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2006/04/25 R3
Introduction
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Otitis externa Mayer in 1844, a fungus infection Chronic otitis externa McLaurin et al. in 1964, laryngoscope; persistent external otitis 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 the epithelial lining of the external auditory canal 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/o Two clinical stage Initial stage: 1. intense and persistent pruritus (most frequently); painlessness 2. Otorrhea (scant, watery or milky, odorless, not very troublesome) 3. Progressive narrowing of EAC End stage 1. 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 epithelium rarely becomes trapped between the blind end and TM)
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), water exposure (swimming) Traumatic Infective Multifactor; 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 resistant organisms with the use of ototopical medications?
1. 2. 3. 1. 2. 3.
1998-2000, US, 2039 AOE subjects (2240 diseased ears) Top 3 most frequent P. aeruginosa (38%) S. epidermidis (9.1%) S. aureus (7.8%) Resistance S. epidermidis S. aureus Neomycin 23% 6.3% Oxacillin 11% 2.7% 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 frequently recovered organism Slow-growing fungi might be missed (special detection techniques: immunofluorescence microscopy) an id reaction: a focus of fungal infection elsewhere in the body can cause an secondary inflammatory process in the external auditory canal
A type IV hypersensitivity reaction; a delayed-type hypersensitivity reaction Characterized by severe pruritis leading to scratching by the patient causing prolongation of the inflammation
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 the earring touches
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 the ear canal -6/22(27%) contact allergy to the ear mould on patch testing; (methyl methacrylate and ethylene glycol methacrylate)
Iatrogenic Prolong use of topical preparations in the treatment of otitis externa Most common: neomycin; crossover with framycetin, gentamycin; avoid systemic aminoglycoside Diagnosis: skin patch test(gold standard; 4872 hrs) Tx: identify antigen and avoid contact
Dermatophytid reaction:
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Hematologic spread of fungi or their allergenic products from a primary focus of fungal infection Id reaction: A demonstrable primary focus containing the pathogenic fungi, remote from the id lesion Absence of fungi in the skin lesion at the id reaction Spontaneous resolution of the dermatitis when the primary focus fungal infection has been eradicated A positive immediate skin test response, demonstrating a type 1, immunoglobulin E (IgE)mediated reaction to an intradermal test of the fungal antigen
Dermatophytid reaction:
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Common sites for the primary focus of fungal infection: Nails (onchomycoses), skin (chronic tinea pedis infections; athlete`s foot), 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 component 3. control of any complicating secondary bacterial infections
Foot and Ear Disease- The Dermatophytid Reaction 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 otitis externa. [Journal Article] Clinical
A prospective age/sex-matched control study Chronic otitis externa: more than 4weeks of duration and/or four or more episodes 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 control pH=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 patient with chronic external otitis. Seborrheic dermatitis (most common): positive family history, associated scalp and retroauricular area involvement, flexor surfaces of the extremities Psoriasis Neurodermatitis
Differential diagnosis
Carcinoma of the EAC Dermatomycosis Psoriasis Seborrhetic dermatitis Contact eczematoid dermatitis (e.g., to hearing aid ear mold or eye glasses) A dermatophytid reaction
Treatment
Restoration of the external auditory canal to its normal anatomic and physiologic 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 irritating than helpful)
Medical treatment
Steroid (the most critical component) Only one well-controlled study Jacobsson et al. Clinical efficacy of budesonide in the treatment of eczematous external otitis. Eur Arch Otorhinolaryngol 1991, 248; 246-9 1. A double-blind, placebo-controlled, crossover trial of budesonide 2. Decreased pruritus and otorrhea significant
Medical treatment
The more potent steroids are more effective Systemic steroid, impractical (long term 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 with powdered dexamethasone (adhere to wet surfaces; more consistent level of drug delivery than topical drops)
Medical treatment
Acidic solutions for the treatment of acute and 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 with Pseudomonas aeruginosa or Candida albicans cured by use of a topical group III steroid, without any antibiotics. [Journal Article] Acta Oto-Laryngologica.
A rat model (Male Sprague-Dawley rats) Right EAC was mechanically irritated by exposure to 400 rotations of a plastic cone (80 rev/min) under microscope Left ear: control
Groups
1. 2. 3. 4.
Group A: P. aeruginosa 0.1ml within 1 min A1: untreated A2: 0.1ml of 0.05% BD (betamethasone dipropionate) A3: 0.1ml of HCPB (hydrocortisone + oxytetracycline + polymyxin B) 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
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 cause Fabricant`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 outcomes data) Tradition and opinion and that no longterm 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 must be removed
Surgical treatment
Reconstruction: local flaps (preconchal and postauricular flap); advantage: 1. less scaring because of increased vascularity; 2. the contractural forces that develop during healing tend to pull the canal open
Surgical treatment
1. 2. 3. 4.
1. 2.
Full-thickness grafts Provide greater resistance to trauma contain glandular elements that provide lubrication; less likely to contract than split-thickness grafts; hair follicles (make postoperative management more difficult) Split-thickness grafts Easier to obtain; harder to place
Surgical treatment
Selesnick et al. Surgical treatment of acquired external auditory canal atresia. Am J Otol 1998;19.123-30 Three requirements of the successful surgical repair of medial canal stenosis 1. Complete removal of the cicatrix 2. Performance of a bony canaloplasty 3. Resurfacing of the bony canal with epithelium Success: >80%
Surgical treatment
Follow-up Slattery and Saadat`s series of 24 patients; (3.6 years follow-up) mean pre-op ABG: 25dB; post-op ABG:15dB
Surgical treatment
Recurrence: 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 during the 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 Slattery WH 3rd. Saadat P. Postinflammatory medial canal fibrosis. [Journal Article] American Journal of Otology. Sood S. Strachan DR. Tsikoudas A. Stables GI. Allergic otitis externa . [Review] [26 refs] [Journal Article. Review] Clinical Derebery J, Berliner KI. Foot and ear disease--the dermatophytid 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 Goodman WS. Middleton WC. The management of chronic external otitis . [Case Reports. Journal Article] Journal of Emgard P. Hellstrom S. Holm S. External otitis caused by infection with Pseudomonas aeruginosa or Candida albicans cured by use of a topical group III steroid, without any antibiotics. [Journal Article] Acta Oto-Laryngologica.
Roland PS. Stroman DW. Microbiology of acute otitis externa. [Journal Article] Laryngoscope. 112(7 Pt 1):1166-77, 2002 Jul.
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