of cerumen that are beieved to
be inhibitory or bactericidal.
*Excessive cerumen is not a disease. In some, cerumen can cake and form
a solid plug; in others, a large amount with buttery consistency blocks the
canal. The patient may experience a sense of blockage or pressure. When a
solid plug of cerumen becomes moistened (bathing), it may swell and
cause temporary hearing impairment.
There is a general tendency for older individuals to have drier cerumen
due to physiologic atrophy of apocrine glands with lessening of sweat
component

Impacted Cerumen
have aural fullness, otalgia (ear pain)
Why otalgia? ex. if you swim it gets wet and swell can no longer be
accommodated in the ear canal and cause pain
There is also conductive hearing loss
Not all cerumen is taken out - serves as lubrication and protection
from foreign bodies.
Cerumen moisturize external ear, if removed skin becomes dry and
itchy.
Symptoms:
Aural fullness
Otalgia
Hearing loss
Uses:
Lubrication
Prevent dryness
Protection from foreign bodies

KERATOSIS OBTURANS

Etiology:
overproduction of squamous epith and squamous plugs
faulty migration of the epithelium
EAR CANAL EXOSTOSES/OSTEOMAS

IRRADIATION OSTEITIS OF TYMPANIC MEMBRANE

HERPES ZOSTER OTICUS

Keratin formation that involves ear canal due to

ACCUMULATION OF CHOLESTEROL
Warrants removal because it sticks to canal skin, very
itchy and cause widening of ear canal
Grows in the bony portion of the ear canal causing
widening, bone deformation, and becomes prone to
foreign body
may present as a keratin plug occluding the external
auditory canal
usually bilateral and may be associated with
bronchiectasis and chronic sinusitis

Symptoms:
Otalgia (pain): dominant feature
Hearing loss

benign tumor of EAC

small, smooth, white, excrescences or growth of bone
in the bony ear canal
May cause conductive hearing loss
consist of a rounded protuberance of hypertrophic
canal bone
usually multiple and bilateral
composed of cortical bone often multiple

Cause:
stated that most of these growths occur more fequently in people who do a great
deal of swimming in cold waters.

Signs:

Widening of the external canal

hyperplasia and inflammation of the epithelium and subepithelium
No bony erosion

Treatment:
Management is to remove and always clean the canal
Plug removal and treatment of inflammation

Treatment:
Managed only if it covers the whole of canal - drill the bone
Usually require no treatment, although they may result in more frequent canal
blockage by cerumen in some individuals
careful removal if not responsive to medical treatment
Carefully chiseled from the canal wall with the aid of the operating microscope

Develop after squamous cell carcinoma of external

just clean the canal thoroughly
Presence of clumps of blisters along a specific dermatome seen most often in the concha or superficial ear canal
Patient complains of severe pain because herpes zoster virus usually attacks the nerve
You cannot eradicate this (severe pain) for 1 year even if blisters are gone
Caused by reactivation of herpes zoster in the GENICULATE GANGLION
Pain and vesicles appear in the external auditory canal and patients lose their sense of taste in the anterior two-thirds of the tongue while
developing ipsilateral facial palsy
Often, the eighth cranial nerve is affected as well
Triad:
o Ipsilateral facial paralysis
o Ear pain
o Vesicles in auditory canal/auricle or hard palate or anterior 2/3 of tongue
Neuropathy of CN V, IX, X
o Tinnitus, Hyperacusis, Lacrimation, Taste perception, vertigo
More severe than Bells palsy
Treatment:
o Antivirals + Steroids (Treat within 3 days of symptoms onset

BULLOUS MYRINGITIS

Membrane inflammation limited to tympanic membrane and nearby canal

Multiple reddened, inflamed blebs
Hemorrhagic vesicles
Commonly associated with an acute upper respiratory tract infection
Presents as an ear infection with more severe pain than usual
Hemorrhagic or serous blisters (bullas) may be seen on the tympanic membrane
Difficult to differentiate from acute otitis media because a large bulla may be confused with a bulging tympanic membrane
Organisms involved are the same as those that cause acute otitis media

Treatment: empiric antibiotic therapy and pain medications

FOREIGN BODIES: EXTERNAL EAR CANAL

KELOIDS

AURAL POLYP

Inanimate Objects: most common is pellet from pellet gun

Animate:
o Cockroach (most common in adults), ants (most common in children), ticks
o Treatment: kill insect first with oil (any oil, even cooking oil. Fill the entire ear canal; it will not harm the ear unless with history of otitis media)
then remove with forceps or suction, etc.

Proper removal with the proper instrument never attempt to remove if without proper instrument because it will only do more harm
Resembles a self-limiting benign tumor
Excessive deposition of scar tissue beyond the original site of injury
Does not tend to diminish with time
Can occur following ear piercing
Occur predominantly in blacks
Treatment: surgical excision and intralesional steroid

Small tumor-like growth obstructing partially or totally the external acoustic canal
Should not be mistaken as a primary tumor of the external ear
Rarely arises from the epidermal surface of external acoustic canal
Sometimes is an extension of a tumor developing in the nasopharyngeal area; went up via Eustachian tube

OTITIS EXTERNA
Collection of diseases involving primarily the auditory meatus
Results from a combination of heat and retained moisture with desquamation and maceration of the epithelium of the outer ear canal
Can be: localized, diffuse, chronic, and invasive
All forms are predominantly bacterial in origin

Definition
Otitis externa is an inflammation of the skin of the external auditory
meatus (EAM)

OTITIS EXTERNA CIRCUMSCRIPTA

Pathology
The skin of the EAM comprises in the outer third an epithelial layer
containing hair follicles, ceruminous glands and sebaceous glands,
lying on a thin dermal bed containing sweat glands.
The skin of the bony ear canal lacks appendages and thins from
without in. The secretions of the sebaceous glands keep the stratum
corneum water-tight and supple.
Sweat gland secretions keep the secretion at a pH between three
and five which is lethal for most human pathogens.
Usually the EAM is sterile or contains Staphylococcus albus
commensals. Staphylococcus aureus and non-haemolytic
streptococci are unusual.
In the acute phase of otitis externa there are dilated dermal blood
vessels of increased permeability which cause signs of a red, hot,
oedematous and tender ear canal
The epithelial reaction consists of vesication, parakeratosis and
spongeosis
Aka Acute localized otitis externa/furunculosis
Due to obstruction of apopilosebaceous unit
Pathogen: S. aureus
Involves the lateral third of the ear canal
Can be caused by punggod (pimple) or insect bite
Develop in the outer third of the ear canal where skin overlies cartilage
and hair follicles are numerous
This common condition is confined to the fibrocartilaginous portion of
the external auditory meatus
Furunculosis begins in a pilosebaceous follicle and is usually caused by
Staph aureus or S. albus
In most severe cases, surrounding cellulitis may extend beyond this area

Treatment:
- Oral antistaphylococcal penicillin (e.g., dicloxacillin or cephalexin)
- Incision and drainage in cases of abscess formation

Predisposing factors
Heat, humidity, bathing, swimming.
Trauma, especially from dirty fingernails, cotton buds and hairgrips.
Inheritednarrow ear canals and non-atopic eczema.

ACUTE DIFFUSE OTITIS EXTERNA (SWIMMERS EAR)

Pathogen: Pseudomonas aeruginosa, Staphylococcus albus, E. coli, Enterobacter aerogenes

After swimming in an infected pool/body of water, with excessive scratching of the ear canal
Can develop even in patients who have not recently been swimming
Heat, humidity and the loss of protective cerumen leads to excessive moisture and elevation of pH in the ear canal leading to skin maceration and irritation
followed by infection.
Illness often starts with itching and progresses to severe pain usually elicited by manipulation of the pinna or tragus.
Onset of pain is generally accompanied by the development of an erythematous, swollen ear canal, often with scant white, clumpy discharge
The stroma overlying the bone of the inner third of the canal is very thin, allowing minimal room for swelling. Thus, the subjective discomfort the patient
experiences is often out of proportion to the extent of the disease visualized
Because of the degree of circumferential canal wall edema often seen, a wick may be required to bring medication into contact with most of the canal wall

Diagnostic Features:
Tragal tenderness
Severe pain
Canal wall swelling involving most of the canal
Scanty discharge
Normal or slightly diminished hearing
Absence of obvious fungal particles
Possible presence of tender regional adenopathy
Treatment:
o Cleansing the canal to remove debris and enhance the activity of topical therapeutic agents
Hypertonic saline
Mixtures of alcohol and acetic acid
o Inflammation can also be decreased by adding glucocorticoids
o Burows solution (aluminum acetate in water)
o Antibiotics are most effective when given topically usually combine neomycin with polymyxin
Systemic antimicrobial typically are reserved for severe disease or infections in immunocompromised hosts
ASPERGILLUS OTITIS EXTERNA

Otomycosis
Common in diabetics and in patients who do habitual cleaning of their ears
o Ear canal is acidic, especially the cerumen thats why it is protective. If you remove all the cerumen you alkalinize the surface of the external ear making
it very conducive for fungal growth
May cause only a superficial scaling similar to dandruff of the scalp, may be associated with an inflammatory seborrheic dermatitis, or may form the basis on
which more uncomfortable infections develop, such as furuncles or eczematous changes
It is sometimes found in the canal in the absence of any symptoms except for a sense of blockage or it may be involved in an inflammatory process, invading
the epithelium of the canal or drumhead and causing acute symptoms

Treatment
Careful cleansing of the canal by wiping, suctioning, and, at times, even gentle irrigation followed by drying
Otic solutions such as VoSol andOtic Domeboro are of value in most cases

MALIGNANT (NECROTIZING) OTITIS EXTERNA

DESCRIPTION
Also known as invasive otitis externa
Is an aggressive and potentially life-threatening disease
Occurs predominantly in elderly diabetic patients and other immunocompromised persons
Begins in the external canal as a soft tissue infection that progresses slowly over weeks to months
ETIOLOGY
P. aeruginosa is the most common pathogen
S. aureus, S. epidermidis, Aspergillus, Actinomyces and some gram-negative bacteria have been also associated with the disease.
DIAGNOSTIC FINDINGS
GRANULATION TISSUE EXTERNAL AUDITORY CANAL FLOOR
Purulent secretions
Occluded canal and obscured tympanic membrane
Cranial nerve V, X and IX involvement
Usually, necrotizing and you can see a mass
Differentiated from an aural polyp or squamous cell carcinoma through biopsy
Often is difficult to distinguish from a severe case of chronic otitis externa because of presence of:
o Purulent otorrhea
o Erythematous swollen ear and external canal
Severe, deap-seated otalgia out of proportion to findings on examinatio
CHARACTERISTIC FINDING:
Granulation tissue in the posteroinferior wall of the external canal near the junction of bone and cartilage
If left unchecked, can migrate to the base of the skull (skull-base osteomyelitis) and onward to the meninges and brain with a high mortality rate.
Facial nerve usually affected first and most often
Thrombosis of the sigmoid sinus can occur if infection extends to that area

CHRONIC CANDIDAL OTITIS EXTERNA

CHRONIC OTITIS EXTERNA

TREATMENT:
o IV Antibiotic therapy given for a prolonged course (6-8 weeks) and directed toward the recovered pathogen
In necrotizing otitis externa, recurrence is documented up to 20% of the time
Aggressive glycemic control in diabetics is important not only for effective treatment but also for prevention of recurrence
Sometimes mistaken as otitis media due to the purulent discharge
Does not respond to antibiotics

Also with purulent discharge but the difference vs. chronic otitis media is in chronic otitis externa, you have an intact tympanic membrane
Due to cotton bud abuse

OTITIS MEDIA
The eustachian tube (ET) appears to be central to the pathogenesis of all forms of OM. The failure of any or all of these normal functions of ET can result in OM:
1. maintain the gaseous pressure within the middle ear cleft at a level that approximates atmospheric pressure
2. prevent reflux of the contents of the nasopharynx into the middle ear
3. clear secretions from the middle ear by both mucociliary transport and a pump action of ET
Anatomic obstruction: most commonly caused by inflammation of ET mucosa or extrinsic compression by tumor or large adenoids
Functional obstruction: usually a result of either failure of the normal muscular mechanism of ET opening, as seen in cleft palate, or insufficient stiffness of the cartilaginous portion of ET, often seen in infants and young
children
Breastfeeding appears to have a protective effect against OM (when exclusively done for at least the first 36 months of life)
Diagnosis of AOM and OME can be made by direct visualization of the TM using an otoscope or pneumatic otoscope
Classification of Otitis Media
Acute Otitis Media
o Suppurative
o Nonsuppurative
o Recurrent
Chronic Otitis Media
o Suppurative
Tubotympanic
Cholesteotoma
o Nonsuppurative
Otitis Media with Effusion
Definition
inflammatory process localized to the middle ear cleft.
The term otitis media can be separated into two distinct
categories:

1.

Acute Otitis Media

is characterized by a rapid onset of signs and symptoms,
such as pyrexia and otalgia, leading to inflammation of
the middle ear.
AOM is the most accurate term used to describe middle
ear inflammation in absence of effusion.
Nonsuppurative AOM: inflammation of the middle ear
cleft mucosa occurs either without formation of an
effusion or with a sterile effusion; often seen prior to,

Pathogenesis
MIDDLE EAR CLEFT
is a continuous space that begins at the Eustachian tube orifice in the
nasopharynx and extends to include the mastoid air cells
The cleft comprises three different contiguous components: the Eustachian
tube, the middle ear, and the mastoid air cells (including the petrosa).
The middle ear cleft is lined with variable epitheliumranging
from thick, ciliated respiratory epithelium found in the Eustachian tube to the
thin, nonglandular cuboidal epithelium in the mastoid cell
EUSTACHEAN TUBE
The main function of the Eustachian tube is to aerate the middle ear space,
providing pressure equivalent to atmospheric pressure.
Additionally, the Eustachian tube plays a role in mucociliary clearance of the
middle ear space and furthermore, prevents nasopharyngeal contents from
entering the middle ear.

Clinical Manifestations

AOM
Otalgia, fevers, decreased
appetite,upper respiratory infection,
and fatigue
In children less than 2 years old,
otalgia is evidenced by fussiness,
insomnia, and generalized irritability
Otoscopy in AOM classically
demonstrates a thickened, hyperemic,
immobile TM.

OME
is often asymptomatic
The most common complaint
associated with OME is
decreased hearing.
Otoscopy demonstrates a dull
gray- or yellow-tinged,
immobile TM.
If the TM is clear, bubbles or air
fluid levels can be elucidated.
Tympanometry and audiometry
are complimentary diagnostic
tools used

or in the resolution stage of, the acute suppurative OM

Recurrent AOM: > 3 episodes of acute suppurative OM
in a 6-month period, or > 4 episodes in a 12-month
period, with complete resolution of symptoms and signs
between the episodes
2.

Otitis Media with Effusion

is characterized by an inflammation of the middle ear
space with the presence of effusion
Because effusions localized to the middle ear space may be
asymptomatic or sterile and/or contain bacteria or even
purulence, it is a misnomer to describe all effusions as
secretory or serous or transudative.

one of the most common infectious diseases seen in

children, with its peak incidence in the first 2 years of life

Antecedent viral URTI disruption of Eustachian tube function

inflammation of the middle ear mucosa defective
clearance via the obstructed ET effusion provides favorable
medium for proliferation of bacterial pathogens suppuration

EUSTACHIAN TUBE DYSFUNCTION

The underlying pathogenesis of all forms of OM (with
the exception of cholesteatoma-related OM
Obstruction of the Eustachian tube, whether it is functional (eg, failure of
contraction of tensor veli palatini during swallowing) or
anatomic (eg, adenoid hypertrophy), results in the development of OM
OTITIS MEDIA
In patients with OM, there is an increase in the number of goblet cells found
in the respiratory epithelium lining the Eustachian tube.
While most episodes of AOM are preceded by viral infections, the majority of
AOM have a bacterial component.
Despite the environmental differences, the results are
universalthe most common bacterial pathogens found in
AOM are Streptococcus pneumoniae, Haemophilus influenzae, and
Moraxella catarrhalis.
OTITIS MEDIA WITH EFFUSION
OME has a similar pathogenesis to AOM in that Eustachian tube dysfunction
is nearly universal in children with OME
as well.
OME develops following untreated or unresolved
episodes of AOM.
persistent effusion (>30 days) in 40% of children after their first episode of
AOM, and continued effusion (up to 3 months) in 10%.
RISK FACTORS:
Parental smoking, Absence of breast feeding, day care attendance, craniofacial
anomalies, adenoid hypertrophy, and allergic rhinitis

TREATMENT

A. NONSURGICAL MEASURES
1. Watchful waitingThe current practice guidelines advise on an initial watchful waiting without antibiotic therapy for healthy 2-year-olds or older children with nonsevere illness (mild otalgia and fever < 39 C)
because AOM symptoms improve in most within 13 days. However, guidelines should not replace clinical judgment. Watchful waiting is not recommended for children < 2 years old if AOM is certain.
2. Antibiotic therapyIf AOM does not settle after the watchful waiting period, then antibiotic therapy should begin. The use of antibiotics is probably beneficial, but there is a trade-off between benefits and side
effects. Amoxicillin (80 mg/kg/d given in three divided doses for 10 days) remains the first-line therapy for AOM, although with increasing numbers of resistant strains of bacteria, it may be necessary to use more
broad-spectrum antibiotics in the future. In resistant cases, amoxicillin should be given in combination with clavulanate.
3. Adjunctive therapyThe adjunctive therapy for AOM should include analgesics and antipyretics. There is no role for oral decongestants or antihistamines in the treatment of AOM
B. SURGICAL MEASURES
- A minority of patients with AOM fail to respond to medical therapy or develop a complication. Myringotomy is then indicated to allow the drainage of pus from the middle ear space. Randomized trials have shown
myringotomy to be ineffective in uncomplicated AOM.

Tympanometry
is an objective and quantitative way to evaluate TM mobility and middle ear function.
It is defined as the measurement of the acoustic immittance of the ear as a function of ear canal air pressure.
- The procedure involves placing a probe into the external auditory canal and measuring the amount of sound energy returned. Patients with OME demonstrate flattened tracings on tympanometry indicating fluid in
the middle ear space.
UNCOMPLICATED OTITIS MEDIA
as long as the inflammatory process is confined to the mucoperiosteal lining of these air spaces
COMPLICATED OTITIS MEDIA
If the inflammatory process affects any part of the bony walls or spaces beyond these walls into adjacent structure
Inflammation of the middle ear
May also involve inflammation of mastoid, petrous apex, and perilabyrinthine air cells
Classification
o Acute OM: < 3 wks course; rapid course
o Subacute OM: 3 wks to 3 mos
o Chronic OM: 3 mos or longer
ACUTE SUPPURATIVE OTITIS MEDIA
acute purulent otitis media
abscess of the ear
simple acute otitis media
an infection of the mucoperiosteal lining of the middle ear cleft by pyogenic microorganisms produces a cycle of inflammatory changes of potentially serious nature
Etiology
Upper respiratory tract infection
Acute streptococcal tonsillitis
Chronic infection of adenoids
Contamination of auditory tube by infected water
Epidemiology
Peak incidence in the first 2 years of life (esp. 6- 12 months)
Boys more affected girls
50% of children 1 yr of age will have at least 1 episode
1/3 of children will have 3 or more infections by age 3
90% of children will have at least one infection by age 6.
Occurs more frequently in the winter months that is because we have no winter
Risk Factors
Intrinsic factor
o Age
o Allergies
o Craniofacial abnormalities (cleft palate)
Cleft lip: muscle of palate is also the muscle of upper part of Eustachian tube, so
open palate = lax and open ET, so milk or food goes to and fro the tube
Immunocompromised host

Extrinsic factor
o Seasons
o Upper Respiratory Infections pirme lang gasipon, ubogasaka sa ET

Causes

o
o
o
o
o
o
o
o

CHILDREN <6 WEEKS

Streptococcus pneumoniae
Haemophilus influenza (non-typeable)- causal organism below age 5
Staph aureus
Group A, B- Hemolytic Streptococcus
Moraxella catarrhalis
Escherichia coli
Klebsiella and Enterobacter
Pseudomonas aeruginosa

TUBAL OCCLUSION
Pathophysiology:
Retraction of the membrane

Signs and Symptoms:

muffled hearing (deafness)
ear pain
retraction of the tympanic
membrane
impaired conduction of sound
tinnitus
tuning fork test reveal conductive
deafness
Treatment
local decongestant combined with
swallowing and yawning
ephedrine nasal drops
lozenges
analgesics for earache

o
o
o
o
o
o

ADULT
Streptococcus pneumoniae ***
Haemophilus influenzae
Moraxella catarrhalis
Group A Streptococcus
Staph aureus
Nonpathogens

STAGES IN THE MUCOSA

PRESUPPURATION
SUPPURATION
Pathophysiology:
Pathophysiology:
Hyperemia of the tympanic vessels or diffuse
gross engorgement of the mucosa of
tympanic engorgement of the membrane
the cleft
convex bulging of membrane into the
Signs and Symptoms
meatus
progressive hyperemia
engorgement of vessels visible as Signs and Symptoms
injection
presence of pus in the middle ear
increasing earache and deafness
bulging membrane
temperature begins to rise
tenderness over the mastoid antrum
intense earache
Treatment
sense of pounding in the ear or
antibiotic therapy
pulsatile tinnitus
continued rise of temperature
X-ray of the mastoids for delayed resolution
Treatment
antibiotic therapy
nose drops to encourage auditory
tube patency
analgesics
may require myringotomy if
membrane is still intact and is still
under tension

RESOLUTION
Pathophysiology:
engorgement and bulging begin to
subside and return to normal
Signs and Symptoms
discharge of pus or bursting of
abscess followed at once by relief
of pain
temperature begins to fall
examination of the membrane will
reveal perforation
gradual fading of hyperemia
restoration of normal color and
landmark

RECURRENT ACUTE OTITIS

CHRONIC SUPPURATIVE OTITIS MEDIA

more than three episodes within 6 months or four episodes within 12 months
generally is due to relapse or reinfection
same pathogens responsible for acute otitis media
Treatment:
o antibiotics active against -lactamase-producing organisms.
o Antibiotic prophylaxis (e.g., with trimethoprim-sulfamethoxazole [TMP-SMX] or amoxicillin)
o tympanostomy tubes
o adenoidectomy
Tonsillectomy plus adenoidectomy - questionable; small benefit compared with the potential for complications.
Characterized by persistent or recurrent purulent otorrhea in the setting of TM perforation.
initiated by an episode of acute otitis media (AOM) with rupture of the membrane.
mastoid air cells are invariably involved.
most common etiologic organisms are P. aeruginosa and S. aureus
typical AOM bacterial pathogens may also be the cause, especially in younger children or in the winter months.
Has some degree of conductive hearing loss.
Categorized as active or inactive.
Inactive disease characterized by a central perforation of the TM, which allows drainage of purulent fluid from the middle ear.
When perforation is more peripheral, squamous epithelium from the auditory canal may invade the middle ear through the perforation, forming a mass of keratinaceous debris
(cholesteatoma) at the site of invasion. Mass can enlarge and has the potential to erode bone and promote further infection, which can lead to meningitis, brain abscess, or
paralysis of cranial nerve VII.
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ETIOLOGY
RISK FACTORS
COMPLICATIONS
Intratemporal complication
Infection in infancy or early childhood prevents
Inadequate treatment of acute otitis media
o Mastoiditis
normal cellular development
Chronic dysfunction of Eustachian tube
o Petrositis
Infection within a pneumatized cleft provokes
Persistent perforation of ear drum
o Labyrinthitis SNHL , vertigo
sclerosis with obliteration of the cell
Irreversible change in middle ear
o Facial paralysis from mastoiditis, cholesteatoma
Failure of air cell development predisposes to all
Persistent osteomyelitis in mastoid
varieties of diseases
Persistent disease in nose & sinuses
Intracranial complication (from cholesteatoma invaded into
In all varieties, the predominant organisms found in
base of skull)
the discharge are Gram negative bacilli and in
o Meningitis
particular Pseudomonas aeruginosa and Proteus sp.
o Extradural abscess
They do not normally inhabit the URT. They are
o Brain abscess
secondary invaders from the skins of the external
o Subdural abscess
auditory meatus
o Lateral venous sinus thrombosis
Medical treatment
Surgical treatment
o upper respiratory tract infection
o Tympanoplasty
o solution of 50% peroxide and 50% sterile water
o Mastoidectomy- open in the post auricular area
Radical Mastoidectomy get all of it kay baho baho na ang cholesteaoma, cannot be resolved by
antibiotic alone, no more ossicles kay radical

CLINICAL TYPES
o
o
o
o

SAFE TYPE
Carries no risk to the patient of any serious complications
infective disease is limited to mucosa and to the antero-posterior part of the
middle ear cleft
No risk of erosion of the bone surrounding the middle ear cleft
perforation in the pars tensa

Pathology
Followed by recovery when ear becomes dry
Inactive if discharge seems to have ceased without probability of resumption
Quiescent, term called during an intermission between episodes of discharge
Persistence of a perforation in the tympanic membrane is a predisposing factor
towards infection

OTITIS MEDIA WITH EFFUSION

(SEROUS OTITIS MEDIA)

o
o
o

UNSAFE TYPE
Associated with erosions of the bone
chance to exposing to infection important structure within the temporal bone or
within the skull
Perforation is within the attic or in the posterior regions of the pars tensa, so
called marginal perforation

Pathology
Often associated with osteitis
Granulation tissue may arise from the posterior bony wall of the external
auditory meatus (Polypus)
Cholesterol granules, a granulomatous structure formed by variable numbers of
cholesterol crystals

fluid is present in the middle ear for an extended period in the absence of signs and symptoms of infection.
acute effusions are self-limited; most resolve in 24 weeks.
Chronic effusions are often associated with significant hearing loss in the affected ear.
Majority of cases of otitis media with effusion resolve spontaneously within 3 months without antibiotic therapy.
Antibiotic therapy or myringotomy with insertion of tympanostomy tubes typically is reserved for patients in whom bilateral effusion (1) has persisted for at least 3 months
and (2) is associated with significant bilateral hearing loss.
persistence of a serous or mucoid middle ear effusion for >3 months
also described as chronic secretory otitis media, chronic serous otitis media, and glue ear
Serous OM- due to transudation of plasma from blood vessels into the middle ear space
Mucoid OM - from active secretion from glands and cysts in the lining of the middle ear cleft
PE reveals drumhead immobility on otoscopy
most common cause of hearing loss in children / school-aged children in the developed world and has peaks in incidence at 2 and 5 years of age
may be completely asymptomatic and detected only on routine audiologic screening
most common symptom: hearing loss
another common symptom is a blocked feeling in the ear, which may cause infants and young children to pull at their ears
Tympanometry is a valuable tool for the investigation of OME as it measures the compliance of the middle ear transformer mechanism

Treatment:
A large number of patients with OME require no treatment, particularly if the hearing impairment is mild.
Spontaneous resolution occurs in a significant proportion of patients.
A period of watchful waiting of 3 months from the onset (if known) or from the diagnosis (if onset unknown) before considering intervention is therefore advisable.
Tympanostomy tubes and adenoidectomy: surgical options for OME
Myringotomy and aspiration of middle ear effusion without ventilation tube insertion has a short-lived benefit and is NOT recommended.

CHOLESTEATOMA

Skin within the middle ear cleft

Skin in the wrong place
Consist of all the layers of the skin epithelium including germinative layer
Principal symptom: chronic purulent otorrhea
Principal sign: Observation of pus coming out from the middle ear and a perforation or retraction pocket

Choleastoma is usually first evident through a perforation in the posterior superior quadrant of the tympanic membrane. It develops as a blind epithelium-lined sac with a bottleneck opening. It gradually expands eroding
the surrounding bone
Complications:
Those within the cranial cavity:
o Extradural abscess
o Subdural abscess
o Meningitis
o Brain abscess
Those within the temporal bone
o mastoiditis
o petrositis
o facial paralysis
o labyrinthine infection
Treatment
Objectives of the treatment
o Arrest the disease
o Severe condition that will permit return of tissues to normal or that will allow recovery of function
Medical Treatment
o can be used only for safe disease
o aims at reaching and influencing the disease area with antibacterial and anti-inflammatory agents
o aims at assisting free drainage of inflammatory discharges by means of aural toilet
Types of surgery
o Cortical mastoidectomy
simple mastoidectomy
Schwartz operation
o Classical radical mastoidectomy
required where disease is so extensive as the wholesale ear structure
involves the principle of adequate exposure incision and permanent exteriorization of the disease area
The radical mastoid operation converts the mastoid antrum, the cells and the middle ear into a single cavity, and all the ossicles except the stapes are removed