Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

External auditory canal anatomy pathologies & management

8,591 views

Published on

eac anatomy pathologies & management

Published in: Health & Medicine
  • Hear The Angels Sing: Listen to this free musical composition to clear away all the negativity in your life and welcome in miracles! Download your complimentary "Angel Soundscape" now.  http://scamcb.com/manifmagic/pdf
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here
  • 12 Signs From The Universe When You Are On The...  http://t.cn/AiuvUCDd
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here
  • The Surprising Reason 11:11 Keeps Popping-Up: Free report reveals the Universe's secret "Sign Posts" that point the way to success, wealth and happiness. Claim your copy right now! ★★★ https://tinyurl.com/y6pnne55
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here
  • Don't fear hair loss - fight it! Try Profollica� natural two-step hair loss system for visible results you'll see and love! ➤➤ https://tinyurl.com/y49r9d8j
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here
  • The Only Holistic System In Existence That Will Show You How To Cure Your Acne, End The Breakouts, Regain Your Natural Inner Balance and Achieve The Lasting Clear Skin You Deserve! ◆◆◆ https://bit.ly/2xJfKi2
       Reply 
    Are you sure you want to  Yes  No
    Your message goes here

External auditory canal anatomy pathologies & management

  1. 1. Dr. vikas
  2. 2. External Auditory Canal  The supporting framework of the canal wall is cartilage in the lateral one-third and bone in the medial two-thirds.  Length of the canal is approximately 2.4 cm  The lateral cartilaginous portion is about 8 mm long and is continuous with the auricular cartilage.  The two or three variably present perforations in the anterior aspect of the cartilaginous canal are the fissures of Santorini.  The isthmus is the narrowest portion of the EAC, lies just medial to the junction of the bony and
  3. 3.  Cartilaginous part is directed upwards, backwards & medially while bony part is directed downwards, forwards & medially.  The canal is straightened by gently moving the auricle upwards and backwards to counteract the direction of the cartilaginous portion.  In the neonate, there is no bony external meatus as the tympanic bone is not yet developed.  The tympanic membrane is more horizontally placed so that the auricle must be gently drawn downwards and
  4. 4.  The medial border of the meatal cartilage is attached to the rim of the bony canal by fibrous bands.  The bony canal wall, about 1.6 mm long, is narrower than the cartilaginous portion and itself becomes smaller closer to the tympanic membrane.  The medial end of the bony canal is marked by a groove, the tympanic sulcus, which is absent superiorly. Although the tympanic bone makes up the greater part of the canal, and also carries the sulcus, the squamous bone forms the roof.  The tympanomastoid suture is a complex suture line between the anterior wall of the mastoid process and the tympanic bone.
  5. 5.  The external canal is lined with skin.  Body skin normally grows directly from the basal layers towards the surface where it is shed into the surroundings.  If this pattern of growth were to occur in the external ear canal then the canal would soon become filled with desquamated skin.  Instead of maturation taking place directly towards the surface, there is outward, oblique growth of the epidermis of the canal skin and pars flaccida so that the surface layers effectively migrate towards the external opening of the canal.
  6. 6. Atresia  Atresia is the absence of or closure of a passage of the body.  This includes both congenital and acquired lesions.  TOS defines acquired atresia of the external ear as 'intraluminal sequelae of either intraluminal or extraluminal processes of varying aetiology, resulting in a blind sac in the external acoustic meatus'. Epidemiology  1 in 10,000 to 15,000 births  Up to 50% of the time associated with some craniofacial syndrome  Unilateral : Bilateral, about 3:1  30% are bilateral  Atresia : Microtia, 7:1  Slightly more common on the right  Male : Female, 2:1
  7. 7. Atresia Aural atresia associated with craniofacial syndromes  Treacher Collins (Mandibulofacial Dysostosis)  Nager Syndrome (Acrofacial Dysostosis)  Cruzoun’s Craniofacial Dysostosis  Goldenhar’s Syndrome  Hemifacial Microsomia
  8. 8. Atresia Embryology – 7th Month  Canalization complete  Mastoid separation from mandible Normal posterior-inferior growth No mastoid growth Normal Atresia
  9. 9. Atresia Embryology  Mastoid growth affects the facial nerve position Normal 120o Curve Acute Curve in Atresia
  10. 10. Atresia
  11. 11. 11 12/11/2014
  12. 12. Classification of Deformities After Colman-3 types  Minor Aplasia-incomplete recanalization  Moderate Aplasia- the tympanic bone has developed but has failed to recanalize  Severe Aplasia-complete absence of the external canal
  13. 13. Atresia Severe Aplasia- Complete Atresia, no tympanic bone
  14. 14. Atresia Moderate Aplasia  The most common, solid mass of compact bone that has failed to recanalize
  15. 15. Atresia Minor Aplasia-partial recanalization  Middle space constricted, often with severe ossicular abnormalities
  16. 16. Radiological Evaluation  High resolution CT in coronal and axial planes  Axial to delineate malleus, incus and I-S joint and round window  Coronal to delineate stapes, oval window and vestibule  3-D CT of little help
  17. 17. Atresia Surgery  First attempt to surgically correct aural atresia was by Thomson in 1843  Shambaugh, 1967, recommended unilateral surgery only if the cochlear reserve allowed hearing to improve by 25dB  Jahrsdoerfer, 1978, first large series using the anterior approach
  18. 18. Surgical Considerations  Most consider repair in bilateral atresia  Many are reluctant to operate on unilateral cases  Not simply the hearing loss  Expectations of hearing recovery  Lifetime care of mastoid cavity  Potential risks to facial nerve and labyrinth  55-65% achieve 25 dB speech-hearing level
  19. 19. Surgical Considerations  Most surgeons choose the anterior approach to avoid the mastoid cavity  40% of patients with unilateral atresia are not surgical candidates such as those with severe aplasia as in Treacher Collins syndrome  Bilateral atresia- best ear by CT done as child approaches school age
  20. 20. Surgical Considerations Timing of surgery  Usually performed after age 6 or 7 years  This allows for microtia repair to be done first  Canal cholesteatoma in the stenotic ear usually develops in canals less than 2mm in diameter. If ear unfavorable, canalplasty alone is offered
  21. 21. Surgical Technique  Minor aplasia- canal widening and middle ear ossicular work with tympanoplasty  Moderate Aplasia  Mastoid or posterior approach  Anterior approach
  22. 22. Surgical Technique Anterior Approach  Middle ear approached through the atretic bone with a limited mastoid opening
  23. 23. Surgical Technique  The posterior wall of the glenoid fossa becomes the anterior wall of the new ear canal  The epitympanum is the first part of the middle ear encountered  Fused ossicles identified
  24. 24. Surgical Technique  Atretic bone removed at times with a curette  Globular mass separated from the stapes to avoid cochlear trauma  Course of facial nerve determined  Ossiculoplasty performed  Tympanic membrane grafted  Meatoplasty  Split thickness skin graft (.006-.008 inches) lines the canal
  25. 25. Surgical Technique  The Meatoplasty must be aligned with the newly created bony canal
  26. 26. Surgical Technique  3cm X 5cm split thickness skin graft  The graft is positioned in the canal and sewn to the meatal margin  Graft stabilized with Merocel wicks and hydrated with ear drops
  27. 27. MASTOID APPROACH  This employs a more posterior route to the middle ear cleft using the dura of the middle cranial fossa, the sigmoid sinus and sino dural angles as landmarks to the antrum with subsequent identification of the lateral semicircular canal (LSCC), atretic plate and the facial nerve.  The atretic plate is removed in a similar fashion, trying to centre the cavity on the stapes.  The aim is to create a stable, small, cavity lined with squamous epithelium.
  28. 28. Hearing Results  Post-op hearing level of 30 dB or better In 50- 75% of patients with moderate or severe aplasia  20 dB or better in 15-20%  Bellucci 20 dB in 50% @ 2 years  Schuknect similar results at 1.3 years  De La Cruz 56 patients 53% @ 20 dB at 6 mo.  Lambert early 60% @25 dB, 46% >1 yr.
  29. 29. Alternatives to Surgery  Bone anchored hearing aid (BAHA)
  30. 30. Surgical Complications  Persistent or recurrent conductive hearing loss  Lateralization of graft  Scar tissue  SNHL  VIIth Nerve injury  30 % revision rate  Re-stenosis  Graft migration  Inadequate hearing  Chronic cavity infection
  31. 31. Acquired atresia of the external ear
  32. 32.  Atresias may be solid or membranous.  Solid atresia consists of a continuous block of either fibrous or fibrous & bony material which is continuous with the structure of the tympanic membrane and is of variable extent. Solid atresia, obliterating the medial aspect of the bony external ear canal. Extensive funnel-shaped solid atresia.
  33. 33.  Membranous atresia is typified by fibrous tissue that has a covering of ear canal skin on both sides, thus separating the ear canal into a medial and lateral segment.  The medial part inevitably collects keratin from desquamation of the skin; this may become an erosive process and thus be defined as an external auditory canal cholesteatoma. Membranous atresia in lateral external auditory meatus.
  34. 34. Diagnosis  The clinical diagnosis of acquired atresia is supported by the use of computed tomography (CT) scanning  It particularly helps in the differentiation of solid and membranous atresia.  Solid atresia is a safe form of ear disease.  Membranous atresia will inevitably produce associated cholesteatoma and therefore erosion of local structure.  Surgical outcome is superior to solid atresia.
  35. 35. AETIOLOGY Inflammation - otitis externa; - psoriasis, eczema and other dermatological conditions; - active chronic otitis media; - Trauma - burns, (thermal, chemical, electrical or post-irradiation) Surgery –  any operation involving a meatal approach (tympanoplasty, etc,)
  36. 36. Pathogenesis SOLID ATRESIA  In cases associated with otitis externa or media the key development is of granular medial otitis externa with granulations of the tympanic membrane that persist for many months in spite of treatment.  The granulations become fibrotic and the eardrum thickens as the medial meatal mass is re-epitheliazed.  principle complaint is of conductive hearing loss. MEMBRANOUS ATRESIA  This originates in the lateral meatus as a web formation, which is precipitated by a circular irritation from inflammation, trauma or burns and ulceration of the skin around the entire circumference of the external ear canal.  The web-like stenosis forms after fibrosis and re-epitheliazation as with solid atresias.  Associated with medial cholesteatoma, which can potentially produce local erosion and complications.
  37. 37. MANAGEMENT OPTIONS Medical  During the wet phase, the medial granulations can be removed by aspiration and cauterization with silver nitrate or trichloroacetic acid, and the ear packed with ribbon gauze or a wick.  This local treatment may result in a change to the dry phase and prevent further progression of the atresia.  The conductive hearing impairment (if bilateral) may be managed by hearing aid.
  38. 38. Surgery FIBROUS ATRESIA  The principle of surgery in fibrous atresia is to remove the fibrous tissue by elevating it from the ear canal bone, the fibrous annulus and lamina propria of the tympanic membrane.  A circumferential incision is made lateral to the blunt face of the atretic plate and a plane of dissection developed between the bone of the ear canal and the canal skin, followed by the atretic plate and, finally, lateral to the fibrous annulus and lamina propria of the tympanic membrane.  The epithelial defect is repaired by a fine split skin graft which can be laid in single or multiple pieces.  A silastic disc or tube may be inserted to stabilize the epithelial surface. Finally, the ear canal is packed with ribbon gauze soaked in antiseptic.
  39. 39. MEMBRANOUS ATRESIA  Similar to fibrous atresia, membranous atresia can be approached transcanal using an ear speculum.  If the fibrous lesion is very thick a retroauricular approach may be superior, allowing preservation of the lateral and medial epithelial coverings to aid repair of the ear canal skin.  The whole lesion is excised with sacrifice of the minimum of surrounding epithelium.  Silastic sheets are overlaid, holding the lateral and medial skin edges against the bone of the ear canal.
  40. 40. Pathological conditions
  41. 41. Furunculosis  Localized form of otitis externa resulting from infection of a single hair follicle.  Hair follicles are only present in the lateral (cartilaginous) segment of the external auditory canal.  Furunculosis is, therefore, confined to the lateral canal.  Bacterial invasion of a single hair follicle results initially in a well-circumscribed deep skin infection.  As the infection progresses a pustule forms and this progresses to local abscess formation, often with considerable associated cellulitis and oedema.
  42. 42. Furunculosis Furuncle of the external auditory canal. Localized rather than generalized oedema of otitis externa.  The affected ear is extremely painful, feels blocked and exudes a scanty serosanguinous discharge.  The pinna and tragus are tender on palpation.  Otoscopic examination usually establishes the diagnosis
  43. 43.  Characteristically, the oedema and inflammation is restricted to the lateral segment of the canal, with relative sparing of the medial canal and an unaffected tympanic membrane.  If the infection is advanced, the abscess may be seen to be pointing into the canal or have discharged already.  If the oedema and secondary cellulitis spreads to the post -auricular crease, the condition may be mistaken for acute mastoiditis.
  44. 44. AETIOLOGY AND EPIDEMIOLOGY  Staphylococcus aureus is the most common organism causing furunculosis.  Leukocidal toxins of S. aureus trigger lysis of phagocytic cells and may have an important role in cutaneous infection.  Local risk factors include heat, humidity, trauma, maceration.  Recurrent furunculosis presents as repeated episodes of infection at multiple sites.  Conditions associated with recurrent furunculosis include hypogammaglobulinaemia, diabetes mellitus and dysphagocytosis.
  45. 45. OUTCOMES  If untreated, the infection usually progresses to a localized abscess which then discharges into the external ear canal.  With adequate drainage the infection will resolve spontaneously.  The infection can also spread towards the deeper tissues, where it may cause a diffuse soft tissue infection spreading to the pinna, post-auricular skin and parotid gland.  Repeated infection can cause permanent scarring and fibrosis of the external canal with subsequent meatal stenosis.
  46. 46. MANAGEMENT  Furunculosis of the external canal is exquisitely painful and appropriate analgesics should be offered to all patients.  Treatment choices include:  oral or systemic antistaphylococcal antibiotics (penicillinase-resistant penicillin, macrolide, cephalosporin, clindamycin or quinolone);  topical treatment (antibiotics, astringents, hygroscopic dehydrating agents);  incision and drainage.
  47. 47. MANAGEMENT OPTIONS  Oral antibiotic treatment is recommended in the early stages of the disease.  Severe spreading soft tissue infection should be treated with intravenous antibiotic therapy.  Abscess formation is an indication for drainage.  After the abscess has discharged, surgically or spontaneously, topical treatment is preferable.  Topical antibiotics are prescribed.  Insertion of a wick into the ear canal facilitates treatment in the presence of severe canal oedema and narrowing.
  48. 48.  Glycerol and ichthammol solution has a specific antistaphylococcal action and is hygroscopic, thus causing dehydration of the canal tissue. Aluminium acetate solution is an astringent as well as a hygroscopic agent.  Options include:  eradication therapy with nasal mupirocin;  eradication therapy with oral flucloxacillin for 14 days;  bacterial interference therapy:  Deliberately implanting a nonpathogenic strain of S. aureus(strain S02A is the most popular) to recolonize the nares and skin.
  49. 49. BuIlous myringitis  Bullous myringitis (myringitis bullosa haemorrhagica) is the finding of vesicles in the superficial layer of the tympanic membrane. PATHOLOLOGY  The vesicles occur between the outer epithelium and the lamina propria of the tympanic membrane.
  50. 50. AETIOLOGY  Cultures from aspirates of the vesicles and middle ear fluid are similar to that in acute otitis media.  An infection by influenza virus or by Mycoplasma pneumoniae has been suggested as the aetiological agent but no evidence for this, other than circumstantial, has been presented.  Bullous myringitis occurs in all age groups but children, adolescents and young adults are more frequently affected
  51. 51. SYMPTOMS  Sudden onset of severe, usually unilateral, often throbbing pain in the ear is the most common presentation?  The symptoms usually set in during or following an upper respiratory tract infection.  A blood stained discharge can be present for a couple of hours.  Hearing impairment (conductive and/or sensorineural) is common in the affected ear.
  52. 52. SIGNS  Otoscopy reveals blood-filled, serous or serosanginous blisters involving the tympanic membrane and sometimes the medial aspect of the ear canal.  A serosanginous secretion can be seen if the blisters rupture.  The tympanic membrane is intact.  In young children with bullous myringitis, middle ear fluid was present in the majority (97 percent) but is an uncommon finding in other age groups.  The site of the sensorineural hearing loss is the cochlea; however, the‘ pathogenic base is not understood.
  53. 53. DIAGNOSIS  The clinical entity, bullous myringitis is based on physical examination. Vesicles in the superficial layer of the tympanic membrane are present.  The main differential diagnoses are acute otitis media or herpes zoster oticus. Bullae on the tympanic membrane
  54. 54. Investigations  Inspection of the ear using a microscope is essential for diagnosis. Pneumatic otoscopy and tympanometry help determine whether the middle ear contains fluid.  Pure-tone audiogram including bone conduction thresholds is essential for detection of sensorineural hearing impairment.  A serologic sample for herpes zoster is of value in cases with sensorineural hearing loss and may be of help in the differential diagnosis.
  55. 55. MANAGEMENT OPTIONS  In cases without middle ear affection and without sensorineural hearing loss, only analgesics are recommended.  When the middle ear is affected, antibiotics can be used as in the treatment of acute otitis media.  In children less than two years of age, acute bullous myringitis should be treated as acute otitis media.  Antibiotics have also been recommended in cases with sensorineural hearing impairment. Effect of management  Spontaneous resolution of the blisters and middle ear effusion.  Complete recovery of the sensorineural impairment within three months occurred in between 60 and 100 percent of affected patients treated with amoxicillin.
  56. 56. Granular myringitis DEFINITION  Characterized by granulation tissue on the lateral aspect of the tympanic membrane with possible involvement of the external ear canal  Some authors have suggested there are two distinct entities:  Myringitis externa granulosa- has granulations on the lateral surface of the drum and the medial part of the ear canal skin.  Granular myringitis- only involves the eardrum.
  57. 57. PATHOLOGY  Microscopic examination shows oedematous granulation tissue with capillaries and diffuse infiltration of chronic inflammatory cells.  Large areas of the granulation tissue have no covering epithelium.  It has been suggested that a non-specific injury involving the lamina propria of the tympanic membrane suppresses epithelialization which leads to the development of granulation tissue.
  58. 58. AETIOLOGY  The incidence of granular myringitis is not related to sex, age, systemic disease or season,  High-ambient temperature, swimming, lack of hygiene, local irritants and foreign bodies have all been suggested as causative factors.  bacterial and sometimes fungal infection is present in the affected ear.  Granular myringitis is also occasionally seen as a postoperative complication of tympanic membrane grafting.  An incidence of up to 5 percent has been reported and the use of tympanic homo grafts seems to result in a higher incidence (8 percent).
  59. 59. SYMPTOMS  The dominant symptom is a foul-smelling discharge from the affected ear.  There is usually little or no pain.  Some individuals have a sensation of fullness or irritation in the ear.  The hearing is either not at all or only slightly impaired.  Associated tinnitus is uncommon.  Some patients can be asymptomatic
  60. 60. SIGNS  Purulent secretion is seen in the affected ear.  The tympanic membrane is covered with secretions that sometimes crust.  After aural toilet the granulation tissue is revealed.  There seems to be a localized and a diffuse form of granular myringitis.  The localized form is most common, in that small areas of the drum are affected or one or more polyps are present.  Most commonly, the granulations are situated posterosuperior on the eardrum and may affect the adjacent canal wall.  A slightly raised carpet of granulations, which covers the tympanic membrane, is seen in the diffuse form.  Perforation of the tympanic membrane is not present
  61. 61. Right granular myringitis. (a) There is pus in the canal but the pars tensa appears intact. However, there is granulation tissue arising from it posteriorly extending on to the adjacent canal wall. The intactness of the pars tensa can be confirmed by pneumatic otoscopy or tympanometry. (b) The ear is active, there being pus in the canal and granulation
  62. 62. DIAGNOSIS  In granular myringitis a discharge from the ear is present.  Inflammation and granulation tissue are seen on the lateral aspect of the tympanic membrane with possible involvement of the external ear canal.  Differential diagnoses are-  chronic (suppurative) otitis media  diffuse external otitis.  Most cases can readily be differentiated by the normal movement of the tympanic membrane on pneumatic otoscopy and no signs of an inflammatory reaction in the lateral ear canal.  The lack of a conductive hearing impairment and a normal computed tomography (CT) scan excludes chronic otitis media.
  63. 63. Investigations  Inspection of the ear using a microscope is essential for diagnosis and treatment.  Pneumatic otoscopy and tympanometry -to confirm that the middle ear is normal and no perforation is present.  Pure-tone audiometry - to exclude a conductive hearing impairment due to chronic otitis media.  Culture for bacteria as well as for fungi is important in detecting the pathogens if conservative treatment with ear drops fails.  Gram-negative bacteria (Pseudomonas aeruginosa, Proteus species and Staphylococcus aureus) and Candida albicans are most commonly Cultured.  The bacterial culture does not differ from specimens found in external otitis and chronic otitis media.  HRCT scan can help exclude chronic otitis media.  biopsy for histological examination should be carried out to exclude carcinoma. If the granulations do not resolve with treatment,
  64. 64. OUTCOMES, NATURAL HISTORY AND COMPLICATIONS  Granular myringitis has a chronic course and granulations may continue to grow slowly for years; however, healing may happen spontaneously.  The inflammation in the epithelial layer and lamina propria of the tympanic membrane sometimes leads to replacement with proliferating granulation tissue, fibrosis and an atresia forming from the medial part of the ear canal.  When the fibrosis and atresia has extended laterally, the atresia ceases to grow.
  65. 65. MANAGEMENT OPTIONS
  66. 66. Benign necrotizing otitis externa  Idiopathic necrosis of a localized area of bone of the tympanic ring, with secondary inflammation of the overlying soft tissue and skin. There are a number of synonyms for the condition:  benign necrotizing otitis externa;  benign necrotizing osteitis of the external auditorymeatus canal;  benign osteonecrosis of the external auditory meatus;  aseptic necrosis of the external auditory meatus;  idiopathic tympanic bone necrosis;  necrosis and sequestration of the tympanic bone;  necrosis and sequestration of the tympanic part of the temporal bone;  focal or circumscribed osteonecrosis of the external auditory
  67. 67. PATHOLOGY  The pathology is nonspecific.  The characteristic necrotic sequestrum of bone appears to involve the superficial cortical layer primarily or exclusively.  Histology of the bone reveals dead lamellar bone with inflammatory cells filling the marrow spaces.  Usually there are very limited and mild inflammatory changes of the adjacent skin and soft tissue (subcutaneous tissue) of the external auditory meatus.  Apart from the normal skin flora a wide range of bacteria may be cultured, with Staphylococcus aureus being the most frequent isolate.
  68. 68. AETIOLOGY  The cause of this condition is unknown.  Suggested etiologies include-  vascular insufficiency because of its relatively poor blood supply  The micro angiopathy of diabetes  Small arterial emboli have been suggested.  Repeated local trauma is a popular theory, for example ear bud abuse, picking of the ear or the use of hearing aids.  Aassociation with respiratory tract inflammatory conditions
  69. 69. DIAGNOSIS History  The symptoms are characteristic of mild local inflammation with perhaps pruritis, otorrhea or otalgia.  Exclude underlying conditions such as previous radiotherapy, diabetes mellitus or systemic disease with depression of the immune system.  There should also not be persistent deep boring otalgia, suggestive of malignant otitis externa. Examination  The condition is diagnosed clinically by the characteristic positive findings of a small area of deficient skin and soft tissue in the external auditory meatus revealing a segment of necrotic superficial bone.  The condition is usually unilateral.
  70. 70.  Clinical examination should exclude the characteristic granuloma and evidence of deep osteitis of the temporal bone, such as cranial nerve palsies, found in malignant otitis externa.  There should be no evidence of an exophytic tumour and no obstructive collection of keratin debris expanding the canal as found in keratosis obturans.  The bony necrosis is usually limited
  71. 71. Diffrential diagnosis  (a) Normal external auditory canal.  (b) Benign necrotizing otitis externa. There is deficient area of skin, and bony sequestrum.  (c) Canal cholesteatoma. A sac of canal skin invades bone.  (d) Keratosis obturans. The bony canal is 'ballooned' out.  Of these, the condition most similar to benign necrotizing otitis externa is canal cholesteatoma, the only real difference being the absence of a lining of
  72. 72. Investigations  These are seldom indicated.  If gross infection is present a pus swab may be taken. Should Pseudomonas be cultured, the diagnosis should be queried in favour of malignant otitis externa,  Computed tomography may be indicated in order to identify the extent of bone necrosis.  If prominent inflammatory or granulation tissue coexists, chronic 'granulomatous' conditions including syphilis and tuberculosis should be excluded.  Exophytic lesions in the ear canal may require brush cytology and biopsy to exclude neoplastic conditions.  Audiometry should be normal unless debris in the external canal causes a mild conductive hearing impairment.
  73. 73. OUTCOMES. INCLUDING NATURAL HISTORY AND COMPLICATIONS  Separation of the sequestrum, followed by epithial growth to cover the bony defect, as encouraged by conservative management, is the most likely outcome.  Canal cholesteatoma might be a consequence of benign necrotizing otitis externa.  Once there is an area of necrotic bone, squamous epithelium might grow from the ulcer margins, under the sequestrum, in an attempt to demarcate the sequestrum.
  74. 74. MANAGEMENT OPTIONS  Traditional conservative management consists of removing the bony sequestrum once it separates spontaneously with local toilet and local treatment to control any infection.  An oral antibiotic may be used.  A more aggressive surgical approach has been advocated, with early surgical removal of them sequestrum down to healthy bone.  Adjunctive hyperbaric oxygen may be considered when there is progression despite intensive local and systemic treatment and when there is necrosis beyond the tympanic plate.
  75. 75. Malignant otitis externa DEFINITION  Malignant otitis externa is an aggressive and potentially life-threatening infection of the soft tissues of the external ear and surrounding structures, quickly spreading to involve the periostium and bone of the skull base. NOMENCLATURE  Also called 'skull base osteomyelitis' and 'necrotizing external otitis'  It has been suggested that  necrotizing external otitis should be used for aggressive soft tissue infection in the absence of bony involvement  skull base osteomyelitis be used for the condition once bone infection is confirmed.  Malignant otitis externa is a misnomer as it is not a neoplastic process
  76. 76. STAGING Stage 1 Clinical evidence of malignant otitis externa with infection of soft tissues beyond the external auditory canal, but negative Tc-99 bone scan 2 Soft tissue infection beyond external auditory canal with positive Tc-99 bone scan 3 As above, but with cranial nerve paralysis 3a Single 3b Multiple 4 Meningitis, empyema, sinus thrombosis or brain abscess
  77. 77. PATHOLOGY  Malignant otitis externa is the end -stage of a severe infection thatoriginates from the external auditory canal and progresses through cellulitis, chondritis, periostitis, osteitis and finally osteomyelitis.  Infection is thought to spread out of the cartilaginous external auditory canal through the fissures of Santorini, congenital defects in the floor of the external auditory canal.  Malignant otitis externa mainly affects the Haversian system of compact bone and involvement of the pneumatized portion of the temporal bone is a late finding.  The otic capsule is usually spared
  78. 78. Predisposing factors  Elderly diabetic (both type I and type II) patients  impaired host response to Pseudomonas  microangiopathy in diabetic tissues, exacerbated by the vasculitic properties of Pseudomonas.  The cerumen in diabetic patients is also of a higher pH than that of normal controls, which may reduce the bactericidal properties of their cerumen.  Non-diabetics accounted for almost a third of one large series.  Children more commonly have a facial nerve palsy and involvement of the middle ear.  Other causes of immunocompromise, especially conditions that affect cell-mediated immunity (e.g. AIDS), can also predispose to malignant otitis externa
  79. 79. DIAGNOSIS  Malignant otitis externa is a clinical diagnosis made on the basis of pain, exudate, granulations and oedema of the external auditory canal , often supported by a positive bone scan and/or the presence of microabscesses at surgery.  The combination of pain, granulations, otorrhea and resistance to local therapy for at least eight to ten days are highly sensitive for making a diagnosis of malignant otitis externa.  Diabetes or other immunocompromised state, Pseudomonas aeruginosa onculture, a positive bone scan and cranial nerve palsy are confirmatory factors that enhance the specificity of the diagnosis.  The erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels are nonspecific measures of inflammation that are significantly raised in untreated cases.  The ESR is often over 100 mm/hour. Malignant otitis externa with granulations of the floor of the right external auditory canal
  80. 80. RADIOLOGY  Technetium (Tc-99m) radio nuclide bone scans will detect bony involvement even before high-resolution computed tomography (CT) scans can demonstrate bone destruction.  As the isotope is absorbed by osteoclasts and osteoblasts that continue remodelling after the infection has resolved, the scan may remain positive for up to nine months.  As such, Tc-99m is only useful for detecting initial bony involvement.  Gallium (Ga-67) is absorbed by leukocytes and is a more sensitive monitor of infection.  The scan quickly returns to normal after the infection has resolved and as such, is a good measure to ascertain when to terminate treatment.  In recent years, magnetic resonance imaging (MRI) has added much to the management of this infection.  Increased signal in the soft tissues beneath the skull base as a result of inflammation does much to establish the extent of the disease. In addition, it
  81. 81. MANAGEMENT OPTIONS Aural toilet  Local toilet to the external auditory canal is essential to control the granulations and improve local pain control.  The use of topical antibiotics is controversial.  They are likely to alter the microbiological flora of the external auditory canal and prevent adequate culture and sensitivities at a future date Systemic antibiotics  The treatment of choice for the management of malignant otitis externa is systemic anti-Pseudomonas antibiotics.  The drug often needs to be given for at least six weeks and in advanced cases, several months.  These are often given initially, with transition to oral antibiotics once the CRP and ESR start to fall. Hyperbaric oxygen
  82. 82. MANAGEMENT OPTIONS Surgery  There is now widespread agreement that surgical intervention for malignant otitis externa should be reserved for a few selected cases and no longer has the goal of removing all the infected tissue.  Surgery for the removal of sequestra, collections of pus and debridement of necrotized and granulating tissues can be beneficial,but should only be used if the patient is deteriorating clinically and if definable surgical goals can be easily achieved.
  83. 83. Keratosis obturans and primary auditory canal cholesteatoma  Keratotis obturans is the accumulation of a large plug of desquaminated keratin in the external auditory meatus, while primary auditory canal cholseteatoma is the invasion of squamous tissue from the ear into a localized area of bony erosion. The keratoma has been removed from the right ear with keratosis obturans and shows expansion of the bony canal just lateral to the tympanic membrane
  84. 84. Comparison of keratosis obturans and primary auditory canal cholesteatoma. keratosis obturans primary auditory canal cholesteatoma Aetiology Abnormal epithelial migration. Abnormal bone leading to migration of epithelium into this bone Clinical symptoms and findings Severe otalgia Conductive hearing loss Younger ages Occasionally bilateral Association with lung and sinus disease Can present with a plugged feeling Otorrhoea Normal hearing Itchiness or pain Older populations Usually unilateral Pathology Keratin plug occluding canal Tympanic membrane thickened Ear canal ballooned Hyperaemia of canal skin sometimes with granulations Keratin in random pattern Tympanic membrane normal Localized osteitis/erosion of ear canal usually Posterioinferior Sequestration of bone Treatment Removal of plug Local treatments of granulations Biopsy May need continued cleanings Surgically remove cholesteatoma and abnormal bone Graft with fascia Biopsy Differential diagnosis Wax impaction with infection Neoplastic disease Necrotizing otitis externa Benign sequestrum Neoplastic disease
  85. 85. Otitis externa  Otitis externa is a generalized condition of the skin of the external auditory canal that is characterized by general oedema and erythema associated with itchy discomfort and usually an ear discharge. Predisposing factors for otitis externa Type Factor Anatomical Narrow external auditory meatus Obstruction of normal meatus DermatologicaI Eczema, sebhorrhoeic dermatitis Allergic Atopy, nonatopic allergy, exposure to topical medications Physiological Humid environment, immunocompromisation Traumatic Skin maceration (bathing), ear probing, laceration, radiotherapy Microbiological Active chronic otitis media, exposure to P. Aeruginosa (50-65%) or fungi
  86. 86. PATHOLOGY  pre-inflammatory stage-protective lipid/acid balance (normal pH 4-5) of the ear is lost  acute inflammatory stage-progressively thickening exudate, further oedema, obliteration of the lumen and increasing pain.  chronic inflammatory-thickening of the external canal skin and fibrous canal stenosis
  87. 87. DIAGNOSIS clinical diagnosis based on the following symptoms and signs: pain, itch, oedema and erythema of the external auditory canal with purulent otorrhoea and debris in the meatus Debris and inflammation in the left external auditory meatus. After removal of debris, the swollen oedematous canal skin of otitis externa can be seen
  88. 88. MANAGEMENT OPTIONS  Aural toilet-most effective single treatment for otitis externa  Topical medication-  Steroid-antibiotic medication in the form of drops or sprays  Glycerol and ichthammol (90:10 percent) aural wick (dehydrating and antiinflammatory properties and antibacterial activity)  Systemic antibiotics Prevention of recurrence-  avoidance of water penetration into the ear (Cotton wool with petroleum jelly)
  89. 89. Otomycosis  Otomycosis accounts for approximately 10 percent of all cases.  More common in hot, humid climates  Often secondary to prolonged treatment with topical antibiotics.  Diabetes and immunocompromised states also predispose to the condition.
  90. 90. Otomycosis with Aspergillus niger. •Aspergillus accounts for 80-90 percent of cases •Candida being responsible for the remaining 10-20 percent. CLINICAL FINDINGS •The most common finding is black, grey, green, yellow or white discharge with debris that is often said to resemble wet newspaper. •Sometimes debris is seen with visible fungal hyphae
  91. 91. MANAGEMENT  Treatment is aural toilet and removal of the debris and topical antifungal drops,  In cases of resistant otomycosis, it is essential to exclude fungal infection elsewhere, including athelete's foot.  The 'foot and ear’ dermatophytid reaction can occur from a fungal infection in a remote location.  Immunotherapy with dermatophyte Trichophyton , Oidiomycetes and Epidermophyton (TOE) extracts and dust mite, is the treatment of choice.
  92. 92. Exostoses and Osteoma  External auditory exostoses and osteomas are benign clinical entities characterized by hyperplastic growth of bone in the osseous EAC.  Both types of lesions are most commonly noted incidentally in asymptomatic patients.  However,as EAC obstruction worsens, symptoms of chronic debris trapping, recurrent otitis externa, and hearing loss develop.
  93. 93. Exostoses Osteomas  Bilateral & multiple  Non-neoplastic bony outgrowth  Broadly based protrusions originating from the anterior and posterior canal walls  Lacks fibrovascular channels  EAC obstruction seen.  Associated with cold water exposure  More often unilateral,  Benign slow growing tumor  Pedunculated growth located at suture lines  Fibrovascular channels are present  lesser degrees of EAC obstruction.  Etiology is unknown
  94. 94. Multiple exostosis osteoma
  95. 95. DIAGNOSIS  characteristic otoscopic appearances of multiple and usually bilateral sessile, hemispherical, bony swellings arising deep in the external auditory canal, adjacent to the tympanic membrane.  In the presence of a tight stenosis of the deep ear canal, a high resolution computed tomography (CT) scan will help differentiate large exostoses from other causes of stenosis, such as chronic otitis externa.  A scan will also demonstrate complications, such as a canal cholesteatoma, developing medial to the exostoses.
  96. 96. MANAGEMENT  Treatment is usually unnecessary in small exostoses,  but advice to avoid further cold water exposure may be appropriate  Management of exostoses and osteomas consists of periodic cerumen disimpaction and débridement and treatment of infection as necessary.  In cases refractory to medical treatment, a meatoplasty operation may be necessary.
  97. 97. Foreign bodies in the ear •Consider the nature of the foreign body when choosing management options Type of foreign body Method of removal Living insects First kill with oil Irregular/graspable objects Remove with crocodile forceps organic/vegetabIe Do not syringe Button batteries Do not syringe Round, hard, smooth, non-graspable Syringe/remove with wax hook/removal under anaesthetic
  98. 98.  Inexpert or ill-advised attempts at removal may cause serious complications such as canal lacerations, tympanic membrane perforations and ossicular fractures or dislocations.  Firmly impacted foreign bodies medial to the isthmus may warrant removal in theatre and may
  99. 99. Herpes zoster oticus DEFINITION  Herpes zoster oticus is defined as a herpetic vesicular rash on the concha, external auditory canal or pinna with a lower motor neurone palsy of the ipsilateral facial nerve PATHOLOGY  The disease is a reactivated varicella zoster infection from dormant viral particles resident in the geniculate ganglion of the facial nerve and the spiral and vestibular ganglia of the VIIIth nerve. Diagnosis is clinical  hearing loss, tinnitus and/or vertigo
  100. 100. MANAGEMENT  Improved outcomes obtained if commenced on acyclovir and prednisolone within three days of the onset of symptoms. Haemorrhagic vesicle in the right external auditory canal in herpes zoster oticus
  101. 101. THANK YOU

×