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Management of complications of acute otitis media


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acute otitis media, complications , facial nerve palsy ,extradural abscess , meningitis , subdural abscess , brain abscess , labyrinthitis ,MASTOIDITIS , diagnosis , C T scan , M R I , management ,

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Management of complications of acute otitis media

  1. 1. Management of Complications of Acute Otitis MediaDr . Ibrahim Habib Barakat M.D.Otorhinolaryngology
  2. 2. 2To my family
  3. 3. 4 Anatomy ofthe middle ear cavity
  4. 4. 5Anatomy of the middle ear cavity• Site : inside the petrous part of the temporal bone.• Shape: small biconcave box.• Surfaces: roof, floor & 4 walls: ant., post., medial &lat.
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  7. 7. 8 Middle ear cleft, Tympanum• The middle ear cleft includes the tympanum (middle ear cavity proper), the eustachean tube, and the mastoid air cell system. The tympanic cavity is an air filled irregular space contained within the temporal bone. It also contains the three auditory ossicles (malleus, incus and stapes) along with their attached muscles. For the purpose of description the tympanic cavity may be considered as a box with four walls, a roof and a floor. The corners of this hypothetical box is not sharp.
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  10. 10. 11 Surfaces of the middle earRoof (tegmental Formed by thin plate of bone called « tegmen tympani »wall) It separates the middle ear cavity from the temporal lobe in the middle cranial fossaThe floor Formed by thin plate of bone called « jugular wall » Separates the middle ear cavity from jugular fossa containing the sup.bulb of the I.J.V. It is pierced by the tympanic branch of glussopharryngeal nerve.Lateral wall Formed mainly by the ear drumAnterior wall Contains the following structures (arranged from above downwards): 1. The opening for the canal of tensor tympani m 2. The opening for Eustachian tube. 3. A plate of bone separating the middle ear from the I.C.A in the carotid canal.
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  12. 12. 13 Surfaces of the middle earMedial wall Separates the middle ear cavity from the internal ear & shows the following features: 1. A well marked rounded bulge « Promontary » which is produced by the first turn of the cochlea of the inner ear. 2. Oval window: above and behind the promontary. It is closed by the foot of the stapes & leads to the vestibule of internal ear. 3. Rounded window: lies below & behind the promontry & is closed by 2ry tympanic membrane. 4. The horizontal part of facial canal :arching above the promontary & oval window.
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  14. 14. 15Surfaces of the middle earPosterior Contains the following structureswall (arranged from above downwards): 1.The aditus ( opening ) leading to the mastoid antrum 2.The pyramid: a hollow conical process containing the stapedius m. 3. The vertical part of the facial canal ( for facial n.) med. To the aditus.
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  16. 16. 17 Contents of middle ear1. 3 ossicles : malleus, incus & stapes.2. 2 muscles: stapedius & tensor tympani.3. 2 nerves: chorda tympani & tympanic plexus.4. Air.
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  20. 20. 21Figure showing malleus and its articular facets
  21. 21. 22Figure showing incus and its articular facets
  22. 22. 23Figure showing stapes bone
  23. 23. 24 Arterial supply1. Ant. Tympanic a ( branch of maxillary a.)2. Post. Tympanic a ( branch of post. Auric a.)3. Superior tympanic a (branch of middle meningeal a.)4. Inf. tympanic a. (from asc. Pharyngeal a.)
  24. 24. 25 Lymphatic drainage• The lymphatics of the middle ear & mastoid antrum drain into parotid LNs & upper deep cervical LNs.
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  26. 26. 27Middle ear functions
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  29. 29. ‫( ومه آَاجه اوك جسي األزض خاشعة فإذا أوزلىا علُها الماء اهحزت وزبث إن الرٌ‬‫أحُاها لمحًُ المىجً اوه علً كل شٍء قدَس) – فصلت : 93.‬
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  34. 34. ‫{ لخلق السمىات واألزض اكبس مه خلق الىاس ولكه أكثس الىاس ال َعلمىن }‬ ‫غافر : 75‬
  35. 35. 36 Complications of A.O.M.• Def. spreading of infection beyond the confines of pneumatized spaces and the attendant mucosa of middle ear
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  37. 37. 38 AuralComplications of A.O.M.Aural complications :1- mastoiditis .2-labyrinthitis .3- petrositis .4- facial paralysis .
  38. 38. 39Intracranial complications1- extradural abscess or granulation tissue .2- dural venous sinus thrompophlebitis .3- brain abcess .4- otitic hydrocephalus .5- subdural abscess .6- meningitis .
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  40. 40. 41Extradural complications:. Extradural abscess. Meningitis. Sigmoid sinus thrombosis
  41. 41. 42 Intradural complications:. Subdural abscess. Brain abscess. Otitic hydrocephalus
  42. 42. 43Intratemporal complications:. Facial palsy. Labyrinthitis. Petrositis. Subperiosteal abscess. Internal carotid artery aneurysm
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  44. 44. 45 Extratemporal complications :• . Subclavian vein thrombosis• . Lucs abscess• . Citellis abscess• . Bezolds abscess
  45. 45. 46Route of spread of infection from the ear:1- extension through bone :demineralised during acute infections, cholesteatoma, chronic disease of the ear..2. Spread through venous channels:Thrombophlebitis from the lateral sinus mayspread to the cerebellum, and from the superiorpetrosal sinus may spread to the temproral lobeof the brain.
  46. 46. 473. Spread through oval / round windows.Spread may also occur through thecochlear and vestibular aqueducts.Certain areas may have dehiscent bone i.e.bony covering of the jugular bulb,dehiscent areas in the tegmen tympani,and dehiscent suture lines of the temporalbone.
  47. 47. 484. Spread may occur through trauma,(accident, surgical) or by erosion due toneoplasia.5. Spread may occur through surgicaldefects as caused by fenestration of theoval window during stapedectomyprocedures.6. Spread may occur directly into the braintissue through the peri arteriolar spaces ofVirchow Robin.
  48. 48. 49Diagramatic representation showing the various routes of spread of infection from the middle ear cavity.
  49. 49. 50Factors that determine the spreadof infection:I. Patient attributes: Patients generalcondition andimmunologic statusII. Bacterial attributesthe virulence of the infecting organism Forexample acute infections caused by Strep.pneumoniae type III, and H. Influenza type Bhave immense potential to spread.
  50. 50. 51 Etiology and pathogenesis1- streptococcus pneumoniae .2- haemophilus influnzae3- pseudomonas .
  51. 51. 52Otoscopic examination
  52. 52. 54Congested bulged eardrum ( impending rupture )
  53. 53. 55Signs and symptoms of impending complications1- persistent acute infection for two weeks .2- recurrent symptoms of infection within two weeks .3- acute , fetid exacerbation of chronic infection .4- fetid discharge during treatment .5- H . Influnzae , type B , or anaerobes cultured from the ear .6- fever in the presence of a chronically perforated tympanic membrane with or without cholesteatoma .
  54. 54. 56Severe earache Otoscopic examination
  55. 55. 57Acute otitis media with bulged eardrum
  56. 56. 58Left ear discharge in a case of complicated otitis media
  57. 57. 59Aural swab for culture and sensetivity
  58. 58. 60 The most obvious complications1- facial paralysis .2- labyrinyhitis .3- meningitis .4- mastoiditis with subperiosteal abscess .
  59. 59. 62clinical presentation of complications of acute otitis media
  60. 60. 63Facial nerve paralysis
  61. 61. 64Clinical presentation of facial paralysis - If it occurs due to A.O.M. usually the only complication . - if it occurs due to cholesteatoma , horrizontal scc fistulae may exist .
  62. 62. 65Acute otitis media complicated with right facial paralysis
  63. 63. 66labyrinthitis
  64. 64. 67Clinical presentation of labyrinthitis 1- ipsilateral SNHL . 2- Nystagmus , towards contralateral side . 3- vertigo .
  65. 65. 68 Classifications of labyrinthitis serous suppurative chronicCause toxins bacteria cholesteatomaHearing Preserve destroy all Preserved Hearing some hearing hearingAssociated Isolated meningitis ±SSC horizontalComplications Complica - (H) fistulae tion ± dehiscence of Fallopian canal ±facial paralysis
  66. 66. 69meningitis
  67. 67. 70Clinical presentation of meningitisCauses1- in A.O.M. , haematogenous dissemination .2- In C.S.O.M. , dehiscence in dura .
  68. 68. 71meningitis:It is also known as Leptomeningitis.(only thepiamater and arachnoid are involved). Thisis a major and serious complication ofmiddle ear infection. Nowadays, recovery isusual provided early diagnosis and prompttreatment is initiated.. Childhood otogenicmeningitis is commonly caused by acutemiddle ear infections … it is a frequentcomplication of chronic middle ear disease.
  69. 69. 72meningitis. Spread to the meninges may occur via anyof the dehicences in the bony barrier orpreformed channels or suppurativelabyrinthitis . Rarely rupture of brainabscess into the subarachnoid space maylead on to meningitis.
  70. 70. 73causative organisms in meningitis:acute infection :H. Influenza type B, and Strep. pneumoniaetype III.chronic ear diseases :gram negative enteric organisms, proteus,and psuedomonas. Anaerobes andbacteriodes have also been reported.
  71. 71. 74 Pathogenèses of meningitisThe initial inflammatory response of the pia arachnoidto infection is an outpouring of fluid into thesubarachnoid space, with a rise in CSF pressure. TheCSF becomes permeated with white blood cells andrapidly multiplying bacteria. These bacteria feed onglucose present in the CSF reducing its level in CSF acharacteristic finding in meningitis. Pus initiallyaccumulates in the basal cisterns, and more rarely inthe vertex. The free flow of CSF is impeded by theexudate obstructing the ventricular foramina to causea non communicating hydrocephalus.
  72. 72. 75 Pathogenèses of meningitisObstruction to CSF in the subarachnoid spaces maycause communicating hydrocephalus. Irritation of theupper cervical nerve roots by the exudate cause neckpain and neck stiffness which are the characteristicfeatures of this condition. Exudates around the exitforamina of cranial nerves could cause nerve palsiesduring the late stage of the disease. Spread ofinfection through virchow robin spaces into the brainsubstance may lead to the formation of brain abscess
  73. 73. 76Clinical features of meningitis: - headache and neck stiffness. At first the headache localised to the side of the affected ear but later it could become generalised and bursting in nature. - malaise and pyrexia. Initially neck stiffness shows resistance only to flexion, but later full rigidity or retraction may develop. During early stages the patient may have mental hyperactivity and restlessness.
  74. 74. 77Clinical features of meningitis:• Tendon reflexes becomes exaggerated during this stage. Photophobia is another constant presenting feature, and the patient may be prompted to lie curled up away from the light. Vomiting projectile in nature is another important feature. As the condition worsens the symptoms also become progressively severe. When neck stiffness is marked the patient may manifest poitive kernigs sign. The stiffness may become more severe enough to cause opisthotonus.
  75. 75. 78 Diagnosis of meningitisexamination of CSF..increased white cellsreduced glucose levels from 1.7-3 mmol/l to 0..Chloride content may fall from 120 mmol/l to80mmol/l.Bacteria may also be isolated from the CSF. Recently polymerase chain reaction have been usedto detect bacterial DNA from CSF.
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  78. 78. 81mastoiditis
  79. 79. 83 Clinical presentation of mastoiditis1- masked mastoiditis :- mild discomfort in the ear with or without mastoid tenderness .- may exist with or without bone destruction .
  80. 80. 84 Clinical presentation of mastoiditis2- obvious mastoiditis( mastoiditis with subperiosteal abscess ) .- mastoid tenderness .- pain.- swelling .- anteroinferior displacement of the ear .- Spread to neck through incisura digastrics , ( Bezold ‘s abscess )- spread under temporalis muscle through external auditory canal ( Luc’ s abscess )
  81. 81. 85 Clinical presentation of mastoiditisN.B.Mastoiditis may occur alone but often result in a silent accumulation of extradural abscess , or granulation tissue .
  82. 82. 86Acute mastoiditis in children and adult
  83. 83. 87Acute otitis media with mastoiditis + Bulged ear drum
  84. 84. 88Acute otitis media complicated with mastoiditis (left)
  85. 85. 89Right coalescent mastoiditis
  86. 86. 91Less obvious complications1- subdural abscess .2- otitic hydrocephalus .3- petrositis .
  87. 87. 92Subdural abscess
  88. 88. 93Subdural abscess (Empyema):• Spread of infection breaches the dura it exposes the subdural space to the perils of the infection. It may initially be associated with Leptomeningitis, or if the infection is contained as subdural effusions or subdural abscess –• extremely rare .• devastatingly obvious by coma and focal neurological signs .
  89. 89. 94Pathogenesis of Subdural Abscess• Spread of infection breaches the dura it exposes the subdural space to the perils of the infection. The granulation tissue which develops on the inner side of the dura obliterates the subdural space.• Initially seropurulent effusion develops in the subdural space, and eventually this becomes frankly purulent.• The spread of this effusion is limited by the granulation tissue which attempts to obliterate the subdural space.
  90. 90. 95 Pathogenesis Subdural Abscess• The subdural pus tends to accumulate near the falx cerebri, that too particularly where it joins the tentorium cerebelli. Healing is always associated with fibrosis and obliteration of the subdural space in the area where granulation was present.• The cortical veins in the adjacent area may become involved by thrombophlebitis. This may also produce multiple small abscess in the brain adjacent to the area of subdural infection. One or numerous multiloculated abscesses over the convex surface of the cerebral hemispheres may be seen. Commonly Non haemolytic streptococci have been implicated
  91. 91. 96 Clinical features of subdural abscessheadache and drowsiness.Focal neurological symptoms like irritative fits andparalysis. Fits are usually of Jacksonian type, starting locallyand spreading to affect one side of the body this isusually caused by cortical thrombophlebitis. Paralysis may start with one upper or lower limb andmay gradually become hemiplegia. If dominant lobe is involved aphasia develops.Papilloedema is highly uncommon, and similarlypalsies involving individual cranial nerves are alsorare.
  92. 92. 97 Clinical features of subdural abscessMeningism may accompany headache, distinguishedfrom meningitis by the presence of characteristicneurological localising signs. In children suspected of meningitis, subduralempyema should be considered if there is noresponse to treatment, or if motor seizures occur.
  93. 93. 98 Diagnosis of subdural abscess•CT scan is diagnostic.• M.R.I. is diagnostic ( easily )•CSF examination :•CSF pressure may be elevated,•the sugar contents are normal ,• the cultures are invariably sterile.• In places where CT scan facilities are unavailable exploratory burr holes may be made to clinch the diagnosis•.
  94. 94. 99Otitic hydrocephalus
  95. 95. 100 Otitic hydrocephalus Is one of the common complication of middle ear infection. It is a syndrome of raised intracranial pressure during or following middle ear infection. This condition is also known as Pseudotumor cerebri.The onset may occur many weeks after acute otitis media, or many years after the start of the chronic middle ear disease.usually associated with occlusive sigmoid sinus thrombophlebitis and extradural abscess .
  96. 96. 101 Pathogenesis of otitic hydrocephalus• The aetiology is unknown. The relationship of this condition with that of lateral sinus thrombosis has been documented.• The inference is that obstruction of the lateral sinus affects cerebral venous outflow, or the extension of the thrombus into the superior sagittal sinus impedes CSF resorption by pacchionian bodies.
  97. 97. 102Clinical presentation of otitic hydrocephalus Characteristically present with headache , some degree of lethargy , severe papilledema( blurred vision ) nausea ,vomiting , Lateral rectus palsy on one or both sides (stretching of the 6th nerve due to increased intracranial pressure ). C.T. is diagnostic
  98. 98. 103petrositis
  99. 99. 104 Clinical presentation of petrositis- rarely ,if ever , present without mastoiditis .- Intracranial complications are more frequent with petrositis .- Triad of Gradinigo :- ear infection .- ipsilateral retro – orbital pain .- abducent palsy .
  100. 100. 105Silent but exteremely serious complications i. Masked mastoiditis ii. Extradural abscess, or granulation tissue. iii. Dural venous sinus thrombophlebitis. iv. Brain abscess.
  101. 101. 106Extradural abscess
  102. 102. 107 Extradural abscess:Is always associated with involvement ofdura mater by the spreading disease,constituting pachymeningitis.This is commonly preceded by loss ofbone, either through demineralisation inacute infection or erosion bycholesteatoma in chronic disease..
  103. 103. 108 Extradural abscessIf the cholesteatoma is non infected it maysimply expose the dura without any inflammatoryreaction. If cholesteatoma is infected it is associated withformation of granulation tissue over the dura.Dura is tough and resists infection. It attempts to wall off the infection, andcollection of pus occur between the dura and thebone.This is known as extradural abscess and is thecommonest of all intracranial complications.
  104. 104. 109Figure showing extradural abscess
  105. 105. 110 Extradural abscessA middle cranial fossa extradural mass may stripthe dura from bone on the inner surface ofsquamous temporal bone.Such an enlarging mass may cause increasingintracranial tension, causing focal neurologicalsigns and papilloedema. Sometimes it could erodethe skull from inside to the exterior causing asubperiosteal abscess i.e. the classic Potts puffytumor. Rarely an extradural abscess may developmedial to the arcuate eminence over the petrousapex.
  106. 106. 111 Extradural abscessThis irritates the Gasserian ganglion of thetrigeminal nerve, and the 6th cranial nerve.This produces the classic Gradenigossyndrome (includes facial pain, diplopia andaural discharge). Posterior fossa extraduralabscess is limited by the attachments of thedura laterally to the sigmoid sinus.Posterior extension of this abscess aroundthe sigmoid sinus produces the perisinusabscess. This could also extend to the neckthrough the jugular vein
  107. 107. 112 Clinical feature of extradural abscessDepends on the site of the abscess, its size,duration and rate of development. In mostpatients the symptoms are vague, and nonspecific. Sometimes it could be a incidentalfinding during mastoid surgery. The commoncomplaint of the patient being headacheaccompanied by malaise. If the abscesscommunicates with the middle ear the patientmay have interim relief following an episodeof aural discharge.
  108. 108. 113Extradural abscess, or granulation tissue• May occur in case of cholesteatoma.• Often result from mastoiditis.• Site:1. In the middle fossa at the tegmen.2. Along extraluminal surface of the lateral wall of the sigmoid sinus.
  109. 109. 114Lateral sinus thrombosis
  110. 110. 115Dural venous sinus thrombophlebitis• Begins as silent non-occluding phlebitis of the sinus wall and induced mural thrombus, sigmoid sinus thrombophlebitis.• NB:Sigmoid sinus thrombophlebitis & Extradural granulation tissue should be thought preoperatively and intraoperatively in every case of suspected or operated mastoiditis
  111. 111. 116 Lateral sinus thrombosis:Thrombophlebitis can develop in any of the veinsadjacent to the middle ear cavity. Of these the lateralsinus, which comprise of the sigmoid and transversesinuses is the largest and most commonlyaffected.Formerly it was commonly associated with acute otitismedia in childhood; now it is commonly seen in patientswith chronic ear disease. In the preantibiotic era thecommonest infecting organism was beta hemolyticstreptococci. This organsim was known to causeextensive destruction of red blood cells causing anaemia.Now a days the infection is by a mixed flora
  112. 112. 117Fig showing the various stages of lateral sinus thrombosis
  113. 113. 118 Pathogenèses of latéral sinus thrombosIsLateral sinus thrombosis is usually preceded by anextradural perisinus abscess.The mural thrombus partly fills the sinus.The clot progressively expands and eventually occludethe lumen.The clot may later become organised, and partly brokendown and may even be softened by suppuration.During this stage there is a release of infecting organismand infected material into the circulation causingbacteremia, septicemia and septic embolisation
  114. 114. 119 Pathogenesis of lateral sinus thrombosisExtension to the confluence of the sinuses,and to the superior sagittal sinus. Invasion of the superior and inferior petrosalsinuses may cause the infection to spread tothe cavernous sinus.This spread into the brain substance accountsfor the very high association of with brainabscess. Downward progression of thrombus into andthrough the internal jugular vein can reach thesubclavian vein.
  115. 115. 120 Clinical features of lateral sinus thrombosis :.The patients manifest with severe fever, wasting illness inassociation with middle ear infection. The fever is high andswinging in nature, when charted it gives an appearance of Picketfence. It is always associated with rigors. The temperature rose rapidly from 39 - 40 degree Centigrade.Headache is a common phenomenon, associated with neck pain.The patient appear ematiated and anaemic.When the clot extended down the internal jugular vein, it will beaccompanied by perivenous inflammation, with tendernessalong the course of the vein. This tenderness descended downthe neck along with the clot, and would be accompanied byperivenous oedema or even suppuration of the jugularlymph nodes.
  116. 116. 121 Clinical features cont. :Perivenous inflammation around jugular foramen cancause paralysis of the lower three cranialnerves.Raised intracranial pressure produce papilloedemaand visual loss.Hydrocephalus could be an added complication ifthe larger or the only lateral sinus is occluded by thethrombus, or if the clot reaches the superior sagittalsinus. Extension to the cavernous sinus canoccur via the superior petrosal sinus, and may causechemosis and proptosis of one eye.
  117. 117. 122 Clinical feature cont. :If circular sinus is involved it could spread to theother eye. The propagation of the infected embolimay cause infiltrates in the lung fields, and mayalso spread to joints and other subcutaneoustissues.. These distant effects usually developedvery late in the disease, these could be the presentingfeatures if the disease is insiduous in onset. Maskingby antibiotics could be one of the causes. Patientsalways feel ill, and persisting fever is usual.
  118. 118. 123Clinical features cont. :The patients may have ear ache, in association withmastoid tenderness, and stiffness along thesternomastoid muscle.The presence of anaemia is rare now a days.Papilloedema is still a common finding. Othercoexisting intracranial complications must be expected inmore than 50 percent of patients.
  119. 119. 124 Clinical features cont. :.Extension of infected clot along the internal jugular vein isalways accompanied by tenderness and oedema along thecourse of the vein in the neck, and localised oedema over thethrombosed internal jugular vein may still be seen. One rare finding is the presence of pitting oedema over theoccipital region, well behind the mastoid process, caused byclotting within a large mastoid emissary vein, this sign is known asthe Griesingers sign. Infact there is no single pathognomonic sign for lateral sinusthrombosis and a high index of suspicion is a must indiagnosing this condition
  120. 120. 125Investigations of lateral sinus thrombosis :A lumbar puncture must be performed, ifpapilloedema does not suggest that raised intracranialpressure may precipitate coning.Examination of CSFIn uncomplicated lateral sinus thrombosis the whiteblood count in the CSF will be low when the cause ischronic middle ear disease, and somewhat raised inacute otitis media.The CSF pressure is usually normal.The variations in the level of CSF proteins and sugar arenot useful.
  121. 121. 126Investigations cont. :Queckenstedt test: This is also known as Tobey - Ayertest. This is recommended whenever lumbar puncture fora possible intracranial infection is performed.The test involves measurement of the CSF pressure andobserving its changes on compression of one or bothinternal jugular veins by fingers on the neck. In normalhumans compression of each internal jugular vein in turnis followed by an increase in CSF pressure, of about 50 -100mm above the normal level. When the pressure overthe internal jugular vein is released then there is a fall inthe CSF pressure of the same magnitude
  122. 122. 127CT scanning:It may show filling defects within the sinus, andincreased density of fresh clots. When contrast materials like Iothalamate (conray) isused failure of opacification of the affected lateral sinusmay become evident. The presence of septic thrombosis shows intenseinflammatory enhancement of the sinus walls and of theadjacent dura. This enhancement of the walls, but not ofthe contents of the sinus constitutes the empty triangleor delta sign. It can also exclude accompanying complications likebrain abscess and subdural empyema.
  123. 123. 128Angiography :It helps to demonstrate the obstruction, its site and theanatomical arrangement of the veins.There is animpending risk of displacing the infected thrombusArteriography:Performed with radio opaque dye injected into the carotidartery can show the venous outflow during the venousphase. This can be clearly visualised in digital subtractionangiography.This technique involves precise superimposition of anegative arteriogram on a positive film of bone structures.This effectively cancels out the skeletal image thus clearlyrevealing the vascular pattern.
  124. 124. 129MRI:Is sufficiently diagnostic hence angiography canbe avoided if MRI could be taken. Established thrombus shows increased signalintensity in both T1 and T2 weighted images.MRI can also be used to show venous flow.Gadolinum enhancement may show a delta signcomparable with that seen on CT scans
  125. 125. 130MR venogram that shows nonfilling of the lateral sinus on the left side
  126. 126. 131Brain abscess
  127. 127. 132Otogenic brain abscess always develop in thetemporal lobe or the cerebellum of the same sideof the infected ear. Temporal lobe abscess is twice as common ascerebellar abscess.In children nearly 25% of brain abscesses areotogenic in nature, whereas in adults who are moreprone to chronic ear infections the percentagerises to 50%.The routes of spread of infection :Retrograde thrombophlebitis of cerebral orcerebellar veins from inflammed sigmoid sinus orother adjacent dural sinuses ..the commonest being the direct extension throughthe eroded tegment plate.
  128. 128. 133Although dura is highly resistant toinfection, local pachymeningitis may befollowed by thrombophlebitis penetratingthe cerebral cortex, sometimes the infection could extent viathe Virchow - Robin spaces in to thecerebral white matter. Cerebellar abscess is usually preceded bythrombosis of lateral sinus.Abscess in the cerebellum may involve thelateral lobe of the cerebellum, and it maybe adherent to the lateral sinus or to apatch of dura underneath the Trautmannstriangle.
  129. 129. 134
  130. 130. 135 Stages of formation of brain abscess:Stage of cerebral oedema: This is infact the first stage of brain abscessformation. It starts with an area of cerebral oedema andencephalitis. This oedema increases in size withspreading encephalitis.Walling off of infection by formation of capsule:Brain attempts to wall off the infected area with theformation of fibrous capsule. This formation of fibroustissue is dependent on microglial and blood vesselmesodermal response to the inflammatory process.This stage is highly variable. Normally it takes 2 to 3weeks for this process to be completed.
  131. 131. 136 Stages of formation of brain abscess:Liquefaction necrosis: Infected brain within the capsule undergoesliquefactive necrosis with eventual formation of pus.Accumulation of pus cause enlargement of theabscess.Stage of rupture: Enlargement of the abscess eventually leads torupture of the capsule containing the abscess and thismaterial finds its way into the cerebrospinal fluid asshown in the above diagram.
  132. 132. 137 Pathological stages of Brain abscess1. Invasion( cerebritis):SymptomsVague,mild headache, lethargy, malaise for several days then resolve.2. Localization : quiescence & latency.Symptoms: totally silent for weeks3. Enlargement :in which most abscesses manifest with seizures or focal neurological signs.4. Termination: the abscess catastrophically rupture into the ventricle or subarachnoid space.
  133. 133. 138Pathological stages of Brain abscessNB: brain abscess detected few weeks from onset either clinically or radiologically. It is prudent to look for brain abscess in case of mastoiditis initially and again 3-4 weeks later
  134. 134. 139 The focal features of cerebellar abscess:Weakness and muscle incoordination on the same side of the lesion. Ataxia causes the patient to fall towards the side of the lesion.Intention tremors which may become manifest by the finger nose test.Spontaneous nystagmus.Dysdiadokinesis is also positive in these patients.
  135. 135. 140Abscess in the cerebellum involves the lateral lobe of the cerebellum
  136. 136. 141 The focal features of Cerebral (Temporo sphenoidal abscess):Nominal aphasia, where the cerebral abscess in the dominant hemisphere .Visual field defects arise from the involvement of optic radiations. Commonly there is quadrantic homonymous hemianopia, affecting the upper part of the temporal visual fieldsThe visual field loss are on the side opposite to that of the lesion. This can be assessed by confrontation method.Upward development affects facial movements on the opposite side, and then progressively paralysis of the upper and lower limbs.Paralysis first affects the leg , then arm and finally the face , if the expansion occur in inward direction .
  137. 137. 142
  138. 138. 143 Investigations for brain abscess :CT scan and MRI scans with contrast media.Reveal the position and size of the abscess,the presence of localised encephalitis can bedistinguished from that of an encapsulated abscess.Associated conditions such as subdural abscess, andlateral sinus thrombosis can also be seen.Lumbar puncture:Is frought with danger because of the risk of coning.Lumbar puncture must be performed in these patientsonly in a neurosurgical unit where immediateintervention is possible if coning occurs
  139. 139. 144 Diagnosis of complicationsin acute otitis media
  140. 140. 145 Diagnosis of complications in acute otitis media1. History & physical examination: In history , look for symptoms :i. Suggesting impending complicationsii. Retro-orbital or deep boring head painiii. Lethargy, headache or both, currently and with the past 2 months.
  141. 141. 146 DiagnosisIn physical examination , look for signs :i. Suggesting impending complicationsii. Diagnostic of obvious complicationsiii. Catastrophic neurologic disease.iv. Fuduscopic examination for papilledema.
  142. 142. 147 Early finding associated with impending or established intratemporal or itracranial complications1. Pain & fever ˃ 4 days despite appropriate ttt for AOM2. Persisting fever & headache.3. Radiographic evidence of a lytic lesion4. Presence of anaerobes.5. Excessive granulation tissue at surgery associated with CSOM.6. Chronic SOM with fever , headache , ear pain or vertigo.7. Increasing otorrhea, meningeal signs , or impairment of consciousness.8. Headache with vomiting in patient with CSOM
  143. 143. 148Diagnosis (cont.) 2. When a complication is suspected , high resolution C.T. for temporal bone and associated brain with or without contrast infusion is indicated. MRI is indicated if bone eroded over sigmoid sinus or at the tegmen.
  144. 144. 149
  145. 145. 150
  146. 146. 1511. Normal transverse cross sectional anatomy ofthe temporal bone at consecutive levels frombottom to top.A) Junction between the hypotympanun and themesotympanun at the level of the round windowniche (2). The tensor tympani muscle can beseen extending towards the handle of themalleus (6) and the tympanic membrane.B) At the level of the basal turn of the cochlea(3) forming the promontory which is part of themedial wall of the mesotympanum.C) At the level of the internal auditory meatus(17) and the oval window (15). Thesuprastructures of the stapes can be seen (8).D) Epitympanon (20) housing the head of themalleus (6) and the incus (7). The horizontalportion of the facial nerve canal is passingunderneath the lateral semicircular canal.E) Epitympanon (20) at the level of the lateralsemicircular canal (18) and the aditus ad antrum(22).F) Cross section of the two limbs of the superiorsemicircular canal (18) at the level of the tegmentympani.
  147. 147. 152
  148. 148. 153 Advantages of MRI over C.T1. It is more sensitive in detecting early cerebritis & cerebral edema.2. It is the most sensitive diagnostic tool in identifying the site & size of epidural, subdural , and brain edema or abscess.3. It is more sensitive in detecting extraparenchymal spread to subarachnoid space or ventricle4. If mastoiditis or sigmoid sinus phlebitis is surgically proven, repeat MRI is indicated 3-4 weeks post operatively to detect subsequent development of an occult brain abscess.
  149. 149. 154 diagnosis• Angiography: is a definitive investigation of lateral sinus thrombosis. It helps to demonstrate the obstruction, its site and the anatomical arrangement of the veins. There is an impending risk of displacing the infected thrombus.• Arteriography: performed with radio opaque dye injected into the carotid artery can show the venous outflow during the venous phase. This can be clearly visualised in digital subtraction angiography. This technique involves precise superimposition of a negative arteriogram on a positive film of bone structures. This effectively cancels out the skeletal image thus clearly revealing the vascular pattern.
  150. 150. 155Apex petrositis in a 50-year-old woman with Gradenigo syndrome atclinical evaluation. (a) Axial T1-weighted MR image shows an irregularlesion at the tip of the petrous apex (arrow). (b) Contrast-enhancedaxial T1-weighted MR image shows right-sided apex petrositis as anenhancing lesion along the courses of cranial nerves V and VI (arrow).
  151. 151. 156 Diagnosis (cont.)3. Funduscopic examination: in case of suspected meningitis or otitic hydrocephalus. or intracranial abscess.4. Lumber puncutre: in case of suspected meningitis or otitic hydrocephalus.• Finding in meningitis: high protein, low glucose level, presence of micro-organisms on Gram’s stain.• Finding in otitic hydrocephalus: normal protein & glucose levels, -ve gram’s stain & elevated opening pressure.5. Surgical exploration.
  152. 152. 157 Treatmentof complications of acute otitis media
  153. 153. 158Treatment of complications of acute otitis media For all complications: i. Admission ii. I.V. antibiotics iii. Surgical intervention.
  154. 154. 159 I. Acute coalescent mastoiditis and masked mastoiditis with or without subperiosteal abscess:Wide myringotomy, complete canal wall up mastoidectomy, and wide facial recess to maintain the aditus & antrum patent.
  155. 155. 160II. Petrositis :Total resection of tympanic membrane ossicles insitu with resection of posterosuperior canal wall (Modified radical mastoidectomy).Later on reconstruction of the tympanic membrane in healed ear.NB:If persistent infection: middle fossa app. combined with lat. app.
  156. 156. 161III. Chronic mastoiditis:Canal wall up or canal wall down procedure.reconstruction of the middle ear at the same setting.NB: during mastoidectomy for suppurative disease, inspection of the dura of the tegmen, sigmoid sinus, and facial nerve through thin bone is crucial. To avoid leaving unrecognized and untreated granulation tissue.
  157. 157. 162IV. Labyrinthitis (acute) :Myringotomy.V. Labyrinthitis in C.S.O.M with or without cholesteatoma:Tympanoplasty and mastoidectomy.If fistula is in the cochlea, better to leave the chlesteatoma matrix on the fistula, remove it after healing.If fistila in semicircular canals, the chlesteatoma matrix carefully removed and fascia placed over the fistula. But if matrix attache to membranous labyrinth, matrix left and removed later.As suppurative labyrinthitis may soon associated with meningitis, hospitalization and IV antibiotics continued until infection eradicated
  158. 158. 163VI. Facial paralysis : Myringotomy.(in acute infection).Facial paralysis in chronic or subacute infection:Mastoidectomy to eradicate disease & to explore the fallopian canal for invasive granuloma.
  159. 159. 164
  160. 160. 165Myringotomy with ventilation tube insertion
  161. 161. 166VIII.Extradural granulation tissue: wide exposure of abnormal dura, careful attempt to bluntly remove excess granulation tissue.
  162. 162. 167Extradural abscessSurgery must be done as early as possible.Drainage into the mastoid. If abscess isencountered, canal wall up should be takendown so that complete drainage is ensured.Granulation tissue over the dura should notbe disturbed because it could breach theonly defence and the infection could spreadto the brain.
  163. 163. 168
  164. 164. 169IX. Dural venous thrombophlebitis: Complete mastoidectomy. I.V antibiotic Reduce I.C pressure by : hyperventilation, therapeutic lumber puncture, mannitol & dexamethazone. Careful opening of sinus to explore for intraluminal abscess, drained into mastoid . or intraluminal fibrotic, non abscessing mural thrombus. If bleeding occur with sinus opening, can be controlled with extraluminal piece of surgical , a piece of fascia may be placed lateral to surgical.
  165. 165. 170IX. Dural venous thrombophlebitis ( contin.): Internal jugular vein ligation: if continuing sepsis, extension of thrombus, pulmonary complication with contiunous spiking fever. Anticoagulants & thrombolytics: if associated with otitic hydrocephalus. Direct intrasinus thrombolytic ttt with urokinase and streptokinase: in case with progressive neurologic deterioration with evolution of thrombus, transvenosus.
  166. 166. 171X. Brain abscess: ttt under the guidance of neurosurgery. Empiric ttt with penicillin or β-lactam antibiotic, chloramphenicol, and metronidazole and IV dexamethazone. Mannitol ,hyperventilation (to decrease I.C.P) Burr hole aspiration and stereostatic drainage. Serial stereostatic aspiration (procedure of choice) Concurrent craniotomy and mastoidectomy. Avoid reinfection , results in a single , shorter hospital stay.
  167. 167. 172 Repeated aspiration arepreferred to complete excision 1. Multiple abscesses in deep or dominant location. 2. With concomitant meningitis with early response to antibiotics 3. Abscesses <3cm
  168. 168. 173XI. Otitic hydrocaphalus: ttt mastoiditis, extradural granulation & sigmoid sinus thrombophlebitis. Most cases resolve spontaneously in months ttt with acetzolamide and furosemide or systemic steroid. Lumoperitoneal shunt: for patient with deterioration of vision or for patient with disabling pulsatile tinnitus. Ophthalmologist follow the patient’s vision. Long term care of intracranial hypertension by neurologist.NB: Blindness or brain herniation are serious concerns.
  169. 169. 174XII.Subdural abscess: ttt under the guidance of neurosurgery. ttt : I.V antibiotics, anticonvulsants and steroids. Neurosurgical drainage with mastoidectomy may be done together or sequentially. Surgical control of mastoiditis, extradural granulation or abscess , and sigmoid sinus thrombophlebitis is crucial for recovery.
  170. 170. 175XIII.Meningitis : Appropriate I.V antibiotics and dexametasone. Myringotomy.NB: meningitis from CSOM (pus directly from ear into subarachnoid space) Radical mastoidectomy with exploration of all dural surfaces directly or through thin bone is necessary. Repair dural defect with fascia placed intradurally and extradurally.
  171. 171. ‫النساء :‬ ‫{ .... وعلمك ما لم جكه جعلم وكان فضل هللا علُك عظُما }‬ ‫311‬
  172. 172. ‫اجلاثية : 63‬ ‫{فلله احلمد رب السموات ورب األرض رب العاملني}‬
  173. 173. 178 THANK YOU Dr, IBRAHIM HABIB BARAKAT,M.D. ( Otorhinolaryngology )