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 GRADE II GRADE III ANOTIA

- 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

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

- aka classic microtia or peanut ear - has few or no recognizable landmarks of the

auricle - ear lobule usually present and anteriorly

positioned

- 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. 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

ATRESIA AND STENOSIS OF EXTERNAL AUDITORY CANAL

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 50–70 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

CONGENITAL MIDDLE-EAR MALFORMATIONS

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

CONGENITAL CHOLESTEATOMA

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, 30–40 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

EXTERNAL EAR DISORDERS

PREAURICULAR SINUS/CYST

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 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

PERICONDRITIS Infection of the tissue that covers the cartilage Cause:

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

Symptoms:

o Swelling of the whole pina o Accumulation of blood, excise and drain blood o If not drained will be infected and will have pus o Early perichondritis and cellulitis are both characterized by skin that is red, edematous, and tender. o 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.

RELAPSING POLYCHONDRITIS

Polychondritis Perichondritis

WHOLE EAR AFFECTED

responsive to antibiotics

Tx: Give corticosteroids

whole ear affected

responsive to antibiotics

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 DRY

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

Mongoloid races and American Indian - dry, scaly, “rice band” phenotype is more frequent

*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

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

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

EAR CANAL EXOSTOSES/OSTEOMAS

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.

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

IRRADIATION OSTEITIS OF TYMPANIC MEMBRANE

Develop after squamous cell carcinoma of external

just clean the canal thoroughly

HERPES ZOSTER OTICUS

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 Bell’s 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 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

KELOIDS

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

AURAL POLYP 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 Pathology Predisposing factors

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

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

• Heat, humidity, bathing, swimming. • Trauma, especially from dirty fingernails, cotton buds and hairgrips. • Inherited—narrow ear canals and non-atopic eczema.

OTITIS EXTERNA CIRCUMSCRIPTA

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

ACUTE DIFFUSE OTITIS EXTERNA (SWIMMER’S 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 Burow’s 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 that’s 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 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

CHRONIC CANDIDAL OTITIS EXTERNA

Sometimes mistaken as otitis media due to the purulent discharge

Does not respond to antibiotics

CHRONIC OTITIS EXTERNA 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 3–6 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 Pathogenesis Clinical Manifestations

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,

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 epithelium—ranging

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.

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

universal—the 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 waiting—The 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 1–3 days. However, guidelines should not replace clinical judgment. Watchful waiting is not recommended for children < 2 years old if AOM is certain. 2. Antibiotic therapy—If 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 therapy—The 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 Extrinsic 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

o Seasons o Upper Respiratory Infections –pirme lang gasipon, ubo…gasaka sa ET

Causes

CHILDREN <6 WEEKS ADULT

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

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

STAGES IN THE MUCOSA

TUBAL OCCLUSION PRESUPPURATION SUPPURATION RESOLUTION

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

Pathophysiology: Hyperemia of the tympanic vessels or diffuse tympanic engorgement of the membrane Signs and Symptoms progressive hyperemia engorgement of vessels visible as

‘injection’ increasing earache and deafness temperature begins to rise

Treatment antibiotic therapy

X-ray of the mastoids for delayed resolution

Pathophysiology: gross engorgement of the mucosa of

the cleft convex bulging of membrane into the

meatus Signs and Symptoms presence of pus in the middle ear bulging membrane tenderness over the mastoid antrum intense earache sense of pounding in the ear or

pulsatile tinnitus continued rise of temperature

Treatment antibiotic therapy nose drops to encourage auditory

tube patency analgesics may require myringotomy if

membrane is still intact and is still under tension

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 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 β-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.

CHRONIC SUPPURATIVE OTITIS MEDIA 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.

=

ETIOLOGY RISK FACTORS COMPLICATIONS

Infection in infancy or early childhood prevents normal cellular development

Infection within a pneumatized cleft provokes sclerosis with obliteration of the cell

Failure of air cell development predisposes to all varieties of diseases

In all varieties, the predominant organisms found in the discharge are Gram negative bacilli and in particular Pseudomonas aeruginosa and Proteus sp.

They do not normally inhabit the URT. They are secondary invaders from the skins of the external auditory meatus

Inadequate treatment of acute otitis media

Chronic dysfunction of Eustachian tube

Persistent perforation of ear drum

Irreversible change in middle ear

Persistent osteomyelitis in mastoid

Persistent disease in nose & sinuses

Intratemporal complication o Mastoiditis o Petrositis o Labyrinthitis SNHL , vertigo o Facial paralysis from mastoiditis, cholesteatoma

Intracranial complication (from cholesteatoma invaded into base of skull)

o Meningitis o Extradural abscess o Brain abscess o Subdural abscess o Lateral venous sinus thrombosis

Medical treatment o upper respiratory tract infection o solution of 50% peroxide and 50% sterile water

Surgical treatment o Tympanoplasty 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

SAFE TYPE UNSAFE TYPE

o Carries no risk to the patient of any serious complications o infective disease is limited to mucosa and to the antero-posterior part of the

middle ear cleft o No risk of erosion of the bone surrounding the middle ear cleft o 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

o Associated with erosions of the bone o chance to exposing to infection important structure within the temporal bone or

within the skull o 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

OTITIS MEDIA WITH EFFUSION (SEROUS OTITIS MEDIA)

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 2–4 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