EAC Bacteria Fungal Viral OE OE Related Otomycosis Herpes NOE RT Bullous COE AOE Acute Inflammatory Granular Preinflammatory Mild Moderate Severe AOE Acute Inflammatory Preinflammatory Mild Moderate Severe AOE Acute Inflammatory Preinflammatory Mild Moderate Severe
Otitis externa Is inflammation or infection of the external auditory canal, auricle or both May be classified into: Acute localised otitis externa Acute diffuse otitis externa Chronic otitis externa Eczematous otitis externa Necrotising otitis externa otomycosis
Localised otitis externa May be: Furunculosis Infection of a single apopilosebaceous unit (hair follicle) Cabuncle Infection of multiple hair follicles
Localised OE Only occurs in the outer 2/3 of EAC No hair follicles in medial 1/3 Commonly caused by S. aureus Others: Strep pyogenes Common risk factors Repeated ear trauma e.g scratching Hormonal changes in adolescents Atopic people Immuno -compromised individuals
Presentation Early: Aural fullness Tenderness in EAC Exaggerated compared to size of lesion Pain on pulling pinna Trismus
Presentation ctd Canal edema Boil formation May later form a small abscess Periaural cellulitis E.g. over mastoid Cervical lymphadenopathy Hearing loss if EAC is blocked
presentation ctd
Management Early: Analgesia Local heat application Oral antibiotic Antistaphylococcal Ear pack with ichthymol glycerine Ichthymol : antiseptic Glycerine: dehydrates hence less edema Late( abscess has formed) Do Incision and drainage on the abscess Topical antibiotic Analgesia Ear wick
Recurrent furunculosis May occur in patients that have nasal colonies of staphylococci Management Eradicate risk factors Oral flucloxacillin for 2 weeks Eradicate nasal colonies with nasal mupirocin
Diffuse otitis externa Aka: Swimmer’s Ear or Dirty South Ear Is inflammation involving the meatal skin. May extend to the epidermal layer of the TM or the pinna It may be acute (<6weeks) or chronic (>6weeks)
Epidemiology Affects 0.4% of the population annually(US) 10% of the population is affected atleast once in their lifetime 80% occur in Summer or during humid conditions Age: peak is 7-12 yrs Increased incidence in > 65yrs due to increased hearing aid use and comobidities
Aetiological theories Moisture in EAC Causes maceration of the skin Alters the pH from acidic to alkaline which promotes bacterial growth esp Pseudomonas Trauma to the EAC Breaks continuity in skin Provides an entry point for bacteria
Pathological staging of OE Clinical course of OE may be divided into 3: 1. Pre-inflammatory phase Protective pH and lipid acid balance is lost Stratum corneum becomes edematous blocking off sebaceous and apocrine glands There is disruption of the epithelial layer and invasion by pathogens Characterised by fullness and itching
Pathology ctd 2. Acute inflammatory phase Progressive edema and thickening with exudate formation May be mild, moderate of severe inflammation Different degrees of lumen obstruction Lymphadenopathy 3. Chronic inflammatory phase Less pain, more itching Lichenification and thickening of EAC Canal stenosis
Mild to moderate stage Severe stage
Presentation Otalgia Aural fullness Hearing loss Tinnitus Fever Ear discharge On examination Pain worse on: pulling pinna jaw mov’t Tragal pressure Purulent discharge Debri in canal Hyperemia of EAC skin Lymphadenopathy
Management Aural toilet More important factor in treatment May be removed by suction/ dry mopping/ curette Analgesia Topical antibiotics With steroid clear infection in 85-97% of patients May insert a wick Keep a dry ear to avoid exacerbating condition Topical acidifying and drying agents
Acidification of EAC Normal pH of EAC is 6.0 – 6.5 In presence of moisture and absence of cerumen, bacteria grow in more alkaline pH Acidic pH is toxic to many bacterial and fungal species esp in pre inflammatory phase E.g. 2-2.5% Acetic acid solutions (sometimes diluted in half by 90-95% EtOH / ABx in acidic solutions) 2.5 % acetic acid = a 50% dilution of white vinegar
Oral antibiotics Oral antibiotic use is controversial Oral antibiotic may be used if: Extra canal manifestations (e.g. auricular cellulitis, cervical adenopathy , parotitis ) (i.e. severe acute inflammatory stage) Moderate acute OE in elderly, immuno -compromised, DM patients
COE: Treatment Similar to that of AOE Topical antibiotics Culture and sensitivity guided if discharge is present Frequent cleanings Topical Steroids Surgical intervention Failure of medical treatment Goal is to enlarge and resurface the EAC
OTOMYCOSIS Is a fungal infection of the external ear Occurs in upto 10% of all AOE patients Risk factors Poor ear hygiene Prolonged use of topical antibiotics Humid ear conditions Immuno suppression
Aetiology Causative organisms include: Aspergillus species (80-90%) Aspergillus niger (black filaments) Aspergillus fumigatus (green or blue filaments) Candida albicans (10-20%) Appears white Other fungi rarely involved
Treatment Meticulous aural toilet and removal of all fungal hyphae and debri Acidification of EAC (2% acetic acid +/- a 90-95% alcohol solution) Antifungal solutions or creams E.g. nystatin / clotrimazole for candida but do NOT cover Aspergillus ) Oral itraconazole for persistent aspergillus Gentian violet paint has antifungal properties Boric acid powder good for drying out the canal
MYRINGITIS Is inflammation of the epithelial layer of the ear drum May be classified into Bullous myringitis Granular myringitis
Bullous myringitis Is formation of vesicles on the superficial layer of the TM The vesicles develop between the epithelial layer of the TM and the lamina propria May occur in all age groups Children, adolescents and young adults are most affected
Aetiology Primarily viral Influenza virus infection Usually follows an URTI mycoplasma pneumoniae May be the cause in a few cases
Presentation Severe throbbing otalgia Blood stained discharge Hearing loss On otoscopy Visualise bullae on TM TM is intact 30-40% associated with a serous OME Bloody D/C if bullae rapture
Bullous Myringitis
Bullous myringitis Diagnosis Diagnosis made from Hx and otoscopy Investigation are not necessary Treatment Analgesics Topical steroid with Antibiotic drops macrolide or quinolone to cover mycoplasma) Don’t cut blisters
Granular myringitis Granulation tissue forms on the outer layer of the TM The granulation tissue contains capillaries Inflammatory cells
Causes Trauma Swimming Poor aural hygiene Foreign bodies in the ear that are touching the TM Local irritants May be a sequelae of bullous nyringitis Post tympanoplasty (grafting) Infective causes: pseudomonas, proteus
presentation Foul Secretions in EAC Granulation tissue on TM Dx made on Otoscopy
GM: Signs TM obscured by pus “peeping” granulations No TM perforations
Management Debridement To remove all granulation tissue Application of topical caustic agents on the granulation tissue Granulation tissue may be removed and defect covered with perichondrial graft Antibiotic if Sx of infection
Herpes Zoster Oticus Viral infection caused by varicella zoster Infection along one or more cranial nerve dermatomes causing a vesicular rash (shingles) Ramsey Hunt syndrome herpes zoster of the pinna with otalgia and facial paralysis
Pathology Reactivation of dormant varicella zoster particles in the: Geniculate ganglion of the facial n. Spiral ganglion of auditory nerve Vestibular ganglion of the vestibular nerve
Herpes Zoster Oticus : Symptoms Early burning pain in one ear Headache malaise fever Late (3 to 7 days): Vesicles in concha, EAC or pinna (3% of pts have no rash) facial paralysis HL/tinnitus/vertigo
Herpes Zoster Oticus: Treatment Oral steroid Start with in 72 hrs of sx Prednisolone 1mg/kg/d for 5d then taper Antivirals E.g. Acyclovir 800mg q5/ 5d Gentle debridement Topical antivirals Corneal protection
Outcomes If untreated, 60% of patients develop complete paralysis in 7 days Only 10% of patients who present with complete paralysis will recover full function If palsy is incomplete, 60% recover function completely
Poor prognostic factors Complete facial paralysis Elderly >65yrs Late initiation of treatment
Perichondritis/Chondritis Perichondritis : Infection of perichondrium of the pinna Chondritis : infection of the cartilage Perichondritis is used to refer to a quantinum of infection Erysipelas to cellulitis to perichondritis to chondritis
Risk factors Thin skin and subcutaneous tissue of pinna: easy for infection spread Trauma to pinna Surgery Frost bite Burns Chemical injury
Microbiology Pseudomonas aureginosa 70-90% of all infections Staphylococcus aureus 50% in an independent study Others Streptococcal spp Proteus E coli
Pathology Infection causes hyperplasia of the dermal layers with thickening of the subcutaneous tissues Intense infiltration with PMN leukocytes leads to thickening of perichondrium and destruction of cartilage by phagocytes As perichondrium peels off, cartilage dies off.
Presentation Symptoms Dull pain over auricle and EAC initially Pain becomes severe quickly ( well innervated pinna) Pruritus ++++ Swelling of pinna Fever Signs Inflammed auricle (lobule spared) Edema Induration Lymphadenopathy Advanced cases Crusting and weeping cartilage Involvement of soft tissues
Presentation
Diagnosis Is made clinically DDX Relapsing perichondritis Extra Nodal NHL of the pinna
Management Treat the wounds and trauma Mild to moderate Topical antibiotics Oral antibiotics (anti- pseudomonal ) Analgesia I&D as may be required
Severe perichondritis Hospitalisation may be required Broad spectrum antibiotics Oral vs IV If a perichondrial abscess is present, it should be drained If necrotic cartilage is should be removed, an irrigation drain inserted
Severe perichondritis Severe perichondritis with abscess formation
Prognosis If untreated A subperichondrial abscess may form leading to avascular necrosis of cartilage leading to a pinna deformity Septisemia ( esp Staph aureus ) Subacute bacterial endocarditis Necrotising fascitis of the neck
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
Relapsing Polychondritis Aka polychondropathy Episodic and progressive inflammation and degeneration of cartilages Cause: unknown ?Autoimmune Affects cartilages e.g. External ear, larynx, trachea, bronchi, and nose If larynx and trachea are involved, DIB will be a sx
Relapsing Polychondritis Fever, pain Cartilage inflammation Swelling, erythema Ocular inflammation Audiovestibular damage Invx : CBC(Anemia), elevated ESR, CRP, ANCA, - ve RF Biopsy of affected area
Relapsing polychondritis
Treatment High dose steroids Prednisolone 1mg/kg/d to induce remission then 5-10mg daily to suppress recurrence Immunosuppressants Azathioprine and methotrexate (under research) Dapsone (some authors report improvement) NSAIDs Surgery if airway compromise is present
DERMATOSES
Dermatoses of the external ear These may include: Contact dermatitis Aural eczematoid dermatitis Neuro -dermatitis
Aural eczematoid dermatitis Present in patients with dermatitis like d/o e.g Psoriasis Seborrhoeic dermatitis Can occur spontaneously with out a clear trigger
Presentation Intense itching Scaling Redness Clear discharge Peeling of skin Moisture Pain- if superimposed infection
Neuro dermatitis Pt has compulsive itching due to psychological factors Mgt Treat underlying Pyschologic dx Cover ear Treat any superimposed infection if present
Gout May manifest in pts with Gout arthritis Tophi for in the auricle
Management of gout Treat underlying gout Curettage of tophi