Chronic Otitis Externa 20060425

7/28/2019 Chronic Otitis Externa 20060425

http://slidepdf.com/reader/full/chronic-otitis-externa-20060425 1/55

Chronic Otitis Externa

2006/04/25

R3 張維修



Introduction

Otitis externaMayer in 1844, a fungus infection

Chronic otitis externa1. McLaurin et al. in 1964, laryngoscope;

persistent external otitis

2. Otitis externa: clinically into acute,sub-acute, chronic, or recurrent



Introduction

Persistent: chronic or recurrent case of otitis externa

1. An interruption of the continuity of theepithelial lining of the external auditorycanal

2. A change of the PH from the acid to

the alkaline side



Clinical presentation F:M=2:1 Bilateral: 50% (constitutional or systemic factor) First visit of mean age: 50.5 y/oTwo clinical stage Initial stage:1. intense and persistent pruritus (most frequently); painlessness2. Otorrhea (scant, watery or milky, odorless, not very

troublesome)3. Progressive narrowing of EAC End stage1. Hearing loss (conductive hearing loss)

secondary to edema and/or debris accumulation in the EAC



Physical examination:Initial stage Cerumen: usually absent Otorrhea: watery or milky, rarely copious Ear canal: varies (depend on the level of disease activity)

Shiny, hyperemic and/or erythematous, covered with

granulation tissue Almost any intermediate stage imaginable can be seen The lateral canal is less severely affected Lumen progressively narrows (months to years)

End stage:a shiny, cerumen-free, skin-lined blunted sac and no evidence of

active infection or ongoing inflammation (squamous epitheliumrarely becomes trapped between the blind end and TM)



Image (Coronal CT)



Histopathology

Consist of fibrous connective tissue,including focal areas of calcification

Some subepithelial edema area were

slightly infiltrated with lymphocytes Subepithelial mucopurulency can

coalesce to form microabscesses No evidence of neoplasm or significant

acute or specific inflammation



Etiology

Mixed etiology; Unclear; Genetic or constitutional factor (50% bilateral)

Environmental factor: high temperature, high

humidity (hot and humid climate), waterexposure (swimming)

Traumatic

InfectiveMultifactor; Right genetic predisposition and the

right environment



Infectious component:

Bacterial pathogens: Culture: the same as acute bacterial external

otitis

Pseudomonas spp.:30~50%Staphylococcus spp.: 10~20%

other G(-) organism

The development of antibiotic resistantorganisms with the use of ototopicalmedications?



Microbiology of acute otitis externa.

Laryngoscope. 112(7 Pt 1):1166-77, 2002 Jul.

1998-2000, US, 2039 AOE subjects (2240 diseasedears)

Top 3 most frequent1. P. aeruginosa (38%)

2. S. epidermidis (9.1%)3. S. aureus (7.8%) Resistance S. epidermidis S. aureus1.

Neomycin 23% 6.3%2. Oxacillin 11% 2.7%3. Ofloxacin 12% 4.5% P. aeruginosa: resistant to quinolones from only

one subject



Infectious component:Fungal organisms:

Not common in AOE; less well understood in COE

Aspergillus and Candida spp. are the most frequentlyrecovered organism

Slow-growing fungi might be missed (specialdetection techniques: immunofluorescencemicroscopy)

an id reaction: a focus of fungal infection elsewherein the body can cause an secondary inflammatoryprocess in the external auditory canal



Allergic otitis externa

Two basic forms: A contact dermatitis

1. primary contact otitis2. secondary contact otitis

A dermatophytid reaction



Allergic contact dermatitis:

A type IV hypersensitivity reaction; adelayed-type hypersensitivity reaction

Characterized by severe pruritis leadingto scratching by the patient causingprolongation of the inflammation



Primary contact otitis

Not previously inflamed Contact allergen:

1. Metal: nickel (commonest contact allergen),

chrome, silver, gold2. Chemicals: cosmetics, nail polish, soaps,

detergents, shampoo, hairspray, dyes,3. Plastics, rubber, leather, or drugs

Diagnosis: history taking



Primary contact otitis:

Earrings

Nickel (10% of woman), chrome,skin around the site of ear piercing(usually the lobule or around the helix),which spreads to the antihelix,scratching: secondary infection

Dermatitis on the neck area where theearring touches



Primary contact otitis:

Hearing aids the components of and chemical used in the

manufacture of hearing aid moulds Methyl methacrylate is the most common sensitizer

Meding and Ringdahl, 1992, Ear Hear

-22 hearing aids users with chronic dermatitis of theear canal

-6/22(27%) contact allergy to the ear mould on

patch testing;(methyl methacrylate and ethylene glycolmethacrylate)



Secondary contact otitis

Iatrogenic Prolong use of topical preparations in the

treatment of otitis externa

Most common: neomycin; crossover withframycetin, gentamycin; avoid systemicaminoglycoside

Diagnosis: skin patch test(gold standard; 48-72 hrs)

Tx: identify antigen and avoid contact



Reported agents associated

with allergic otitis externa



Dermatophytid reaction: Hematologic spread of fungi or their allergenic

products from a primary focus of fungal infection Id reaction:1. A demonstrable primary focus containing the

pathogenic fungi, remote from the id lesion2. Absence of fungi in the skin lesion at the id reaction3. Spontaneous resolution of the dermatitis when the

primary focus fungal infection has been eradicated4. A positive immediate skin test response,

demonstrating a type 1, immunoglobulin E (IgE)-mediated reaction to an intradermal test of thefungal antigen



Dermatophytid reaction:

Common sites for the primary focus of fungal infection:

1. Nails (onchomycoses),

2. skin (chronic tinea pedis infections;athlete`s foot),

3.

vagina (monilial vaginitis; recurrent vaginitis) The most common fungus: Trichophyton



Dermatophytid reaction:

Treatment:1. identification and treatment of the

primary focus of fungal infection

2. desensitization with allergic extract of the infecting fungus to lessen the

allergic component3. control of any complicating secondary

bacterial infections



Foot and Ear Disease- The DermatophytidReaction in Otology Laryngoscope 106:181-6, 1996



Results



Regional PH in EAC

1938, Dermatologist Marchionini & Hausknetch:

The bactericidal and fungicial functions of

skin are reinforced by superficial skin acidity. Martinez Devesa P. Willis CM. Capper JW.

External auditory canal pH in chronic otitisexterna. [Journal Article] Clinical Otolaryngology & Allied Sciences. 28(4):320-4,

2003 Aug.



External auditory canal PH in

chronic otitis externa

A prospective age/sex-matched controlstudy

Chronic otitis externa: more than4weeks of duration and/or four or moreepisodes per year

18 patients (F:M=11:7); mean age:51.4 y/o



Results

External auditory canal pH in chronic otitis externa pH=6.61; Normal controlpH=5.90 (P<0.004)

Forearm PH in chronic otitis externa pH=5.7; Normal control pH=5.66



Results



Results



Results



Results



Dermatologic conditions: Pre-existing dermatologic processes are being

found with increasing frequency in patientwith chronic external otitis.

Seborrheic dermatitis (most common):positive family history, associated scalp andretroauricular area involvement, flexorsurfaces of the extremities

Psoriasis

Neurodermatitis



Differential diagnosis

Carcinoma of the EAC Dermatomycosis

Psoriasis Seborrhetic dermatitis

Contact eczematoid dermatitis (e.g., tohearing aid ear mold or eye glasses)

A dermatophytid reaction



Treatment

Restoration of the external auditorycanal to its normal anatomic andphysiologic state

Early stage: medical treatment

Surgery; clinically significant conductive

hearing loss (media fibrosis)



Medical treatment

Cleansing: aural toilet Trauma exacerbate the disease process

As atraumatic as possible; a“

no touch”

technique

Ear wick: corticosteroid neomycin

ointment (foreign body, more irritatingthan helpful)



Medical treatmentSteroid (the most critical component) Only one well-controlled study

Jacobsson et al. Clinical efficacy of

budesonide in the treatment of eczematous external otitis. Eur ArchOtorhinolaryngol 1991, 248; 246-9

1. A double-blind, placebo-controlled,crossover trial of budesonide2. Decreased pruritus and otorrhea

significant



Medical treatment

The more potent steroids are moreeffective

Systemic steroid, impractical (longterm nature of the disease)

Steroid injections into the

subepithelial tissues of the EAC(anecdotally, no evidence based)



Medical treatment

Antibiotics (for infectious component) Used cautiously and probably sparingly,

Intermittent use

Powders antibiotics mixed withpowdered dexamethasone (adhere to

wet surfaces; more consistent level of drug delivery than topical drops)



Medical treatment

Acidic solutions for the treatment of acuteand chronic otitis externa:

Aluminium acetate (Lambert, 1981)

97% alcohol + 3% acetic acid (Strauss& Dierker, 1987)

Acetic acid 1-3% (Thorp et al. 1998)



Medical treatment

Emgard P. Hellstrom S. Holm S.External otitis caused by infection withPseudomonas aeruginosa or Candida

albicans cured by use of a topical groupIII steroid, without any antibiotics.

[Journal Article] Acta Oto-Laryngologica.125(4):346-52, 2005 Apr.



Material and methods

A rat model (Male Sprague-Dawley rats) Right EAC was mechanically irritated by

exposure to 400 rotations of a plasticcone (80 rev/min) under microscope

Left ear: control



Groups Group A: P. aeruginosa 0.1ml within 1 min1. A1: untreated2. A2: 0.1ml of 0.05% BD (betamethasone

dipropionate)3. A3: 0.1ml of HCPB (hydrocortisone +

oxytetracycline + polymyxin B)4. A4: 0.1ml of saline, pH:5.0 Group B: C. albicans 0.1ml within 1 min

B1, B2, B3, B4 Group C: not infected; 0.1 ml pH:5.0 saline



Results



Results

Results



Results



Medical treatment Relief of pain or discomfort

Through cleansing of the aural canal

The judicious, limited use of specific

medication Termination of therapy, particularly specific

therapy, as promptly as possible

Elimination or control of predisposing causeFabricant`s dictum: a maximum of inspection

and a minimum of therapy



Medical treatment

Goal: arrest the disease completely,prevent the development of stenosis

Result: disappointed; Only slow the

progression (No long-term outcomesdata)

Tradition and opinion and that no long-term outcomes data are available



Surgical treatment Indication: a significant conductive

hearing loss

Goal: remove the stenotic segment of

the external auditory canal Recreate a physiologically functioning

tympanic membrane

Success: all of the involved skin mustbe removed



Surgical treatmentReconstruction:

local flaps (preconchal and postauricularflap);

advantage:1. less scaring because of increased

vascularity;

2. the contractural forces that develop duringhealing tend to pull the canal open



Surgical treatment Full-thickness grafts

1. Provide greater resistance to trauma2. contain glandular elements that provide lubrication;

3. less likely to contract than split-thickness grafts;

4. hair follicles (make postoperative managementmore difficult)

Split-thickness grafts

1. Easier to obtain;2. harder to place



Surgical treatmentSelesnick et al. Surgical treatment of acquired

external auditory canal atresia. Am J Otol1998;19.123-30

Three requirements of the successful

surgical repair of medial canal stenosis1. Complete removal of the cicatrix2. Performance of a bony canaloplasty

3. Resurfacing of the bony canal withepithelium Success: >80%



Surgical treatmentFollow-up

Slattery and Saadat`s series of 24patients; (3.6 years follow-up)

mean pre-op ABG: 25dB;

post-op ABG:15dB



Surgical treatmentRecurrence: Slattery and Saadat`s series of 14 surgical

procedures;1. recurrence rate: 3/14 (21.4%);2. earliest: more than 3 years following surgery Becker and Tos`s series:1. recurrence rate: 11/47 (23%);2. 3 patient recurrent within 6 months (an

insufficient removal of fibrous tissue duringthe primary operation)



References McLaurin JW. Raggio TP. Simmons M. Persistent external otitis.

[Journal Article] Laryngoscope. 75(11):1699-707, 1965 Nov. Roland PS. Chronic external otitis.[see comment]. [Review] [17

refs] [Journal Article. Review] Ear, Nose, & Throat Journal. 80(6 Suppl):12-6, 2001 Jun.

Slattery WH 3rd. Saadat P. Postinflammatory medial canal

fibrosis. [Journal Article] American Journal of Otology.18(3):294-7, 1997 May.

Sood S. Strachan DR. Tsikoudas A. Stables GI. Allergic otitisexterna . [Review] [26 refs] [Journal Article. Review] Clinical Otolaryngology & Allied Sciences. 27(4):233-6, 2002 Aug.

Derebery J, Berliner KI. Foot and ear disease--thedermatophytid reaction in otology.Laryngoscope. 1996 Feb;106(2 Pt 1):181-6.



References Martinez Devesa P. Willis CM. Capper JW. Externa l auditory

canal pH in chronic otitis externa . [Journal Article] Clinical Otolaryngology & Allied Sciences. 28(4):320-4, 2003 Aug.

Goodman WS. Middleton WC. The management of chronicexternal otitis . [Case Reports. Journal Article] Journal of Otolaryngology. 13(3):183-6, 1984 Jun.

Emgard P. Hellstrom S. Holm S. External otitis caused byinfection with Pseudomonas aeruginosa or Candida albicanscured by use of a topical group III steroid, without anyantibiotics. [Journal Article] Acta Oto-Laryngologica.125(4):346-52, 2005 Apr.

Roland PS. Stroman DW. Microbiology of acute otitis externa.[Journal Article] Laryngoscope. 112(7 Pt 1):1166-77, 2002 Jul.



THE END

Thank You

Documents

Chronic Otitis Externa 20060425