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COMPLICATIONS OF OTITIS MEDIA.pptx
- 2. HISTORICAL NOTES ● Hippocrates (460 B.C) “Acute pain of the ear with continued high fever is to be dreaded for the patient may become delirious & die”
- 3. ● Roman physicist celcus (25 AD) “Inflammation & pains of the ear lead sometimes to insanity & death”. ● Arabian physician Avicenna (980-1037 AD) stated that the ear discharge was due to the brain disease. ● Morgagni (1682-1771), noted that the ear infection comes first before the brain abscess. ● McEwen in 1881 showed great surgical success - 18 patients recovered out of 19 operated cases of brain abscess.
- 4. Factors influencing development of complications ● Infective organism ● Virulence ● Susceptibility to antibiotics ● Adequacy of medication ● Resistance of host ● Type of pneumatization ● History of previous otitis media.
- 5. DEFENSE MECHANISM ● Ability of mucous membrane to localise & overcome infection. ● Intact bony walls of tympanic cavity & pneumatic cells. ● Granulation tissue.
- 6. PATHWAYS OF SPREAD OSTEO THROMBOPHLEBITIS BONE EROSION PREFORMED PATHWAYS
- 7. OSTEOTHROMBOPHLEBITIS ➢ Infection pass from lining mucosa of the middle ear & mastoid through intact bone by progressive thrombophlebitis of small venules. ➢ Occur in acute middle ear infection or acute exacerbations of chronic infection. ➢ Complication occurs early. ➢ Prodromal period is lacking. ➢ Bony walls of the middle ear & mastoid is intact. ➢ Bone & mucoperiosteum lining of mastoid air cells are inflamed and bleed easily.
- 8. BONE EROSION ➢ Nearly always the manner of spread in COM. ➢ Complication occurs several weeks later. ➢ A prodromal period of partial or intermittent involvement precedes diffuse involvement. ➢ At operation, dehiscence of the bony barrier is found. ➢ A layer of granulation cover the exposed soft tissue of neighbouring structure. ➢ Treatment should always include the removal of suppurating, bone eroding focus.
- 9. PREFORMED PATHWAYS ● Normal anatomical pathways. ● Developmental dehiscence. ● Acquired.
- 10. COMPLICATIONS ● MENINGITIS ● OTOGENIC BRAIN ABSCESS ● OTOGENIC SUPPURATIVE THROMBOPHLEBITIS ● OTITIC HYDROCEPHALUS ● SUBDURAL EMPYEMA ● EPIDURAL (EXTRADURAL) ABSCESS
- 12. MENINGITIS ❖ MC intracranial complication of otitis media. ❖ Spreads directly through necrotic bone of middle ear. ❖ As a complication of suppurative labyrinthitis, through Internal Acoustic meatus, vestibular & cochlear aqueducts.
- 13. contd... Pia-arachnoid inflamed Outpouring of fluid in the subarachnoid space Raised intracranial pressure White blood cells & multiplying organisms in CSF Irritation of upper cervical nerve roots
- 15. symptoms: ❖ Headache ❖ Fever ❖ Vomiting ❖ Photophobia ❖ irritability ❖ Neck pain ❖ Stiffness ❖ General hyperesthesia
- 16. SIGNS: ❖ KERNIG SIGN ❖ BRUDZINSKI SIGN
- 17. INVESTIGATIONS ❖ HRCT. ❖ MRI with gadolinium contrast. ❖ Lumbar puncture ➢ Turbid,purulent ➢ Glucose nearly to zero ➢ Protein content ➢ Polymorphs in CSF ➢ Gram staining ➢ Culture & sensitivity.
- 18. TREATMENT ❖ HIGH DOSE ANTIBIOTICS ➢ Empirical therapy: 3rd generation cephalosporins + vancomycin. ❖ CORTICOSTEROIDS ➢ A 4 day regime of 0.6 mg/kg/day in four divided doses started before or with the antibiotics. SURGERY : surgical exterenation of the diseased mastoid once patient is stabilised.
- 19. OTOGENIC BRAIN ABSCESS ➢ Focal suppurative process within the brain parenchyma surrounded by a region of encephalitis. ➢ Often the result of venous thrombophlebitis rather than direct dural extension. ➢ Can occur in temporal lobe or cerebellum. ➢ Polymicrobial culture including anaerobes: ○ Gram +ve-> streptococcus & staphylococcus species ○ Gram -ve -> E coli, proteus, klebsiella & pseudomonas. ○ Anaerobic -> bacteroides.
- 20. STAGES
- 21. SYMPTOMS ● GENERAL : toxic, drowsy, deep bony pain, triad of headache, high grade fever, focal neurological deficits,papilloedema. ● TEMPORAL LOBE ABSCESS: ○ seizures. ○ Nominal aphasia. ○ Quadrantic Homonymous hemianopia. ○ Motor paralysis of contralateral side. ● CEREBELLAR ABSCESS: ○ Ataxia. ○ Nystagmus. ○ Dysmetria. ○ Dysdiadochokinesia.
- 22. INVESTIGATIONS CT BRAIN WITH CONTRAST: RING SIGN -
- 23. TREATMENT ➢ MEDICAL ○ High dose IV broad spectrum antibiotics ○ Dexamethasone ○ Anti epileptic- phenytoin. ➢ SURGICAL: ○ Neurosurgical intervention of draining the abscess is quintessential ○ Once the patient is stable , mastoidectomy can be done.
- 24. OTOGENIC SUPPURATIVE THROMBOPHLEBITIS ➢ Simultaneous presence of venous thrombosis & suppuration in the intracranial cavity. ➢ Often associated with perisinus extradural abscess. ➢ Can also occur by osteo thrombophlebitic extension via small venules. ➢ The infected mural thrombus can extend cranially to sagittal sinus or cavernous sinus via superior & inferior petrosal sinus. ➢ It can also extend caudally to Internal Jugular vein thereby to the right atrium.
- 27. PATHOGENESIS Erosion of the bone covering the sigmoid sinus Immune status of host osteothrombophlebitic extension Perisinus abscess/inflammation Inflammation of outer wall (dura) of sinus Inflammation of intima (inner wall of sinus) Platelet, RBCs,fibrin,WBCs Adhere to inflamed area MURAL THROMBUS Mural thrombus propagates, obliterating lumen
- 28. CLINICAL FEATURES ➢ Picket fence fever, with diurnal temp exceeding 103℉ ➢ Headache ➢ Griesinger ’s sign ➢ Papilloedema ➢ Vision loss ➢ Tenderness along the anterior border of sternomastoid muscle ➢ Proptosis & chemosis - CST ➢ Otalgia ➢ Queckenstedt or Tobey-ayer test.
- 30. INVESTIGATION ➢ Blood culture ➢ Lumbar puncture test ➢ CECT - DELTA “𝚫” sign in lateral sinus thrombosis ➢ MR angiography.
- 31. TREATMENT ➢ High dose antibiotics ➢ Anticoagulation if CST present. ➢ Surgical exploration & removal of clot. ➢ Internal jugular vein ligation.
- 32. OTITIC HYDROCEPHALUS ➢ Raised intracranial pressure with normal CSF findings. ➢ Benign raised intracranial tension. ➢ Commonly associated with sigmoid sinus thrombosis. ➢ Spontaneous recovery.
- 33. MECHANISM ➢ SYMOND: retrograde extension of thrombophlebitis from sigmoid sinus to superior sagittal sinus Blockage of arachnoid villi CSF absorption & secretion ➢ Increase in CSF volume ➢ Secondary to brain edema ➢ Disruption in venous circulation.
- 34. CLINICAL FEATURES ➢ Headache ➢ Drowsiness ➢ Vomiting ➢ Blurring of vision ➢ Diplopia ➢ Papilloedema ➢ 6th cranial nerve palsy ➢ Optic atrophy
- 35. INVESTIGATIONS ➢ LUMBAR PUNCTURE ○ Elevated CSF pressure with normal biochemistry. ○ Done with caution. ➢ CT SCAN ➢ MRI: ○ Imaging modality of choice. ○ Allows superior evaluation of venous sinuses.
- 36. TREATMENT ➢ Eradicate ear disease. ➢ Lowering of CSF pressure: ○ Decompression of sigmoid sinus. ○ CSF drainage procedures. ○ Optic sheath decompression : to prevent optic atrophy. ➢ MEDICAL: ○ Corticosteroids. ○ Mannitol. ○ Acetazolamide. ○ Diuretics.
- 37. EPIDURAL (EXTRADURAL) ABSCESS ➢ Occurs after bone demineralisation or bone erosion adjacent to the middle or posterior fossa sura. ➢ Middle fossa extradural abscess: ○ Lateral: erosion of tegmen tympani, strip a large area of dura from the inner surface of squamous temporal bone. ○ Medial: infection of petrous apex causes middle fossa extradural abscess medial to arcuate eminence, irritates trigeminal nerve & 6th cranial nerve. ( gradenigo syn). ➢ Posterior fossa extradural abscess: ○ In close association with lateral sinus. ○ Spread is laterally limited by internal acoustic meatus.
- 38. CLINICAL FEATURES ➢ Usually asymptomatic ➢ Gradenigo syndrome: ○ Otorrhea ○ Retro orbital pain ○ Diplopia ➢ Persistent headache on the side of otitis media. ➢ General malaise with low grade fever. ➢ Disappearance of headache with free flow of pus from the ear ( spontaneous abscess drainage).
- 39. ➢ DIAGNOSIS: Contrast enhanced CT or MRI. ➢ TREATMENT: Antimicrobial therapy. Surgical exploration.
- 40. SUBDURAL EMPYEMA ➢ Collection of pus between dura and arachnoid mater. ➢ Spread of infection through the dura with formation of granulation tissue in the subdural space.
- 41. PATHOLOGY: OTITIS MEDIA EROSION OF TEGMEN BRAIN ABSCESS THROMBOPHLEBITIS EROSION OF DURA BRAIN ABSCESS RUPTURES INFECTION IN SUBDURAL SPACE EXPANDING MASS LESION
- 42. CLINICAL FEATURES ➢ Meningeal irritation: ○ Fever. ○ Headache. ○ Malaise, drowsiness. ○ Kernig sign ➢ Thrombophlebitis: ○ Aphasia ○ Hemianopia ○ Hemiplegia ○ Jacksonian convulsions ➢ Raised ICP ○ 3rd nerve involvement ○ papilloedema
- 43. DIAGNOSIS by CT or MRI ➢ TREATMENT: ○ Surgical drainage of abscess. ○ High dose IV antibiotics. ○ Once stabilised neurologically, then underlying ear disease managed. ○ Antiepileptic medication
- 44. Extracranial (intratemporal) complications ● Mastoiditis ● Petrositis ● Labyrinthitis ● Facial paralysis
- 45. Extracranial ( extratemporal) complications ● Subperiosteal abscess ● Bezold’s abscess ● Zygomatic ( Luc’s abscess/Meatal) ● Digastric ( Citelli’s abscess)
- 46. ACUTE MASTOIDITIS ● It is the extension of middle ear inflammation into antrum & mastoid air cells. ● Mastoid antrum & epitympanum communicate freely through aditus ad antrum. ● Common in children. ● Causative organisms include strep. pneumoniae , strep pyogenes, staph aureus, Haemophilus influenzae, and pseudomonas aeruginosa.
- 47. Pathogenesis ● Following otitis media - tympanomastoiditis. ● Blockade of aditus - loculation of mucopurulent material within antrum and air cells. ● Persistent blockade of aditus - retrograde thrombophlebitis - edema and cellulitis of tissues overlying mastoid. ● If pus not drained - necrosis and demineralisation of bony trabeculae - ‘coalescent mastoiditis’. ● Where the entire mastoid becomes a single cavity filled with pus.
- 48. Clinical features Symptoms: ● Earache ● Fever ● Ear discharge - profuse and purulent Signs: ● Mastoid tenderness. ● Sagging of postero-superior meatal wall ● TM perforation ● Swelling, redness, bulging over the mastoid (ironed out mastoid) ● Hearing loss ( conductive)
- 49. investigations ● Aural swab for culture & sensitivity ● HRCT temporal bone
- 50. TREATMENT ● Hospitalization. ● IV antibiotics. ● Myringotomy. ● Cortical mastoidectomy.
- 51. Sequelae of acute coalescent mastoiditis ● Subperiosteal abscess ● Bezold’ abscess ● Citelli’s abscess ● Luc’s abscess ● Petrositis ● Labyrinthitis ● Facial paralysis ● Meningitis ● Brain abscess ● Sigmoid sinus thrombophlebitis.
- 52. Sites of pneumatization of mastoid air cell system in relation to types of mastoid abscess
- 53. MASKED MASTOIDITIS Slow destruction of mastoid air cells. Acute sign & symptoms of acute mastoiditis are absent. Inadequate antibiotic therapy - dose, frequency, duration. Pain, discharge, fever, mastoid swelling - absent. Mostly progress to complication. Mastoidectomy - extensive destruction of air cells Granulation tissue Dark gelatinous material filling the mastoid.
- 54. PETROSITIS Inflammation of pneumatized spaces of the petrous part of the temporal bone. Petrous bone - two groups of air cell tracts- communicate mastoid & middle ear to the petrous apex. Postero superior tract: in continuity with mastoid antrum, epitympanum that clusters around semicircular canals at the base of pyramid. Antero inferior tract: In continuity with the mesotympanum, protympanum, and hypotympanum & passes around the cochlea to petrous apex. Petrositis may be acute or chronic.
- 55. ● Acute petrositis ● Middle ear inflammation- antrum and mastoid air cells - medial progression involving petrous pyramid. ● If inflammatory products are retained- osteitis of petrous apex . ● Gradenigo syndrome - ● Ear discharge ● Retro Orbital pain (Trigeminal nerve) ● Diplopia ( lateral rectus palsy - Abducens nerve) ● Chronic petrositis ● In addition to inflammatory changes - new bone formation & resorption
- 56. Management : Investigations: ● CT temporal bone. Treatment : ● Systemic antibiotics. ● Radical mastoidectomy with skeletonization of semicircular canals to remove disease from middle ear and petrous apex. ● Approaches to petrous apex ● Eagleton’s approach. ● Thornwalt’s operation. ● Almoor’s approach. ● Ramadier’ s operation. ● Freckner’s operation.
- 57. Surgical approaches to petrous apex
- 58. FACIAL NERVE PARALYSIS Complication of both acute and chronic otitis media. ROUTES OF SPREAD: ● Natural dehiscence - dehiscence of fallopian canal. ● Natural pathways - ex, canal for stapedius, neurovascular bundle. ● Direct extension - ex, osteitis around fallopian canal. Toxins and ischemia probably have an ancillary role. TREATMENT: In AOM- myringotomy & appropriate antibiotic for 10 days. In COM - CWD mastoidectomy with decompression of the fallopian canal, antibiotics.
- 59. LABYRINTHITIS Inflammation of inner ear/ labyrinth. Pathogenesis: -spread through round window, fistula, preformed pathways. -inflammatory products pass into perilymph of scala tympani by diapedesis from adjacent labyrinthine vessels. - fibrillary precipitate accumulates in perilymphatic and endolymphatic spaces.
- 60. Symptoms & signs ● Vertigo ● Loss of balance ● nausea/ vomiting ● nystagmus ● High frequency SNHL ● Hearing distortion ● diplacusis
- 61. Treatment ● Complete bed rest - with restriction of head movement ● Parenteral chlorperazine / cinnarizine ● Dehydration - IV fluids. ● IV antibiotics. ● Acute infection - Myringotomy ● Chronic infection - mastoid exploration
- 62. Labyrinthine fistula Complication of COM Results from erosion of endochondral bone of bony labyrinth- movement of perilymph and structures of endolymphatic compartments when pressure in EAC changes. Most commonly - dome of lateral SCC. Cholesteatoma found in all cases. Incidence of fistula in cholesteatoma is 7-10%
- 63. symptoms/signs ● Short periods of imbalance. ● Vertigo ● Tullio’s phenomenon - feeling of imbalance on sudden exposure to loud noises. ● Fistula sign - positive. ● Investigations ● CT - erosion of lateral SCC ● cholesteatoma
- 64. Treatment Canal wall down mastoidectomy - All cholesteatoma is removed except for small area around fistula site. After careful removal of cholesteatoma debri without disturbing matrix. Matrix is elevated. A small piece of tissue / thin cap of bone placed over site and secured with fibrin glue / packing after the cholesteatoma is removed. - Risk of removing cholesteatoma from fistula is total / partial loss of hearing.
- 65. THANK YOU