Otitis

Externa
(OE)

Ahmed
AlMumtin
MD
Anatomy and Physiology
• Consists of the auricle and EAM
• Skin-lined apparatus
• Approximately 2.5 cm in length
• Ends at tympanic membrane
 Anatomy and Physiology
• Auricle is mostly skin-lined cartilage
• External auditory meatus
• Cartilage: ~40%, Bony: ~60%
• S-shaped, Narrowest portion at bony-cartilage junction
Anatomy and Physiology
 EAC is related to
various contiguous
structures
 Tympanic membrane
 Mastoid
 Glenoid fossa
 Cranial fossa
 Infratemporal fossa
Anatomy and Physiology
 Innervation: cranial nerves V, VII, IX, X,
and greater auricular nerve
• Arterial supply: superficial temporal,
posterior and deep auricular branches
• Venous drainage: superficial temporal and
posterior auricular veins
• Lymphatics
Anatomy and Physiology
 Squamous
epithelium
 Bony skin – 0.2mm
 Cartilage skin
 0.5 to 1.0 mm
 Apopilosebaceous
unit
Otitis Externa
 Bacterial, viral or fungal infection of
external auditory canal
 Categorized by time course
 Acute
 Chronic
 Speculum findings:
• the canal may be so swollen that a view into
the ear is impossible
• In swimmers, divers and surfers, chronic
water exposure can lead to the growth of
bony swellings in the canal known as
exostoses.
These can interfere with the drainage of wax
and predispose to infection.
Differential diagnoses:
• Otitis media
• Ramsay Hunt syndrome Furuncle
• Skull base osteomyelitis Preauricular
• cyst and fistula Lacerations
• Atopic dermatitis Cerumen impaction
• Exostosis and osteoma Foreign
• body
• Acute (bullous) and chronic (granular)
• myringitis
•
•
Organisms
1. Pseudomonas species
2. Staphylococci
3. Streptococci/Gram negative rods
4. Fungi (Aspergillus/Candida species)
Labs/workup
Usually after failed empiric therapy:
• bacterial and fungal culture
• Adults with otitis externa: screening blood
glucose and/or a urine dipstick test to
rule out occult diabetes.
• Additional tests (if available):
 Gram stain of d/c
 KOH prep smear (within 10 min)
Acute Otitis Externa (AOE)
• “swimmer’s ear”
• Preinflammatory stage
• Acute inflammatory stage
 Mild
 Moderate
 Severe
Factors contributing to AOE
• High humidity Water exposure
• Maceration of canal skin
• High environmental temperature
• Local trauma
• Perespiration Allergy Stress
• Removal of normal skin lipids
• Absence of cerumen
• Alkaline pH of canal
•
•
•
AOE: Preinflammatory Stage
 Oedema of stratum corneum and plugging
of apopilosebaceous unit
 Symptoms: pruritus and sense of fullness
 Signs: mild edema
 Starts the itch/scratch cycle
AOE: Mild to Moderate Stage
 Progressive
infection
 Symptoms
 Pain
 Increased pruritus
 Signs
 Erythema
 Increasing edema
 Canal debris,
discharge
AOE: Severe Stage
 Severe pain, worse
with ear
movement
 Signs
 Lumen obliteration
 Purulent otorrhoea
 Involvement of
periauricular soft
tissue
 AOE: Treatment
• Most common pathogens: P. aeruginosa and S. aureus,
E.coli and proteus.!
• Four principles
 Frequent canal cleaning; swap or suction
 With sever EO, palcement of a wick made of sponge or
gauze provides a pathway for drops to be delivered to the
EAC wall skin for 48-72 hours!
 Topical antibiotics, and if sever>> Systemic PO,ABT
 Pain control
 Instructions for prevention
AT A GLANCE. . .
• Ostalgia
• Tenderness on palpation or manipulation
(tragus sign)
• Ear fullness
• Conductive hearing loss. Erythaema of
• meatus and canal Swelling and
• obstruction of canal Crusting and
• discharge
• Odor!
Furunculosis
• Acute localized infection
• Lateral 1/3 of posterosuperior canal
• Obstructed apopilosebaceous unit
• Pathogen: S. aureus
Furunculosis: Symptoms
• Localized pain Pruritus
• Hearing loss (if lesion occludes canal)
•
Furunculosis: Signs
 Edema
 Erythema
 Tendernes
s
 Occasional
fluctuance
Furunculosis: Treatment
 Local heat
 Analgesics
 Oral anti-staphylococcal antibiotics
 Incision and drainage reserved for
localized abscess
 IV antibiotics for soft tissue extension
- tri-adcortyle!
Erysipelas
 Acute superficial
cellulitis
• Group A, beta
hemolytic streptococci
• Skin: bright red; well-
demarcated, advancing
margin
• Rapid treatment with
oral or IV antibiotics if
insufficient response
Otomycosis
 Mostly in children who are
exposed to warm, moist
climates or who have a Hx
of chronic use of
antibiotic ear drops.
• Fungal infection of EAC
skin

• Primary or secondary
• Most common organisms:
Aspergillus and Candida
Otomycosis: Signs
 Canal erythaema
 Mild oedema
 White, gray, green,
yellow or black fungal
debris
Otomycosis: Symptoms
 Often indistinguishable from
bacterial OE
 Pruritus deep within the ear
 Otorrhoea
 Dull pain
 Hearing loss (obstructive)
 Tinnitus
 Otomycosis: Treatment
• Thorough cleaning and drying of canal Topical
• antifungals (clotrimazole for eg.,
amphotericine B, oxytetracycline-polymyxin, and
nystatin are very effective!)
• Acidifying of the EAC with drops like 2% acetic acid,
3% boric acid or sulzberger’s powder are also helpful
in the t/t of fungal infections.
Necrotizing (malignant) External Otitis(NEO)
 Potentially lethal infection of EAC and
surrounding structures
• Pseudomonas aeruginosa is the usual
culprit
• Risk Factors:
- Diabetes Mellitus
- Elderly
- Immunocompromised state
- Human Immunodeficiency Virus (HIV)
• Typically seen in diabetics and
immunocompromised patients
 NEO: Signs & Symptoms
• Similar to Otitis Externa except
• Severe, unrelenting Ear Pain and Headache
• Persistent discharge
• Does not respond to topical medications
• Commonly associated with Diabetes
• Granulation
Mellitus tissue in posterior and inferior canal
• Pathognomonic for necrotizing otitis
• Occurs at bone-cartilage junction
• Extra-auricular findings
• Cervical Lymphadenopathy Trismus (TMJ
• involvement)
• Facial Nerve Palsy or paralysis (Bell's Palsy)
 Associated with poor prognosis
 NEO: Dx, Prevention and T/T:

• Prognosis; Reportedly mortality 20-53%

• Dx: Hx, PE, Labs and Imaging:
- Labs; FBC, Culture of discharge, ESR, Serum glucose, Serum
creatinine.
- Radiology; CT, or MRI (ear),Tc 99m medronate methylene bone
scanning, Ga 67 scintography.
• Prevention:
- Avoid use of cotton swabs in ear and other canal trauma.
- Use caution when irrigating ear of high risk patients.
- Treat eczema of ear canal and other pruritic dermatitis
NEO: Treatment
 Intravenous antibiotics for at least 4 weeks
– with serial gallium scans monthly
 Local canal debridement until healed
 Pain control
 Use of topical agents controversial
 Hyperbaric oxygen experimental
 Surgical debridement for refractory cases
 NEO: Diagnosis
• Cohen and Friedman – criteria from review: They were divided into two
categories: obligatory and occasional. The obligatory criteria are: pain, edema,
exudate, granulations, microabscess (when operated), positive bone scan or
failure of local treatment often more than 1 week, and possibly pseudomonas in
culture. The occasional criteria are diabetes, cranial nerve involvement,
positive radiograph, debilitating condition and old age. All of the obligatory
criteria must be present in order to establish the diagnosis. The presence of
occasional criteria alone does not establish it. The importance of Tc99 scan in
detecting osteomyelitis is stressed. When bone scan is not available, a trial of
1-3 weeks of local treatment is suggested. Failure to respond to such
treatment may assist in making the diagnosis of MEO.
NEO: Mortality
 Death rate essentially unchanged despite
newer antibiotics (37% to 23%)
• Higher with multiple cranial neuropathies
(60%)
• Recurrence not uncommon (9% to 27%)
• May recur up to 12 months after treatment
Perichondritis/Chondritis
• Infection of perichondrium/cartilage
• Result of trauma to auricle
• May be spontaneous (overt diabetes)
• Usual pathogens include pseudomonas
species and mixed flora
Perichondritis: Symptoms
• Pain over auricle and deep in canal
• fever
• Pruritus

Perichondritis: Signs
• Tender auricle
• Induration Oedema
• erythaema Advanced
• cases
•  Crusting & weeping
 Involvement of soft
tissues
 Perichondritis: Treatment
• Aspiration of the pus
• Use antibiotics of gram-negative coverage, specifically
anitpseudomonals.
• If frank chondritis develops, incisions should be made in
the cartilage in order to provide adequate drainage.
• Mild: debridement, topical & oral antibiotic Advanced:
• hospitalization, IV antibiotics
• Chronic: surgical intervention with excision of necrotic
tissue and skin coverage
Relapsing Polychondritis
 Uncommon progressive inflammatory disorder that
may affect children, but more commonly in adults.
• Episodic and progressive inflammation of cartilages
• Autoimmune etiology?
• External ear, larynx, trachea, bronchi, and nose may
be involved
• Involvement of larynx and trachea causes
increasing respiratory obstruction
 Relapsing Polychondritis
 Fever, pain
 Swelling, erythaema
 Arthralgia!
 Tenderness of the nasal
septum may progress to
complete destruction of the
septum
Dx and T/t
• Weak +ve RF ANA +ve
-Systemic steroids
• High ESR, Anaemia
such as prednisolone
• And difinitve Dx is made
-In resistant cases;
• by a biopsy from the
dapsone,
• affected cartilage
cyclophosphamide or
azithioprine may be
used
Herpes Zoster Oticus
(Ramsay Hunt Syndrome)
• J. Ramsay Hunt described in 1907
• Viral infection caused by varicella zoster
• Infection along one or more cranial nerve
dermatomes (shingles).
- herpes zoster of the pinna with otalgia.
- facial paralysis
- sensorineural hearing loss Bullus
- myringitis
- A vesicular eruption of the concha of the
pinna and the EAC.
Symptoms

 Early: burning pain in one

ear, headache, malaise and
fever
 Late (3 to 7 days): vesicles,
facial paralysis

Treatment
• Corneal protection
• Oral steroid taper (10 to 14 days)
• Antivirals (eg. Valacyclovir)
• Facial nerve decompression
(controversial)!
Bullous Myringitis
• Viral infection
• Confined to tympanic membrane
• Primarily involves younger children
Bullous Myringitis: Symptoms
• Sudden onset of severe pain No fever
• No hearing impairment
• Bloody otorrhoea (significant) if rupture
•

Bullous Myringitis: Signs

• Inflammation limited to TM & nearby canal
• Multiple reddened, inflamed blebs.
• Hemorrhagic vesicles
Bullous Myringitis: Treatment
• Self-limiting Analgesics
• Topical antibiotics to prevent secondary
• infection
Incision of blebs is unnecessary
•
 Chronic Otitis Externa
• Acute otitis externa occurs in 4 of every 1000 people
per year
• Otitis externa is defined as chronic when the duration
of the infection exceeds 4 weeks or when more than
4 episodes occur in 1 year
 Bacterial, fungal, dermatological aetiologies

COE: Symptoms
• Unrelenting pruritus Mild discomfort
• Dryness, Crusting, and flaking of canal skin
•
 COE: Signs
 Asteatosis
 Dry, flaky skin
 Hypertrophied skin
 Mucopurulent otorrhoea
(occasional)
 COE: Treatment
• Similar to that of AOE
• Topical antibiotics, frequent cleanings
• Topical Steroids
• Surgical intervention
 Failure of medical treatment
 Goal is to enlarge and resurface the EAC
 Radiation-Induced Otitis Externa

 OE occurring after
radiotherapy
 Often difficult to treat
 Limited infection treated
like COE
 Involvement of bone
requires surgical
debridement and skin
coverage
Granular Myringitis (GM)
• Deepithelization of the TM
• Localized chronic inflammation of pars
tensa with granulation tissue
• Sequela of primary acute myringitis,
previous OE, perforation of TM
• Common organisms: Pseudomonas,
Proteus
GM: Symptoms
• Foul smelling discharge from one ear
• Often asymptomatic
• Slight irritation or fullness
• No hearing loss or significant pain
GM: Signs
• TM obscured by pus
• “peeping” granulations
• No TM perforations
GM: Treatment
• Careful and frequent debridement Topical anti-
• pseudomonal antibiotics Occasionally combined with
• steroids At least 2 weeks of therapy
• May warrant careful destruction of granulation tissue if
• no response
 Eczema
• External clue to OE (atopic, contact and
sebrrheoic) dermatitis
• Usual symptom is itching.
• P/E; erythaema, oedema, flaking and crusting.
• T/t:
- Local cleansing.
- Usage of corticosteroid and drying agents.
• Metal sensitivity is the most common form of
chronic dermatitis involving the ear.!
• Nickel is the most common offending metal.
• Women are affected more than men.
- Ear peircing is an important cause of primary
sensitization to nickel.
Conclusions
• Careful History Thorough
• physical exam
• Understanding of various disease
processes common to this area
• Vigilant treatment and patience
Questions/Comments?