Otitis externa Ear nose and throat present

66w8f4sqsp 43 views 82 slides Jul 20, 2024
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About This Presentation

management of otitis externa


Slide Content

INFECTIONS OF THE EXTERNAL EAR DR. NYANZI DANIEL

The ear

Defence Mechanisms Natural Barriers Tragus + Anti-Tragus Skin TM Cerumen Acidic pH Contains Lysozyme Prevents drying and maceration of skin Contains Sloughed Squamous Epithelium

External Ear Infection Auricle EAC TM Dermatoses Auricle

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

Complications of AOE Chronic OE Necrotising OE Mastoiditis CNS complications Cellulitis Lymphadenitis Canal stenosis Perichondritis Chondritis Cellulitis parotitis erysipelas.

Chronic Otitis Externa (COE) Chronic inflammatory process Persistent symptoms (> 2 months) Causative organisms Bacterial ( Proteus ) Fungal Dermatological etiologies

COE: Symptoms Unrelenting pruritus Mild discomfort Dryness of canal skin

COE: Signs Asteatosis Sebaceous gland arrest Dry, flaky skin Hypertrophied skin Mucopurulent otorrhea (occasional) Scant greenish-grey brown secretions

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

Presentation Intense itching Ear discharge Dull pain Ear debri Hearing loss (obstructive) Visible hyphae Canal erythema

otomycosis

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

Auricle Peri/Chondritis Relapsing Polychondritis Erysipelas Herpes

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

Contact dermatitis Caused by allergic triggers Examples Nickle containing jewellery Beauty products Hair sprays Hair dyes

Contact dermatitis From a drug

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

Management Avoid triggers Avoid trauma/ water/ scratching Corticosteroid cream E.g. betamethasone, hydrocortisone +/- oral cortisteroid Burrow soln (diluted aluminiun acetate soln ) Esp in eczematoid dermatitis

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