 Darwin’s tubercle : an inherited cond. Presence
as a small elevation in post-sup part of helix.
 Wildermuth’s ear : Prominence of antihelix and
under-development of helix & assoc. with CHL
& SNHL.
 Mozart’s Ear : an dominant inheritance
presencs as fusion of helix and antihelix.
 Congenital Abnormalities of Auricle :
 Anotia
 Microtia
 Synotia
 Melotia
 Bat ears : Abnormal protrusion of auricle ,
disappered spontanously in first year of life.
 Lop Ear : Crux anhihelics is poorly formed
 Cup Ear : Antihelix is undeveloped
 Pre – Auricular Sinus :
 Faulty fusion of 1st & 2nd arch
 Opening :
1) Anterior border of ascending limb of helix
2) Line extending b/w tragal notch & angle of mouth
3) Pinna (or) Lobule
 Extend upto the level of tympanic ring.
 C/F : Asymptomatic , If infected – chr.discharge ,
recc.abscess & calculus
 Treatment : Excision ( careful for facial nerve)
 Collaural Fistula
 Tract : Line joining the angle of mandible &
Sterno-clavicular joint
Outer opening : Ant border of SCM
Inner opening : Bony Cartilagenous junction of EAC
C/F : Discharge fistula , Abscess , Ear discharge ,
Gran.tissue in EAC
Treatment : Excision of fistula
 Cicatrical Stenosis & Acquired Atresia of EAC
 Aetiology : Following external trauma , mastoid surgery ,
blunting following a lateral graft technique , keloid , COE,
burns , radiation , neoplasms
 Treatment : Surgical Removal of fibrous tissue &
Reconstruction of canal
 Cystic swelling in upper half of the anterior aspect of the
auricle.
 Formed within degenerate cartilage as a cystic space that has
no lining but contains straw coloured fluid.
 Oral Prednisolone ( 4 week period ) – fluid was absorbed and
the intra-cartilaginous fibrosis and granulation was
prevented.
 Insertion of drainage tube into the pseudocyst thro a guide
needle which was left in place for 5 days with pressure
dressing.
 Caused by an extravasation of blood b/w the cartilage
and the perichondrium producing a soft doughy
swelling of the pinna
 If untreated , blood clot becomes organised and the ear
remains permanently thickened – Cauliflower Ear
 Aspiration with wide bore needle
 Incision (along the margin of helix) & Evacuation of clot
 Infection of superficial layer of skin by staphylococci.
 Involve the whole auricle doesnot extend the EAC
 Reddish – purple vesicles filled with serum – later
bursts to exude - dries to form semi-adherent amber
crusts.
 Bathing with warm sterile saline.
 Topical Antibiotic Ointment
 Due to streptococcal infection of the skin producing a
raised red oedematous eruption with a
characterically well – defined edge.
 Auricle – red & swollen
 Assoc with fever and rapid pulse
 Antibiotic theraphy
 Infection or inflammation of perichondrium /
cartilage of Auricle & EAC
 Classification :
 Erysipelas of External ear ( Inf. of overlying skin)
 Cellulitis of External ear (Inf. of soft tissue )
 Perichondritis ( Inf. Involving perichondrium)
 Chondritis ( Inf. Involving cartilage )
 Result of trauma to auricle
 Laceration of auricle , Surgery to ext.ear , frostbite , burns ,
chemical injury , inf. of hematoma of pinna , high piercing
of auricle for insertion of ear rings.
 May be spontaneous (overt diabetes)
 Org : Pseudomonas Aeruginosa , Staph. Aureus
SIGNS & SYMPTOMS
 Pain over auricle and deep in
canal
 Pruritus
 Induration
 Edema
 Advanced cases
 Crusting & weeping
 Involvement of soft tissues
 TREATMENT :
 Topical & oral antibiotics
 Discharge (or) Abscess – Drainage
 Sub-perichondrial Abscess – I & D & Irrigating with 1.5 % acetic acid &
garamycin
 PREVENTION :
 By careful ear piercings away from cartilaginous pinna.
 Avoid Surgery in and around ear – to prevent from trauma
 Hematoma of auricle to drain properly.
 Meticulous management of burn injuries with prophylatic antibodies
against gram neg. bacteria.
 Removal of eschars and crusts.
 Acute localized infection of single hair follicle.
 Lateral 1/3 of posterosuperior canal
 Obstructed apopilosebaceous unit
 Pathogen: S. aureus
SYMPTOMS :
 Localized pain
 Ear blockage
 Exudates a scanty sero-sanguinous discharge
 Pinna & tragus – tender on palpation
 Pruritus
 Hearing loss (if lesion occludes canal)
SIGNS :
 Edema
 Erythema
 Tenderness
 Occasional fluctuance
DD : Ac.mastoiditis
TREATMENT :
 Local heat
 Analgesics
 Oral & systemic anti-staphylococcal antibiotics
 Topical ( antibiotics, Hygroscopic Dehydrating
agents)
 Incision and drainage reserved for localized
abscess
 IV antibiotics for soft tissue extension
 For recurrent : Eradication theraphy with nasal
mupirocin , oral flucloxacillin (14 days)
 Fungal infection of EAC skin
 Common in hot , humid
climates & is often secondary
to prolonged use of topical
Antibiotics.
 Most common organisms:
Aspergillus and Candida
 Occur bcoz the protective
lipid/acid balance of the ear is
lost.
SYMPTOMS :
 Often indistinguishable from bacterial OE
 Pruritus deep within the ear
 Dull pain
 Hearing loss (obstructive)
 Tinnitus
 Canal erythema
 Mild edema
 White, grey ,green , yellow or black fungal debris
( wet newspaper)
TREATMENT
 Thorough aural toilet & removal of debris
 Topical antifungals
 Resistant otomycosis – Exclude fungal inf. anywhere
including Athelete’s foot .
 Gen. cond of skin of the EAC that is charac. by
General edema & Erythema assoc. with itchy
discomfort and usually a ear discharge.
 Predisposing factors :
 Anatomical ( narrow / obstructed ear canal) ,
Dermatological ( Eczema , Sebhorrhoeic dermatitis )
Allergic ( Atopy , Non–atopy , Exposure to top.med)
Physiological ( Humid environment , Imm.comp)
Traumatic ( Skin maceration , ear probing , rad.theraphy )
Microbiological ( P.aeruginosa , Active COM , Fungi )
 Edema of stratum corneum and plugging of
apopilosebaceous unit
 Symptoms: pruritus and sense of fullness
 Signs: mild edema
 Starts the itch/scratch cycle
 Progressive infection
 Symptoms
 Pain
 Increased pruritus
 Signs
 Erythema
 Increasing edema
 Canal debris, discharge
 Severe pain, worse with
ear movement
 Signs
 Lumen obliteration
 Purulent otorrhea
 Involvement of
periauricular soft tissue
 Most common pathogens: P. aeruginosa and S. aureus
 Frequent canal cleaning ( Microscopic Toilet )
 Topical Medications ( IG pack )
 Pain control ( NSAIDS )
 Instructions for prevention ( avoidance of water pentration
into ear – cotton wool with petroleum jelly , custom made
ear moulds , nonprene head bandage)
 Aqua-Ear (or) Ear Calm , Blow driers - will remove the
water
 Unrelenting pruritus
 Mild discomfort
 Dryness of canal skin
 Hypertrophied skin
 Mucopurulent otorrhea
(occasional)
 Similar to that of AOE
 Topical antibiotics, frequent cleanings
 Topical Steroids
 Surgical intervention
 Failure of medical treatment
 To enlarge and resurface the EAC
 Localized chronic inflammation of pars tensa with
granulation tissue with possible involvement of EAC
 Toynbee described in 1860
 Causes : High temp , swimming , lack of hygeine , local
irritants , foreign body , bacterial & fungal infections
 Sequela of primary acute myringitis, previous OE, perforation
of TM
 Common organisms: Pseudomonas, Proteus, Staph.aureus &
Candida albicans
 Myringitis Externa Granulosa :
 Has granulation on lateral surface of drum & medial
part of the ear canal skin
 Granular Myringitis :
 Involves only the ear drum
 PATHOLOGY :
 Odematous granulation tissue with capillaries and diffuse
infiltration of chronic inflammatory cells
SIGNS & SYMPTOMS :
 Foul smelling discharge from one
ear
 Often asymptomatic
 Slight irritation or fullness
 No hearing loss or significant pain
 TM obscured by pus
 Posterio-superior granulations
 No TM perforations
 Careful and frequent debridement
 Specific Anti-microbial drops or powder with or without
steroids for 2 weeks
 Removal of granulation by physical methods
 Appln of caustic agents – Chromic acid , 0.5 % formalin ,
silver nitrate
 Laser evaporation of granulation
 Myringitis Bullosa Hemorrhagica – finding of
vesicles in the superficial layer of TM
 Viral infection ( Influenza ) , Mycoplasma
pnuemoniae
 Confined b/w outer epithelium & lamina
propria of tympanic membrane
 Primarily involves younger children
 Inflammation limited to
TM & nearby canal
 Multiple reddened,
inflamed blebs
 Hemorrhagic vesicles
 Sudden , unilateral throbbiong pain
 Blood stained discahrge
 Hearing loss
 Otoscopy : Serous (or) sero-sanginous discharge
blisters in TM & med. part of Ear canal
 Self-limiting
 Analgesics
 Topical antibiotics to prevent secondary
infection
 Benign NOE : is the clinical cond. of idiopathic necrosis of a
localised area of the bone of the tympanic ring , with
secondary inflammation of the overlying soft tissue and skin.
 Causative organism : Staph.aureus ,
 TM is suspectible to osteonecrosis because of its relatively
poor vascular supply
 Repeated local trauma – ear bud abuse , pricking of ear , use
of hearing aids.
 Poorly controlled diabetic with h/o OE
 Deep-seated aural pain
 Chronic otorrhea
 Aural fullness
 Pruritis
 Hearing loss
 Small area of deficient skin and soft tissue in
EAC revealing a segment of necrotic bone.
 Purulent secretions
 Occluded canal and obscured TM
 Cranial nerve involvement
 Pus swab
 CT Scan – extent of bone necrosis
 Brush cytology & Biopsy – to exclude neoplasm
 Audiometry
 Chronic granulomatous cond like Syphillis & TB should
be excluded.
 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 – necrosis beyond tymp.plate
 Surgical debridement
 Localised necrosis – involves only tympanic plate and leads to
spontaneous sequestration of bone
 Diffuse necrosis – more adjacent neuro-vascular structures
assoc. with more morbidity & lethal seq.
 Limited to tympanic ring - small area of bare bone may
appear on meatal floor , assoc. with pain & irritation , scanty
discharge.
 Conservative management
 Removal of remaining dead bone of the tympanic ring and
reconstitute the soft tissue of the meatus with a graft.
 A very severe dangerous cellulitis and
inflammation of the external auditory canal and
skull base ( temporal bone )
 Caused by psuedomonas organism.
 Majority of these patients are elderly diabetics
 Males
 Spread of this disease occurs through the fissures
of Santorini and osteo cartilagenous junction.
PATHOLOGY
 Immunity is reduced in patients with :
1. Diabetis mellitus
2. Blood cancer
3. HIV infections
4. Patients on anticancer drugs
CLINICAL FEATURES :
 history of trivial trauma to the ear often by ear
buds
 pain and swelling involving the EAC often
severe, throbbing and worse during nights.
 scanty and foul smelling discahrge (When the
discharge is foul smelling it indicates the onset
of osteomyelitis )
C / F :
 Granulation tissue at the bony cartilagenous junction.
 Ear drum is normal.
 EAC skin is soggy and edematous.
 Cranial nerve palsies are common when the disease
affects the skull base.
 The facial nerve is the most common nerve affected.
 Intracranial complications like meningitis and brain
abscess.
 TREATMENT
 MEDICAL:
 Carbenicillin, Pipercillin, Ticarcillin can be used.
 Third and forth generation cephalosporins can be used.
 Ciprofloxacillin in doses of 1.5 g - 2.5 g /day in divided doses can
be administered for a period of 2 weeks.
 Gentamycin can also be administered parenterally in doses of 80
mg iv two times a day in adults.
 Local antibiotic ear drops
 CONTROL OF DIABETES
SURGERY :
 Extensive surgical procedures have failed miserably
to cure this condition.
 Drainage of subperiosteal abscess, removal of
necrotic tissue and sequestrated bone
 Wound debridement in advanced cases.
 Herpes zoster oticus (HZ oticus) is a viral
infection of the inner, middle, and external ear.
 HZ oticus manifests as severe otalgia and
associated cutaneous vesicular eruption,
usually of the external canal and pinna.
 When associated with facial paralysis, the
infection is called Ramsay Hunt syndrome
 Pathophysiology
Reactivation of the varicella-zoster virus (VZV) along
the distribution of the sensory nerves innervating the
ear, which usually includes the geniculate ganglion,
is responsible for HZ oticus.
 Severe otalgia ( burning blisters in and around the
ear, on the face, in the mouth, and/or on the
tongue)
 Vertigo, nausea, vomiting
 Hearing loss, hyperacusis, tinnitus
 Eye pain, lacrimation
 In patients with Ramsay Hunt syndrome, vesicles
may appear before, during, or after facial palsy
 Vesicular exanthem - External auditory canal,
concha, and pinna , post-auricular skin .
 Associated findings
 Dysgeusia (alteration in taste)
 Inability to fully close the ipsilateral eye
 Corneal protection
 Oral steroid taper (10 to 14 days)
 Antivirals
 Keratotic mass of desquamating squamous epithelium in
bony portion of EAC
 Aetiology :
 Faulty migration of squamous epithelial cells from surface of TM
and the adjacent canal – accumulation of squ.epithelial cells and
debris end mixed with cerumen
 Pearlly white & glistening
 Pain – erosion of osseus meatus
 CHL & Otorrohea
 Tm – intact
 Gram (-)ve infection – treated topically
 Irritation of efferent vagal nerve endings in the
bronchi produces a reflex secretion of wax
 Assoc with Yellow Nail Syndrome ( yellow nails ,
lymphodema & plueral effusion )
 Treatment :
 Removal of Kerototic mass
 Refractory cases – canaloplasty
 Mixture of two glands – Ceruminous & Pilo-sabeceous
together with squ.epithelium , dust , forign debris
 Outer 2/3 rd of EAC lined by cuboidal and columnar
epithelium
 Secretion – Exocrine & apocrine Functions
 Stimulation of adrenergic receptors – myoepithelial cells
contract – expel liquid content into EAC
 Wet phenotype
 Caucasians & Negroes
 Moist , honey coloured
 Dry phenotype
 Mangaloid races
 Grey , granular & brittle
 C/F
 Deafness , tinnitus , Reflex cough , Ear ache ,
Fullness & Vertigo
 Treatment
 Ceruminolytics (paradichlorobenzene)
 Syringing
 Suction (or) Hooking
 Syringing – Not in Perf. TM , Middle Ear
Diseases , Previous ear surgeries.
 Insects – first killed by instilling oil in EAC and
then by syringing
 Small Objects – Syringing with water
 Vegetable Objects – Syringing with alchohol
(or) removal by small forceps.
 Large Objects - Using Microscopic control , by
small forceps or blunt hook
 Spherical objects – Cyanoacrylate adhesive
(superglue) applied to blind end of cotton swab
 Buttton batteries – may spontaneously leak
alkaline electrolyte solution on exposure to
moisture – liquefication necrosis – removed in
urgency
 Otolaryngeal Complication :
 LMN Palsy
 Nasal Septal Perforation
 Large FB – Expose the meatus thro’ post-
auricular incision , drilling the bone from the
canal wall
 Lipoma – post-auricular sulcus
 Papilloma
 Viral Papilloma - outer meatus
 Removal – curetting under L.A / laser
 Diffuse Papilloma
 Typical papilliferous apperance
 Extend to deep meatus & obscure TM
 Remove permanently but recur
 Adenoma
 Sebaceous Adenoma
 Arise from sabeceous gland of meatus.
 Smooth , painless skin covered swelling in outer EAC
 Local Excision
 Ceruminoma ( Hidradenoma)
 Arise from modified apocrine sweat gland
 Smooth innervated polypoidal swelling in outer EAC
 Blocking sensation
 Wide Excision
 Indurated ulcer with everted margins
 Biopsy under L.A
 Regional L.N involvement
 Small leisions - Local Excision
 Large leisions – Excision with external beam radiation
 Advanced Cases – Radical ressection of ear including
Parotidectomy , neck dissection & mastoidectomy
 Results from prolifertion of basal epithelium
 Seen in tragus , border of helix , meatal entrance
 Later cases – whole auricle is involved , with underlying
bone and parotid gland involvement.
 First a flat painless slightly raised leision followed by the
development of rolled edge with penetrating ulcer –
bleeds readily
 Treatment – Wide Excision
 Advanced Stages – Wide Excision & radiotheraphy
 Nodular pigmented leision which tends to enlarge
rapidly and eventually to ulcerate
 Regional L.N Involement & Diatant metastasis
 Local Disease – Excision & Skin Graft
 Large Tumours – Wedge (or) Wide Excision
 Radical excision involves complete excision of pinna & and
dissection of regional L.N
 Prognosis is poor
THANK YOU

Diseases of external ear,dr.s.gopalakrishnan, 13.06.17

  • 2.
     Darwin’s tubercle: an inherited cond. Presence as a small elevation in post-sup part of helix.  Wildermuth’s ear : Prominence of antihelix and under-development of helix & assoc. with CHL & SNHL.  Mozart’s Ear : an dominant inheritance presencs as fusion of helix and antihelix.
  • 3.
     Congenital Abnormalitiesof Auricle :  Anotia  Microtia  Synotia  Melotia  Bat ears : Abnormal protrusion of auricle , disappered spontanously in first year of life.  Lop Ear : Crux anhihelics is poorly formed  Cup Ear : Antihelix is undeveloped
  • 4.
     Pre –Auricular Sinus :  Faulty fusion of 1st & 2nd arch  Opening : 1) Anterior border of ascending limb of helix 2) Line extending b/w tragal notch & angle of mouth 3) Pinna (or) Lobule  Extend upto the level of tympanic ring.  C/F : Asymptomatic , If infected – chr.discharge , recc.abscess & calculus  Treatment : Excision ( careful for facial nerve)
  • 5.
     Collaural Fistula Tract : Line joining the angle of mandible & Sterno-clavicular joint Outer opening : Ant border of SCM Inner opening : Bony Cartilagenous junction of EAC C/F : Discharge fistula , Abscess , Ear discharge , Gran.tissue in EAC Treatment : Excision of fistula
  • 6.
     Cicatrical Stenosis& Acquired Atresia of EAC  Aetiology : Following external trauma , mastoid surgery , blunting following a lateral graft technique , keloid , COE, burns , radiation , neoplasms  Treatment : Surgical Removal of fibrous tissue & Reconstruction of canal
  • 7.
     Cystic swellingin upper half of the anterior aspect of the auricle.  Formed within degenerate cartilage as a cystic space that has no lining but contains straw coloured fluid.  Oral Prednisolone ( 4 week period ) – fluid was absorbed and the intra-cartilaginous fibrosis and granulation was prevented.  Insertion of drainage tube into the pseudocyst thro a guide needle which was left in place for 5 days with pressure dressing.
  • 8.
     Caused byan extravasation of blood b/w the cartilage and the perichondrium producing a soft doughy swelling of the pinna  If untreated , blood clot becomes organised and the ear remains permanently thickened – Cauliflower Ear  Aspiration with wide bore needle  Incision (along the margin of helix) & Evacuation of clot
  • 9.
     Infection ofsuperficial layer of skin by staphylococci.  Involve the whole auricle doesnot extend the EAC  Reddish – purple vesicles filled with serum – later bursts to exude - dries to form semi-adherent amber crusts.  Bathing with warm sterile saline.  Topical Antibiotic Ointment
  • 10.
     Due tostreptococcal infection of the skin producing a raised red oedematous eruption with a characterically well – defined edge.  Auricle – red & swollen  Assoc with fever and rapid pulse  Antibiotic theraphy
  • 11.
     Infection orinflammation of perichondrium / cartilage of Auricle & EAC  Classification :  Erysipelas of External ear ( Inf. of overlying skin)  Cellulitis of External ear (Inf. of soft tissue )  Perichondritis ( Inf. Involving perichondrium)  Chondritis ( Inf. Involving cartilage )
  • 12.
     Result oftrauma to auricle  Laceration of auricle , Surgery to ext.ear , frostbite , burns , chemical injury , inf. of hematoma of pinna , high piercing of auricle for insertion of ear rings.  May be spontaneous (overt diabetes)  Org : Pseudomonas Aeruginosa , Staph. Aureus
  • 13.
    SIGNS & SYMPTOMS Pain over auricle and deep in canal  Pruritus  Induration  Edema  Advanced cases  Crusting & weeping  Involvement of soft tissues
  • 14.
     TREATMENT : Topical & oral antibiotics  Discharge (or) Abscess – Drainage  Sub-perichondrial Abscess – I & D & Irrigating with 1.5 % acetic acid & garamycin  PREVENTION :  By careful ear piercings away from cartilaginous pinna.  Avoid Surgery in and around ear – to prevent from trauma  Hematoma of auricle to drain properly.  Meticulous management of burn injuries with prophylatic antibodies against gram neg. bacteria.  Removal of eschars and crusts.
  • 15.
     Acute localizedinfection of single hair follicle.  Lateral 1/3 of posterosuperior canal  Obstructed apopilosebaceous unit  Pathogen: S. aureus
  • 16.
    SYMPTOMS :  Localizedpain  Ear blockage  Exudates a scanty sero-sanguinous discharge  Pinna & tragus – tender on palpation  Pruritus  Hearing loss (if lesion occludes canal)
  • 17.
    SIGNS :  Edema Erythema  Tenderness  Occasional fluctuance DD : Ac.mastoiditis
  • 18.
    TREATMENT :  Localheat  Analgesics  Oral & systemic anti-staphylococcal antibiotics  Topical ( antibiotics, Hygroscopic Dehydrating agents)  Incision and drainage reserved for localized abscess  IV antibiotics for soft tissue extension  For recurrent : Eradication theraphy with nasal mupirocin , oral flucloxacillin (14 days)
  • 19.
     Fungal infectionof EAC skin  Common in hot , humid climates & is often secondary to prolonged use of topical Antibiotics.  Most common organisms: Aspergillus and Candida  Occur bcoz the protective lipid/acid balance of the ear is lost.
  • 20.
    SYMPTOMS :  Oftenindistinguishable from bacterial OE  Pruritus deep within the ear  Dull pain  Hearing loss (obstructive)  Tinnitus
  • 21.
     Canal erythema Mild edema  White, grey ,green , yellow or black fungal debris ( wet newspaper)
  • 22.
    TREATMENT  Thorough auraltoilet & removal of debris  Topical antifungals  Resistant otomycosis – Exclude fungal inf. anywhere including Athelete’s foot .
  • 23.
     Gen. condof skin of the EAC that is charac. by General edema & Erythema assoc. with itchy discomfort and usually a ear discharge.  Predisposing factors :  Anatomical ( narrow / obstructed ear canal) , Dermatological ( Eczema , Sebhorrhoeic dermatitis ) Allergic ( Atopy , Non–atopy , Exposure to top.med) Physiological ( Humid environment , Imm.comp) Traumatic ( Skin maceration , ear probing , rad.theraphy ) Microbiological ( P.aeruginosa , Active COM , Fungi )
  • 24.
     Edema ofstratum corneum and plugging of apopilosebaceous unit  Symptoms: pruritus and sense of fullness  Signs: mild edema  Starts the itch/scratch cycle
  • 25.
     Progressive infection Symptoms  Pain  Increased pruritus  Signs  Erythema  Increasing edema  Canal debris, discharge
  • 26.
     Severe pain,worse with ear movement  Signs  Lumen obliteration  Purulent otorrhea  Involvement of periauricular soft tissue
  • 27.
     Most commonpathogens: P. aeruginosa and S. aureus  Frequent canal cleaning ( Microscopic Toilet )  Topical Medications ( IG pack )  Pain control ( NSAIDS )  Instructions for prevention ( avoidance of water pentration into ear – cotton wool with petroleum jelly , custom made ear moulds , nonprene head bandage)  Aqua-Ear (or) Ear Calm , Blow driers - will remove the water
  • 28.
     Unrelenting pruritus Mild discomfort  Dryness of canal skin  Hypertrophied skin  Mucopurulent otorrhea (occasional)
  • 29.
     Similar tothat of AOE  Topical antibiotics, frequent cleanings  Topical Steroids  Surgical intervention  Failure of medical treatment  To enlarge and resurface the EAC
  • 30.
     Localized chronicinflammation of pars tensa with granulation tissue with possible involvement of EAC  Toynbee described in 1860  Causes : High temp , swimming , lack of hygeine , local irritants , foreign body , bacterial & fungal infections  Sequela of primary acute myringitis, previous OE, perforation of TM  Common organisms: Pseudomonas, Proteus, Staph.aureus & Candida albicans
  • 31.
     Myringitis ExternaGranulosa :  Has granulation on lateral surface of drum & medial part of the ear canal skin  Granular Myringitis :  Involves only the ear drum
  • 32.
     PATHOLOGY : Odematous granulation tissue with capillaries and diffuse infiltration of chronic inflammatory cells
  • 33.
    SIGNS & SYMPTOMS:  Foul smelling discharge from one ear  Often asymptomatic  Slight irritation or fullness  No hearing loss or significant pain  TM obscured by pus  Posterio-superior granulations  No TM perforations
  • 34.
     Careful andfrequent debridement  Specific Anti-microbial drops or powder with or without steroids for 2 weeks  Removal of granulation by physical methods  Appln of caustic agents – Chromic acid , 0.5 % formalin , silver nitrate  Laser evaporation of granulation
  • 35.
     Myringitis BullosaHemorrhagica – finding of vesicles in the superficial layer of TM  Viral infection ( Influenza ) , Mycoplasma pnuemoniae  Confined b/w outer epithelium & lamina propria of tympanic membrane  Primarily involves younger children
  • 36.
     Inflammation limitedto TM & nearby canal  Multiple reddened, inflamed blebs  Hemorrhagic vesicles
  • 37.
     Sudden ,unilateral throbbiong pain  Blood stained discahrge  Hearing loss  Otoscopy : Serous (or) sero-sanginous discharge blisters in TM & med. part of Ear canal
  • 38.
     Self-limiting  Analgesics Topical antibiotics to prevent secondary infection
  • 39.
     Benign NOE: is the clinical cond. of idiopathic necrosis of a localised area of the bone of the tympanic ring , with secondary inflammation of the overlying soft tissue and skin.  Causative organism : Staph.aureus ,  TM is suspectible to osteonecrosis because of its relatively poor vascular supply  Repeated local trauma – ear bud abuse , pricking of ear , use of hearing aids.
  • 40.
     Poorly controlleddiabetic with h/o OE  Deep-seated aural pain  Chronic otorrhea  Aural fullness  Pruritis  Hearing loss
  • 41.
     Small areaof deficient skin and soft tissue in EAC revealing a segment of necrotic bone.  Purulent secretions  Occluded canal and obscured TM  Cranial nerve involvement
  • 42.
     Pus swab CT Scan – extent of bone necrosis  Brush cytology & Biopsy – to exclude neoplasm  Audiometry  Chronic granulomatous cond like Syphillis & TB should be excluded.
  • 43.
     Intravenous antibioticsfor at least 4 weeks – with serial gallium scans monthly  Local canal debridement until healed  Pain control  Use of topical agents controversial  Hyperbaric oxygen – necrosis beyond tymp.plate  Surgical debridement
  • 44.
     Localised necrosis– involves only tympanic plate and leads to spontaneous sequestration of bone  Diffuse necrosis – more adjacent neuro-vascular structures assoc. with more morbidity & lethal seq.  Limited to tympanic ring - small area of bare bone may appear on meatal floor , assoc. with pain & irritation , scanty discharge.  Conservative management  Removal of remaining dead bone of the tympanic ring and reconstitute the soft tissue of the meatus with a graft.
  • 45.
     A verysevere dangerous cellulitis and inflammation of the external auditory canal and skull base ( temporal bone )  Caused by psuedomonas organism.  Majority of these patients are elderly diabetics  Males  Spread of this disease occurs through the fissures of Santorini and osteo cartilagenous junction.
  • 46.
    PATHOLOGY  Immunity isreduced in patients with : 1. Diabetis mellitus 2. Blood cancer 3. HIV infections 4. Patients on anticancer drugs
  • 47.
    CLINICAL FEATURES : history of trivial trauma to the ear often by ear buds  pain and swelling involving the EAC often severe, throbbing and worse during nights.  scanty and foul smelling discahrge (When the discharge is foul smelling it indicates the onset of osteomyelitis )
  • 48.
    C / F:  Granulation tissue at the bony cartilagenous junction.  Ear drum is normal.  EAC skin is soggy and edematous.  Cranial nerve palsies are common when the disease affects the skull base.  The facial nerve is the most common nerve affected.  Intracranial complications like meningitis and brain abscess.
  • 49.
     TREATMENT  MEDICAL: Carbenicillin, Pipercillin, Ticarcillin can be used.  Third and forth generation cephalosporins can be used.  Ciprofloxacillin in doses of 1.5 g - 2.5 g /day in divided doses can be administered for a period of 2 weeks.  Gentamycin can also be administered parenterally in doses of 80 mg iv two times a day in adults.  Local antibiotic ear drops  CONTROL OF DIABETES
  • 50.
    SURGERY :  Extensivesurgical procedures have failed miserably to cure this condition.  Drainage of subperiosteal abscess, removal of necrotic tissue and sequestrated bone  Wound debridement in advanced cases.
  • 51.
     Herpes zosteroticus (HZ oticus) is a viral infection of the inner, middle, and external ear.  HZ oticus manifests as severe otalgia and associated cutaneous vesicular eruption, usually of the external canal and pinna.  When associated with facial paralysis, the infection is called Ramsay Hunt syndrome
  • 52.
     Pathophysiology Reactivation ofthe varicella-zoster virus (VZV) along the distribution of the sensory nerves innervating the ear, which usually includes the geniculate ganglion, is responsible for HZ oticus.
  • 53.
     Severe otalgia( burning blisters in and around the ear, on the face, in the mouth, and/or on the tongue)  Vertigo, nausea, vomiting  Hearing loss, hyperacusis, tinnitus  Eye pain, lacrimation  In patients with Ramsay Hunt syndrome, vesicles may appear before, during, or after facial palsy
  • 54.
     Vesicular exanthem- External auditory canal, concha, and pinna , post-auricular skin .  Associated findings  Dysgeusia (alteration in taste)  Inability to fully close the ipsilateral eye
  • 55.
     Corneal protection Oral steroid taper (10 to 14 days)  Antivirals
  • 56.
     Keratotic massof desquamating squamous epithelium in bony portion of EAC  Aetiology :  Faulty migration of squamous epithelial cells from surface of TM and the adjacent canal – accumulation of squ.epithelial cells and debris end mixed with cerumen  Pearlly white & glistening  Pain – erosion of osseus meatus  CHL & Otorrohea
  • 57.
     Tm –intact  Gram (-)ve infection – treated topically  Irritation of efferent vagal nerve endings in the bronchi produces a reflex secretion of wax  Assoc with Yellow Nail Syndrome ( yellow nails , lymphodema & plueral effusion )  Treatment :  Removal of Kerototic mass  Refractory cases – canaloplasty
  • 58.
     Mixture oftwo glands – Ceruminous & Pilo-sabeceous together with squ.epithelium , dust , forign debris  Outer 2/3 rd of EAC lined by cuboidal and columnar epithelium  Secretion – Exocrine & apocrine Functions  Stimulation of adrenergic receptors – myoepithelial cells contract – expel liquid content into EAC
  • 59.
     Wet phenotype Caucasians & Negroes  Moist , honey coloured  Dry phenotype  Mangaloid races  Grey , granular & brittle  C/F  Deafness , tinnitus , Reflex cough , Ear ache , Fullness & Vertigo
  • 60.
     Treatment  Ceruminolytics(paradichlorobenzene)  Syringing  Suction (or) Hooking  Syringing – Not in Perf. TM , Middle Ear Diseases , Previous ear surgeries.
  • 61.
     Insects –first killed by instilling oil in EAC and then by syringing  Small Objects – Syringing with water  Vegetable Objects – Syringing with alchohol (or) removal by small forceps.  Large Objects - Using Microscopic control , by small forceps or blunt hook  Spherical objects – Cyanoacrylate adhesive (superglue) applied to blind end of cotton swab
  • 62.
     Buttton batteries– may spontaneously leak alkaline electrolyte solution on exposure to moisture – liquefication necrosis – removed in urgency  Otolaryngeal Complication :  LMN Palsy  Nasal Septal Perforation  Large FB – Expose the meatus thro’ post- auricular incision , drilling the bone from the canal wall
  • 63.
     Lipoma –post-auricular sulcus  Papilloma  Viral Papilloma - outer meatus  Removal – curetting under L.A / laser  Diffuse Papilloma  Typical papilliferous apperance  Extend to deep meatus & obscure TM  Remove permanently but recur
  • 64.
     Adenoma  SebaceousAdenoma  Arise from sabeceous gland of meatus.  Smooth , painless skin covered swelling in outer EAC  Local Excision  Ceruminoma ( Hidradenoma)  Arise from modified apocrine sweat gland  Smooth innervated polypoidal swelling in outer EAC  Blocking sensation  Wide Excision
  • 65.
     Indurated ulcerwith everted margins  Biopsy under L.A  Regional L.N involvement  Small leisions - Local Excision  Large leisions – Excision with external beam radiation  Advanced Cases – Radical ressection of ear including Parotidectomy , neck dissection & mastoidectomy
  • 66.
     Results fromprolifertion of basal epithelium  Seen in tragus , border of helix , meatal entrance  Later cases – whole auricle is involved , with underlying bone and parotid gland involvement.  First a flat painless slightly raised leision followed by the development of rolled edge with penetrating ulcer – bleeds readily  Treatment – Wide Excision  Advanced Stages – Wide Excision & radiotheraphy
  • 67.
     Nodular pigmentedleision which tends to enlarge rapidly and eventually to ulcerate  Regional L.N Involement & Diatant metastasis  Local Disease – Excision & Skin Graft  Large Tumours – Wedge (or) Wide Excision  Radical excision involves complete excision of pinna & and dissection of regional L.N  Prognosis is poor
  • 68.